[{"issue":"4","pmid":"1","publication_identifier":{"issn":["1436-6207","1436-6215"]},"citation":{"ieee":"I. Perrar <i>et al.</i>, “Circadian eating patterns track from infancy to pre- and primary school-age, but are not prospectively associated with body composition in childhood - Results of the DONALD cohort study.,” <i>Eur J Nutr</i>, vol. 64, no. 4, p. 165, 2025.","chicago":"Perrar, I, E Hohoff, A Lesani, S Schmitting, Lars Libuda, Bettina Krüger, Bianca Stutz, et al. “Circadian Eating Patterns Track from Infancy to Pre- and Primary School-Age, but Are Not Prospectively Associated with Body Composition in Childhood - Results of the DONALD Cohort Study.” <i>Eur J Nutr</i> 64, no. 4 (2025): 165.","ama":"Perrar I, Hohoff E, Lesani A, et al. Circadian eating patterns track from infancy to pre- and primary school-age, but are not prospectively associated with body composition in childhood - Results of the DONALD cohort study. <i>Eur J Nutr</i>. 2025;64(4):165.","short":"I. Perrar, E. Hohoff, A. Lesani, S. Schmitting, L. Libuda, B. Krüger, B. Stutz, U. Nöthlings, A. Buyken, U. Alexy, N. Jankovic, Eur J Nutr 64 (2025) 165.","bibtex":"@article{Perrar_Hohoff_Lesani_Schmitting_Libuda_Krüger_Stutz_Nöthlings_Buyken_Alexy_et al._2025, title={Circadian eating patterns track from infancy to pre- and primary school-age, but are not prospectively associated with body composition in childhood - Results of the DONALD cohort study.}, volume={64}, number={4}, journal={Eur J Nutr}, author={Perrar, I and Hohoff, E and Lesani, A and Schmitting, S and Libuda, Lars and Krüger, Bettina and Stutz, Bianca and Nöthlings, U and Buyken, Anette and Alexy, U and et al.}, year={2025}, pages={165} }","mla":"Perrar, I., et al. “Circadian Eating Patterns Track from Infancy to Pre- and Primary School-Age, but Are Not Prospectively Associated with Body Composition in Childhood - Results of the DONALD Cohort Study.” <i>Eur J Nutr</i>, vol. 64, no. 4, 2025, p. 165.","apa":"Perrar, I., Hohoff, E., Lesani, A., Schmitting, S., Libuda, L., Krüger, B., Stutz, B., Nöthlings, U., Buyken, A., Alexy, U., &#38; Jankovic, N. (2025). Circadian eating patterns track from infancy to pre- and primary school-age, but are not prospectively associated with body composition in childhood - Results of the DONALD cohort study. <i>Eur J Nutr</i>, <i>64</i>(4), 165."},"page":"165","intvolume":"        64","year":"2025","author":[{"first_name":"I","last_name":"Perrar","full_name":"Perrar, I"},{"full_name":"Hohoff, E","last_name":"Hohoff","first_name":"E"},{"full_name":"Lesani, A","last_name":"Lesani","first_name":"A"},{"last_name":"Schmitting","full_name":"Schmitting, S","first_name":"S"},{"first_name":"Lars","orcid":"0000-0003-1603-3133","last_name":"Libuda","id":"88682","full_name":"Libuda, Lars"},{"first_name":"Bettina","full_name":"Krüger, Bettina","id":"49428","orcid":"0000-0001-5351-1785","last_name":"Krüger"},{"first_name":"Bianca","last_name":"Stutz","id":"77099","full_name":"Stutz, Bianca"},{"first_name":"U","full_name":"Nöthlings, U","last_name":"Nöthlings"},{"first_name":"Anette","full_name":"Buyken, Anette","id":"65985","last_name":"Buyken"},{"first_name":"U","full_name":"Alexy, U","last_name":"Alexy"},{"first_name":"N","full_name":"Jankovic, N","last_name":"Jankovic"}],"date_created":"2025-06-11T08:49:19Z","volume":64,"date_updated":"2025-06-11T08:51:28Z","title":"Circadian eating patterns track from infancy to pre- and primary school-age, but are not prospectively associated with body composition in childhood - Results of the DONALD cohort study.","type":"journal_article","publication":"Eur J Nutr","status":"public","user_id":"92491","department":[{"_id":"22"}],"_id":"60182","external_id":{"pmid":["40285866"]},"language":[{"iso":"eng"}]},{"language":[{"iso":"eng"}],"article_number":"26709","department":[{"_id":"35"},{"_id":"22"}],"user_id":"49428","_id":"60873","status":"public","abstract":[{"lang":"eng","text":"<jats:title>Abstract</jats:title>\r\n          <jats:p>Variations in circadian rhythm-related genes influence the individual chronotype. Here, we hypothesize that the peak of clock gene expression at 7 a.m. differs between young adults with a late chronotype and young adults with an early chronotype. Participants of the Chronotype and Nutrition nutritional trial (ChroNu study) were selected for their chronotype assessed by the Munich Chronotype questionnaire (MCTQ) and actigraphy. Total RNA was isolated from CD14<jats:sup>+</jats:sup> monocytes of participants at 7 a.m. on the run-in day. Expression levels of seven clock genes (<jats:italic>PER1</jats:italic>,<jats:italic> PER2</jats:italic>,<jats:italic> PER3</jats:italic>, <jats:italic>NR1D1</jats:italic>,<jats:italic> NR1D2</jats:italic>, <jats:italic>CRY1</jats:italic> and <jats:italic>CRISPLD2</jats:italic>) of individuals with early (<jats:italic>n</jats:italic> = 11) or late chronotypes (<jats:italic>n</jats:italic> = 19) were analysed by reverse transcription quantitative polymerase chain reaction. Difference in expression levels was tested by Mann Whitney-U test. The relative expression levels of the selected genes were not significantly different between individuals with early and late chronotypes (all <jats:italic>p</jats:italic> &gt; 0.07). Contrary to expectation, clock gene expression levels at 7 a.m. was similar in individuals with early and late chronotypes. Further studies on larger sample sizes with multiple sampling time points should elucidate whether gene expression is altered at other day times underscoring the biological difference between individuals with early or late chronotypes.</jats:p>"}],"publication":"Scientific Reports","type":"journal_article","doi":"10.1038/s41598-025-12423-7","title":"Morning clock gene expression in young adults of early and late chronotypes","volume":15,"date_created":"2025-08-05T05:17:48Z","author":[{"first_name":"Bettina","id":"49428","full_name":"Krueger, Bettina","orcid":"0000-0001-5351-1785","last_name":"Krueger"},{"first_name":"Luisa Sophie","full_name":"Rajcsanyi, Luisa Sophie","last_name":"Rajcsanyi"},{"first_name":"Katharina","last_name":"Hundertmark","full_name":"Hundertmark, Katharina"},{"first_name":"Bianca","full_name":"Stutz, Bianca","id":"77099","last_name":"Stutz"},{"first_name":"Anke","last_name":"Hinney","full_name":"Hinney, Anke"},{"last_name":"Buyken","full_name":"Buyken, Anette E.","id":"65985","first_name":"Anette E."}],"publisher":"Springer Science and Business Media LLC","date_updated":"2025-08-05T05:19:20Z","intvolume":"        15","citation":{"ieee":"B. Krueger, L. S. Rajcsanyi, K. Hundertmark, B. Stutz, A. Hinney, and A. E. Buyken, “Morning clock gene expression in young adults of early and late chronotypes,” <i>Scientific Reports</i>, vol. 15, no. 1, Art. no. 26709, 2025, doi: <a href=\"https://doi.org/10.1038/s41598-025-12423-7\">10.1038/s41598-025-12423-7</a>.","chicago":"Krueger, Bettina, Luisa Sophie Rajcsanyi, Katharina Hundertmark, Bianca Stutz, Anke Hinney, and Anette E. Buyken. “Morning Clock Gene Expression in Young Adults of Early and Late Chronotypes.” <i>Scientific Reports</i> 15, no. 1 (2025). <a href=\"https://doi.org/10.1038/s41598-025-12423-7\">https://doi.org/10.1038/s41598-025-12423-7</a>.","ama":"Krueger B, Rajcsanyi LS, Hundertmark K, Stutz B, Hinney A, Buyken AE. Morning clock gene expression in young adults of early and late chronotypes. <i>Scientific Reports</i>. 2025;15(1). doi:<a href=\"https://doi.org/10.1038/s41598-025-12423-7\">10.1038/s41598-025-12423-7</a>","bibtex":"@article{Krueger_Rajcsanyi_Hundertmark_Stutz_Hinney_Buyken_2025, title={Morning clock gene expression in young adults of early and late chronotypes}, volume={15}, DOI={<a href=\"https://doi.org/10.1038/s41598-025-12423-7\">10.1038/s41598-025-12423-7</a>}, number={126709}, journal={Scientific Reports}, publisher={Springer Science and Business Media LLC}, author={Krueger, Bettina and Rajcsanyi, Luisa Sophie and Hundertmark, Katharina and Stutz, Bianca and Hinney, Anke and Buyken, Anette E.}, year={2025} }","short":"B. Krueger, L.S. Rajcsanyi, K. Hundertmark, B. Stutz, A. Hinney, A.E. Buyken, Scientific Reports 15 (2025).","mla":"Krueger, Bettina, et al. “Morning Clock Gene Expression in Young Adults of Early and Late Chronotypes.” <i>Scientific Reports</i>, vol. 15, no. 1, 26709, Springer Science and Business Media LLC, 2025, doi:<a href=\"https://doi.org/10.1038/s41598-025-12423-7\">10.1038/s41598-025-12423-7</a>.","apa":"Krueger, B., Rajcsanyi, L. S., Hundertmark, K., Stutz, B., Hinney, A., &#38; Buyken, A. E. (2025). Morning clock gene expression in young adults of early and late chronotypes. <i>Scientific Reports</i>, <i>15</i>(1), Article 26709. <a href=\"https://doi.org/10.1038/s41598-025-12423-7\">https://doi.org/10.1038/s41598-025-12423-7</a>"},"year":"2025","issue":"1","publication_identifier":{"issn":["2045-2322"]},"publication_status":"published"},{"title":"Glycemic response to meals with a high glycemic index differs between morning and evening: a randomized cross-over controlled trial among students with early or late chronotype","doi":"10.1007/s00394-024-03372-4","date_updated":"2024-06-30T13:39:12Z","publisher":"Springer","date_created":"2024-06-30T13:38:17Z","author":[{"first_name":"Bianca","last_name":"Stutz","id":"77099","full_name":"Stutz, Bianca"},{"first_name":"Bettina","last_name":"Krueger","orcid":"0000-0001-5351-1785","full_name":"Krueger, Bettina","id":"49428"},{"first_name":"Janina","full_name":"Goletzke, Janina","last_name":"Goletzke"},{"last_name":"Jankovic","full_name":"Jankovic, Nicole","first_name":"Nicole"},{"first_name":"Ute","full_name":"Alexy, Ute","last_name":"Alexy"},{"first_name":"Christian","full_name":"Herder, Christian","last_name":"Herder"},{"last_name":"Dierkes","full_name":"Dierkes, Jutta","first_name":"Jutta"},{"last_name":"Berg-Beckhoff","full_name":"Berg-Beckhoff, Gabriele","first_name":"Gabriele"},{"first_name":"Rasmus","full_name":"Jakobsmeyer, Rasmus","id":"9583","orcid":"0000-0002-9385-0834","last_name":"Jakobsmeyer"},{"first_name":"Claus","id":"48978","full_name":"Reinsberger, Claus","last_name":"Reinsberger"},{"last_name":"Buyken","id":"65985","full_name":"Buyken, Anette E.","first_name":"Anette E."}],"year":"2024","citation":{"ama":"Stutz B, Krueger B, Goletzke J, et al. Glycemic response to meals with a high glycemic index differs between morning and evening: a randomized cross-over controlled trial among students with early or late chronotype. <i>European Journal of Nutrition</i>. Published online 2024. doi:<a href=\"https://doi.org/10.1007/s00394-024-03372-4\">10.1007/s00394-024-03372-4</a>","apa":"Stutz, B., Krueger, B., Goletzke, J., Jankovic, N., Alexy, U., Herder, C., Dierkes, J., Berg-Beckhoff, G., Jakobsmeyer, R., Reinsberger, C., &#38; Buyken, A. E. (2024). Glycemic response to meals with a high glycemic index differs between morning and evening: a randomized cross-over controlled trial among students with early or late chronotype. <i>European Journal of Nutrition</i>. <a href=\"https://doi.org/10.1007/s00394-024-03372-4\">https://doi.org/10.1007/s00394-024-03372-4</a>","short":"B. Stutz, B. Krueger, J. Goletzke, N. Jankovic, U. Alexy, C. Herder, J. Dierkes, G. Berg-Beckhoff, R. Jakobsmeyer, C. Reinsberger, A.E. Buyken, European Journal of Nutrition (2024).","bibtex":"@article{Stutz_Krueger_Goletzke_Jankovic_Alexy_Herder_Dierkes_Berg-Beckhoff_Jakobsmeyer_Reinsberger_et al._2024, title={Glycemic response to meals with a high glycemic index differs between morning and evening: a randomized cross-over controlled trial among students with early or late chronotype}, DOI={<a href=\"https://doi.org/10.1007/s00394-024-03372-4\">10.1007/s00394-024-03372-4</a>}, journal={European Journal of Nutrition}, publisher={Springer}, author={Stutz, Bianca and Krueger, Bettina and Goletzke, Janina and Jankovic, Nicole and Alexy, Ute and Herder, Christian and Dierkes, Jutta and Berg-Beckhoff, Gabriele and Jakobsmeyer, Rasmus and Reinsberger, Claus and et al.}, year={2024} }","mla":"Stutz, Bianca, et al. “Glycemic Response to Meals with a High Glycemic Index Differs between Morning and Evening: A Randomized Cross-over Controlled Trial among Students with Early or Late Chronotype.” <i>European Journal of Nutrition</i>, Springer, 2024, doi:<a href=\"https://doi.org/10.1007/s00394-024-03372-4\">10.1007/s00394-024-03372-4</a>.","chicago":"Stutz, Bianca, Bettina Krueger, Janina Goletzke, Nicole Jankovic, Ute Alexy, Christian Herder, Jutta Dierkes, et al. “Glycemic Response to Meals with a High Glycemic Index Differs between Morning and Evening: A Randomized Cross-over Controlled Trial among Students with Early or Late Chronotype.” <i>European Journal of Nutrition</i>, 2024. <a href=\"https://doi.org/10.1007/s00394-024-03372-4\">https://doi.org/10.1007/s00394-024-03372-4</a>.","ieee":"B. Stutz <i>et al.</i>, “Glycemic response to meals with a high glycemic index differs between morning and evening: a randomized cross-over controlled trial among students with early or late chronotype,” <i>European Journal of Nutrition</i>, 2024, doi: <a href=\"https://doi.org/10.1007/s00394-024-03372-4\">10.1007/s00394-024-03372-4</a>."},"publication_identifier":{"issn":["1436-6215"]},"language":[{"iso":"eng"}],"_id":"54926","department":[{"_id":"35"},{"_id":"22"}],"user_id":"49428","status":"public","publication":"European Journal of Nutrition","type":"journal_article"},{"status":"public","publication":"Appetite","type":"journal_article","language":[{"iso":"eng"}],"department":[{"_id":"35"},{"_id":"22"}],"user_id":"49428","_id":"54927","intvolume":"       200","page":"107569","citation":{"mla":"Stutz, Bianca, et al. “Association between Glucose Dips and the Feeling of Hunger in a Dietary Intervention Study among Students with Early and Late Chronotype-Secondary Analysis of a Randomized Cross-over Nutrition Trial.” <i>Appetite</i>, vol. 200, Elsevier, 2024, p. 107569, doi:<a href=\"https://doi.org/10.1016/j.appet.2024.107569\">10.1016/j.appet.2024.107569</a>.","short":"B. Stutz, J. Goletzke, B. Krueger, N. Jankovic, U. Alexy, C. Herder, R. Jakobsmeyer, C. Reinsberger, A.E. Buyken, Appetite 200 (2024) 107569.","bibtex":"@article{Stutz_Goletzke_Krueger_Jankovic_Alexy_Herder_Jakobsmeyer_Reinsberger_Buyken_2024, title={Association between glucose dips and the feeling of hunger in a dietary intervention study among students with early and late chronotype-secondary analysis of a randomized cross-over nutrition trial}, volume={200}, DOI={<a href=\"https://doi.org/10.1016/j.appet.2024.107569\">10.1016/j.appet.2024.107569</a>}, journal={Appetite}, publisher={Elsevier}, author={Stutz, Bianca and Goletzke, Janina and Krueger, Bettina and Jankovic, Nicole and Alexy, Ute and Herder, Christian and Jakobsmeyer, Rasmus and Reinsberger, Claus and Buyken, Anette E.}, year={2024}, pages={107569} }","apa":"Stutz, B., Goletzke, J., Krueger, B., Jankovic, N., Alexy, U., Herder, C., Jakobsmeyer, R., Reinsberger, C., &#38; Buyken, A. E. (2024). Association between glucose dips and the feeling of hunger in a dietary intervention study among students with early and late chronotype-secondary analysis of a randomized cross-over nutrition trial. <i>Appetite</i>, <i>200</i>, 107569. <a href=\"https://doi.org/10.1016/j.appet.2024.107569\">https://doi.org/10.1016/j.appet.2024.107569</a>","ama":"Stutz B, Goletzke J, Krueger B, et al. Association between glucose dips and the feeling of hunger in a dietary intervention study among students with early and late chronotype-secondary analysis of a randomized cross-over nutrition trial. <i>Appetite</i>. 2024;200:107569. doi:<a href=\"https://doi.org/10.1016/j.appet.2024.107569\">10.1016/j.appet.2024.107569</a>","chicago":"Stutz, Bianca, Janina Goletzke, Bettina Krueger, Nicole Jankovic, Ute Alexy, Christian Herder, Rasmus Jakobsmeyer, Claus Reinsberger, and Anette E. Buyken. “Association between Glucose Dips and the Feeling of Hunger in a Dietary Intervention Study among Students with Early and Late Chronotype-Secondary Analysis of a Randomized Cross-over Nutrition Trial.” <i>Appetite</i> 200 (2024): 107569. <a href=\"https://doi.org/10.1016/j.appet.2024.107569\">https://doi.org/10.1016/j.appet.2024.107569</a>.","ieee":"B. Stutz <i>et al.</i>, “Association between glucose dips and the feeling of hunger in a dietary intervention study among students with early and late chronotype-secondary analysis of a randomized cross-over nutrition trial,” <i>Appetite</i>, vol. 200, p. 107569, 2024, doi: <a href=\"https://doi.org/10.1016/j.appet.2024.107569\">10.1016/j.appet.2024.107569</a>."},"year":"2024","doi":"10.1016/j.appet.2024.107569","title":"Association between glucose dips and the feeling of hunger in a dietary intervention study among students with early and late chronotype-secondary analysis of a randomized cross-over nutrition trial","volume":200,"author":[{"first_name":"Bianca","full_name":"Stutz, Bianca","id":"77099","last_name":"Stutz"},{"first_name":"Janina","last_name":"Goletzke","full_name":"Goletzke, Janina"},{"first_name":"Bettina","id":"49428","full_name":"Krueger, Bettina","last_name":"Krueger","orcid":"0000-0001-5351-1785"},{"first_name":"Nicole","last_name":"Jankovic","orcid":"https://orcid.org/0000-0002-9235-5356","id":"105192","full_name":"Jankovic, Nicole"},{"last_name":"Alexy","full_name":"Alexy, Ute","first_name":"Ute"},{"full_name":"Herder, Christian","last_name":"Herder","first_name":"Christian"},{"id":"9583","full_name":"Jakobsmeyer, Rasmus","last_name":"Jakobsmeyer","orcid":"0000-0002-9385-0834","first_name":"Rasmus"},{"first_name":"Claus","id":"48978","full_name":"Reinsberger, Claus","last_name":"Reinsberger"},{"id":"65985","full_name":"Buyken, Anette E.","last_name":"Buyken","first_name":"Anette E."}],"date_created":"2024-06-30T13:40:19Z","publisher":"Elsevier","date_updated":"2024-06-30T13:41:10Z"},{"year":"2024","citation":{"short":"B. Krueger, B. Stutz, R. Jakobsmeyer, C. Reinsberger, A.E. Buyken, Chronobiology International (2024) 1–10.","mla":"Krueger, Bettina, et al. “Relevance of High Glycaemic Index Breakfast for Heart Rate Variability among Collegiate Students with Early and Late Chronotypes.” <i>Chronobiology International</i>, Informa UK Limited, 2024, pp. 1–10, doi:<a href=\"https://doi.org/10.1080/07420528.2024.2428203\">10.1080/07420528.2024.2428203</a>.","bibtex":"@article{Krueger_Stutz_Jakobsmeyer_Reinsberger_Buyken_2024, title={Relevance of high glycaemic index breakfast for heart rate variability among collegiate students with early and late chronotypes}, DOI={<a href=\"https://doi.org/10.1080/07420528.2024.2428203\">10.1080/07420528.2024.2428203</a>}, journal={Chronobiology International}, publisher={Informa UK Limited}, author={Krueger, Bettina and Stutz, Bianca and Jakobsmeyer, Rasmus and Reinsberger, Claus and Buyken, Anette E.}, year={2024}, pages={1–10} }","apa":"Krueger, B., Stutz, B., Jakobsmeyer, R., Reinsberger, C., &#38; Buyken, A. E. (2024). Relevance of high glycaemic index breakfast for heart rate variability among collegiate students with early and late chronotypes. <i>Chronobiology International</i>, 1–10. <a href=\"https://doi.org/10.1080/07420528.2024.2428203\">https://doi.org/10.1080/07420528.2024.2428203</a>","ieee":"B. Krueger, B. Stutz, R. Jakobsmeyer, C. Reinsberger, and A. E. Buyken, “Relevance of high glycaemic index breakfast for heart rate variability among collegiate students with early and late chronotypes,” <i>Chronobiology International</i>, pp. 1–10, 2024, doi: <a href=\"https://doi.org/10.1080/07420528.2024.2428203\">10.1080/07420528.2024.2428203</a>.","chicago":"Krueger, Bettina, Bianca Stutz, Rasmus Jakobsmeyer, Claus Reinsberger, and Anette E. Buyken. “Relevance of High Glycaemic Index Breakfast for Heart Rate Variability among Collegiate Students with Early and Late Chronotypes.” <i>Chronobiology International</i>, 2024, 1–10. <a href=\"https://doi.org/10.1080/07420528.2024.2428203\">https://doi.org/10.1080/07420528.2024.2428203</a>.","ama":"Krueger B, Stutz B, Jakobsmeyer R, Reinsberger C, Buyken AE. Relevance of high glycaemic index breakfast for heart rate variability among collegiate students with early and late chronotypes. <i>Chronobiology International</i>. Published online 2024:1-10. doi:<a href=\"https://doi.org/10.1080/07420528.2024.2428203\">10.1080/07420528.2024.2428203</a>"},"page":"1-10","publication_status":"published","publication_identifier":{"issn":["0742-0528","1525-6073"]},"title":"Relevance of high glycaemic index breakfast for heart rate variability among collegiate students with early and late chronotypes","doi":"10.1080/07420528.2024.2428203","date_updated":"2024-11-26T10:52:50Z","publisher":"Informa UK Limited","author":[{"full_name":"Krueger, Bettina","id":"49428","orcid":"0000-0001-5351-1785","last_name":"Krueger","first_name":"Bettina"},{"first_name":"Bianca","id":"77099","full_name":"Stutz, Bianca","last_name":"Stutz"},{"orcid":"0000-0002-9385-0834","last_name":"Jakobsmeyer","full_name":"Jakobsmeyer, Rasmus","id":"9583","first_name":"Rasmus"},{"first_name":"Claus","last_name":"Reinsberger","full_name":"Reinsberger, Claus","id":"48978"},{"first_name":"Anette E.","id":"65985","full_name":"Buyken, Anette E.","last_name":"Buyken"}],"date_created":"2024-11-26T10:51:33Z","status":"public","type":"journal_article","publication":"Chronobiology International","language":[{"iso":"eng"}],"_id":"57429","user_id":"49428","department":[{"_id":"35"},{"_id":"22"}]},{"status":"public","publication":"Appetite","type":"journal_article","language":[{"iso":"eng"}],"department":[{"_id":"17"}],"user_id":"49428","_id":"36073","external_id":{"pmid":["36202148"]},"page":"106333","intvolume":"       180","citation":{"ieee":"B. Stutz, A. E. Buyken, A. Schadow, N. Jankovic, U. Alexy, and B. Krueger, “Associations of chronotype and social jetlag with eating jetlag and their changes among German students during the first COVID-19 lockdown. The Chronotype and Nutrition study.,” <i>Appetite</i>, vol. 180, p. 106333, 2023, doi: <a href=\"https://doi.org/10.1016/j.appet.2022.106333\">10.1016/j.appet.2022.106333</a>.","chicago":"Stutz, Bianca, Anette E. Buyken, Alena Schadow, N Jankovic, U Alexy, and Betina Krueger. “Associations of Chronotype and Social Jetlag with Eating Jetlag and Their Changes among German Students during the First COVID-19 Lockdown. The Chronotype and Nutrition Study.” <i>Appetite</i> 180 (2023): 106333. <a href=\"https://doi.org/10.1016/j.appet.2022.106333\">https://doi.org/10.1016/j.appet.2022.106333</a>.","short":"B. Stutz, A.E. Buyken, A. Schadow, N. Jankovic, U. Alexy, B. Krueger, Appetite 180 (2023) 106333.","bibtex":"@article{Stutz_Buyken_Schadow_Jankovic_Alexy_Krueger_2023, title={Associations of chronotype and social jetlag with eating jetlag and their changes among German students during the first COVID-19 lockdown. The Chronotype and Nutrition study.}, volume={180}, DOI={<a href=\"https://doi.org/10.1016/j.appet.2022.106333\">10.1016/j.appet.2022.106333</a>}, journal={Appetite}, author={Stutz, Bianca and Buyken, Anette E. and Schadow, Alena and Jankovic, N and Alexy, U and Krueger, Betina}, year={2023}, pages={106333} }","mla":"Stutz, Bianca, et al. “Associations of Chronotype and Social Jetlag with Eating Jetlag and Their Changes among German Students during the First COVID-19 Lockdown. The Chronotype and Nutrition Study.” <i>Appetite</i>, vol. 180, 2023, p. 106333, doi:<a href=\"https://doi.org/10.1016/j.appet.2022.106333\">10.1016/j.appet.2022.106333</a>.","apa":"Stutz, B., Buyken, A. E., Schadow, A., Jankovic, N., Alexy, U., &#38; Krueger, B. (2023). Associations of chronotype and social jetlag with eating jetlag and their changes among German students during the first COVID-19 lockdown. The Chronotype and Nutrition study. <i>Appetite</i>, <i>180</i>, 106333. <a href=\"https://doi.org/10.1016/j.appet.2022.106333\">https://doi.org/10.1016/j.appet.2022.106333</a>","ama":"Stutz B, Buyken AE, Schadow A, Jankovic N, Alexy U, Krueger B. Associations of chronotype and social jetlag with eating jetlag and their changes among German students during the first COVID-19 lockdown. The Chronotype and Nutrition study. <i>Appetite</i>. 2023;180:106333. doi:<a href=\"https://doi.org/10.1016/j.appet.2022.106333\">10.1016/j.appet.2022.106333</a>"},"year":"2023","pmid":"1","publication_identifier":{"issn":["0195-6663","1095-8304"]},"doi":"10.1016/j.appet.2022.106333","title":"Associations of chronotype and social jetlag with eating jetlag and their changes among German students during the first COVID-19 lockdown. The Chronotype and Nutrition study.","volume":180,"author":[{"last_name":"Stutz","full_name":"Stutz, Bianca","first_name":"Bianca"},{"id":"65985","full_name":"Buyken, Anette E.","last_name":"Buyken","first_name":"Anette E."},{"last_name":"Schadow","full_name":"Schadow, Alena","first_name":"Alena"},{"first_name":"N","full_name":"Jankovic, N","last_name":"Jankovic"},{"full_name":"Alexy, U","last_name":"Alexy","first_name":"U"},{"first_name":"Betina","id":"49428","full_name":"Krueger, Betina","orcid":"0000-0001-5351-1785","last_name":"Krueger"}],"date_created":"2023-01-11T11:49:31Z","date_updated":"2023-01-13T07:17:08Z"},{"date_updated":"2023-10-25T08:39:21Z","publisher":"Springer Science and Business Media LLC","date_created":"2023-10-25T08:38:46Z","author":[{"last_name":"Jankovic","full_name":"Jankovic, Nicole","first_name":"Nicole"},{"first_name":"Sarah","last_name":"Schmitting","full_name":"Schmitting, Sarah"},{"last_name":"Stutz","id":"77099","full_name":"Stutz, Bianca","first_name":"Bianca"},{"first_name":"Bettina","full_name":"Krüger, Bettina","id":"49428","last_name":"Krüger","orcid":"0000-0001-5351-1785"},{"first_name":"Anette","last_name":"Buyken","id":"65985","full_name":"Buyken, Anette"},{"first_name":"Ute","last_name":"Alexy","full_name":"Alexy, Ute"}],"title":"Alignment between timing of ‘highest caloric intake’ and chronotype in relation to body composition during adolescence: the DONALD Study","doi":"10.1007/s00394-023-03259-w","publication_identifier":{"issn":["1436-6207","1436-6215"]},"publication_status":"published","year":"2023","citation":{"bibtex":"@article{Jankovic_Schmitting_Stutz_Krüger_Buyken_Alexy_2023, title={Alignment between timing of ‘highest caloric intake’ and chronotype in relation to body composition during adolescence: the DONALD Study}, DOI={<a href=\"https://doi.org/10.1007/s00394-023-03259-w\">10.1007/s00394-023-03259-w</a>}, journal={European Journal of Nutrition}, publisher={Springer Science and Business Media LLC}, author={Jankovic, Nicole and Schmitting, Sarah and Stutz, Bianca and Krüger, Bettina and Buyken, Anette and Alexy, Ute}, year={2023} }","mla":"Jankovic, Nicole, et al. “Alignment between Timing of ‘Highest Caloric Intake’ and Chronotype in Relation to Body Composition during Adolescence: The DONALD Study.” <i>European Journal of Nutrition</i>, Springer Science and Business Media LLC, 2023, doi:<a href=\"https://doi.org/10.1007/s00394-023-03259-w\">10.1007/s00394-023-03259-w</a>.","short":"N. Jankovic, S. Schmitting, B. Stutz, B. Krüger, A. Buyken, U. Alexy, European Journal of Nutrition (2023).","apa":"Jankovic, N., Schmitting, S., Stutz, B., Krüger, B., Buyken, A., &#38; Alexy, U. (2023). Alignment between timing of ‘highest caloric intake’ and chronotype in relation to body composition during adolescence: the DONALD Study. <i>European Journal of Nutrition</i>. <a href=\"https://doi.org/10.1007/s00394-023-03259-w\">https://doi.org/10.1007/s00394-023-03259-w</a>","ama":"Jankovic N, Schmitting S, Stutz B, Krüger B, Buyken A, Alexy U. Alignment between timing of ‘highest caloric intake’ and chronotype in relation to body composition during adolescence: the DONALD Study. <i>European Journal of Nutrition</i>. Published online 2023. doi:<a href=\"https://doi.org/10.1007/s00394-023-03259-w\">10.1007/s00394-023-03259-w</a>","ieee":"N. Jankovic, S. Schmitting, B. Stutz, B. Krüger, A. Buyken, and U. Alexy, “Alignment between timing of ‘highest caloric intake’ and chronotype in relation to body composition during adolescence: the DONALD Study,” <i>European Journal of Nutrition</i>, 2023, doi: <a href=\"https://doi.org/10.1007/s00394-023-03259-w\">10.1007/s00394-023-03259-w</a>.","chicago":"Jankovic, Nicole, Sarah Schmitting, Bianca Stutz, Bettina Krüger, Anette Buyken, and Ute Alexy. “Alignment between Timing of ‘Highest Caloric Intake’ and Chronotype in Relation to Body Composition during Adolescence: The DONALD Study.” <i>European Journal of Nutrition</i>, 2023. <a href=\"https://doi.org/10.1007/s00394-023-03259-w\">https://doi.org/10.1007/s00394-023-03259-w</a>."},"_id":"48456","department":[{"_id":"22"}],"user_id":"92491","keyword":["Nutrition and Dietetics","Medicine (miscellaneous)"],"language":[{"iso":"eng"}],"publication":"European Journal of Nutrition","type":"journal_article","abstract":[{"lang":"eng","text":"<jats:title>Abstract</jats:title><jats:sec>\r\n              <jats:title>Purpose</jats:title>\r\n              <jats:p>Our aim was to assess alignment in timing of ‘highest caloric intake’ with individual chronotype and its association with body composition in adolescents.</jats:p>\r\n            </jats:sec><jats:sec>\r\n              <jats:title>Methods</jats:title>\r\n              <jats:p>We used repeatedly collected data from <jats:italic>n</jats:italic> = 196 adolescents (age 9–16 years, providing <jats:italic>N</jats:italic> = 401 yearly questionnaires) of the DONALD open cohort study. Chronotype was assessed by the Munich Chronotype Questionnaire from which midpoint of sleep (MSFsc) was derived. A sex- and age-specific diet-chrono-alignment score (DCAS) was calculated as the difference in hours between the chronotype-specific median timing of highest caloric intake of the studied population and the individual timing of ‘highest caloric intake’ or vice versa. Repeated-measures regression models were applied to study cross-sectional and longitudinal associations between the DCAS and body composition, e.g., Fat Mass Index (FMI) or Fat Free Mass Index (FFMI).</jats:p>\r\n            </jats:sec><jats:sec>\r\n              <jats:title>Results</jats:title>\r\n              <jats:p>DCAS ranged from −6:42 h to + 8:01 h and was not associated with body composition. Among adolescents with a later chronotype (<jats:italic>N</jats:italic> = 201) a 1 h increase in DCAS (later consumption of ‘highest caloric intake’ in comparison to the median intake of that group), increased FFMI by 1.92 kg/m<jats:sup>2</jats:sup> (95% CI: 0.15, 3.69, <jats:italic>p</jats:italic> value = 0.04) over a median follow-up of 0.94 year.</jats:p>\r\n            </jats:sec><jats:sec>\r\n              <jats:title>Conclusion</jats:title>\r\n              <jats:p>Alignment of energy intake with individual chronotype appears beneficial for FFMI among those with a late chronotype.</jats:p>\r\n            </jats:sec>"}],"status":"public"},{"article_number":"e0279620","keyword":["Multidisciplinary"],"language":[{"iso":"eng"}],"_id":"36505","user_id":"61597","department":[{"_id":"35"},{"_id":"22"}],"abstract":[{"lang":"eng","text":"<jats:p>Young adults with a later chronotype are vulnerable for a discrepancy in sleep rhythm between work- and free days, called social jet lag (SJL). This study analysed (i) chronotype/SJL association with visceral fat/skeletal muscle mass, (ii) the attribution to physical activity behaviour, and (iii) chronotype-specific changes in physical activity behaviour in young adults during the Covid-19 pandemic lockdown. Chronotype and SJL were derived from the Munich-Chrono-Type-Questionnaire in 320 German students (age 18–25 years) from September 2019 to January 2020, 156 of these participated in an online follow-up survey in June 2020. Body composition was assessed by bioimpedance analysis at baseline. Multivariable linear regression analyses were used to relate chronotype/SJL to body composition; the contribution of self-reported physical activity was tested by mediation analysis. At baseline, a later chronotype and a larger SJL were associated with a higher visceral fat mass (P&lt;0.05), this relation was notably mediated by the attention to physical activity (P&lt;0.05). Chronotype (P = 0.02) but not SJL (P = 0.87) was inversely associated with skeletal muscle mass. During the pandemic lockdown, chronotype hardly changed, but SJL was reduced. Timing and physical activity behaviour remained in most participants and changes were unrelated to chronotype (all P&gt;0.07). A later chronotype/higher SJL may increase the risk of a higher visceral fat mass even in this relatively healthy sample, which may be partly due to their physical activity behaviour. Despite a reduction in SJL during the pandemic lockdown, later chronotypes did not change their physical activity behaviour more than earlier chronotypes.</jats:p>"}],"status":"public","type":"journal_article","publication":"PLOS ONE","title":"The association of chronotype and social jet lag with body composition in German students: The role of physical activity behaviour and the impact of the pandemic lockdown","doi":"10.1371/journal.pone.0279620","date_updated":"2023-01-24T11:54:46Z","publisher":"Public Library of Science (PLoS)","author":[{"first_name":"Betina","orcid":"0000-0001-5351-1785","last_name":"Krueger","id":"49428","full_name":"Krueger, Betina"},{"first_name":"Bianca","last_name":"Stutz","full_name":"Stutz, Bianca","id":"77099"},{"last_name":"Jankovic","full_name":"Jankovic, Nicole","first_name":"Nicole"},{"last_name":"Alexy","full_name":"Alexy, Ute","first_name":"Ute"},{"first_name":"Anna","last_name":"Kilanowski","full_name":"Kilanowski, Anna"},{"first_name":"Lars","id":"88682","full_name":"Libuda, Lars","orcid":"0000-0003-1603-3133","last_name":"Libuda"},{"last_name":"Buyken","id":"65985","full_name":"Buyken, Anette E.","first_name":"Anette E."}],"date_created":"2023-01-13T07:15:13Z","volume":18,"year":"2023","citation":{"chicago":"Krueger, Betina, Bianca Stutz, Nicole Jankovic, Ute Alexy, Anna Kilanowski, Lars Libuda, and Anette E. Buyken. “The Association of Chronotype and Social Jet Lag with Body Composition in German Students: The Role of Physical Activity Behaviour and the Impact of the Pandemic Lockdown.” <i>PLOS ONE</i> 18, no. 1 (2023). <a href=\"https://doi.org/10.1371/journal.pone.0279620\">https://doi.org/10.1371/journal.pone.0279620</a>.","ieee":"B. Krueger <i>et al.</i>, “The association of chronotype and social jet lag with body composition in German students: The role of physical activity behaviour and the impact of the pandemic lockdown,” <i>PLOS ONE</i>, vol. 18, no. 1, Art. no. e0279620, 2023, doi: <a href=\"https://doi.org/10.1371/journal.pone.0279620\">10.1371/journal.pone.0279620</a>.","ama":"Krueger B, Stutz B, Jankovic N, et al. The association of chronotype and social jet lag with body composition in German students: The role of physical activity behaviour and the impact of the pandemic lockdown. <i>PLOS ONE</i>. 2023;18(1). doi:<a href=\"https://doi.org/10.1371/journal.pone.0279620\">10.1371/journal.pone.0279620</a>","bibtex":"@article{Krueger_Stutz_Jankovic_Alexy_Kilanowski_Libuda_Buyken_2023, title={The association of chronotype and social jet lag with body composition in German students: The role of physical activity behaviour and the impact of the pandemic lockdown}, volume={18}, DOI={<a href=\"https://doi.org/10.1371/journal.pone.0279620\">10.1371/journal.pone.0279620</a>}, number={1e0279620}, journal={PLOS ONE}, publisher={Public Library of Science (PLoS)}, author={Krueger, Betina and Stutz, Bianca and Jankovic, Nicole and Alexy, Ute and Kilanowski, Anna and Libuda, Lars and Buyken, Anette E.}, year={2023} }","mla":"Krueger, Betina, et al. “The Association of Chronotype and Social Jet Lag with Body Composition in German Students: The Role of Physical Activity Behaviour and the Impact of the Pandemic Lockdown.” <i>PLOS ONE</i>, vol. 18, no. 1, e0279620, Public Library of Science (PLoS), 2023, doi:<a href=\"https://doi.org/10.1371/journal.pone.0279620\">10.1371/journal.pone.0279620</a>.","short":"B. Krueger, B. Stutz, N. Jankovic, U. Alexy, A. Kilanowski, L. Libuda, A.E. Buyken, PLOS ONE 18 (2023).","apa":"Krueger, B., Stutz, B., Jankovic, N., Alexy, U., Kilanowski, A., Libuda, L., &#38; Buyken, A. E. (2023). The association of chronotype and social jet lag with body composition in German students: The role of physical activity behaviour and the impact of the pandemic lockdown. <i>PLOS ONE</i>, <i>18</i>(1), Article e0279620. <a href=\"https://doi.org/10.1371/journal.pone.0279620\">https://doi.org/10.1371/journal.pone.0279620</a>"},"intvolume":"        18","publication_status":"published","publication_identifier":{"issn":["1932-6203"]},"issue":"1"},{"publication":"European Journal of Clinical Nutrition","type":"journal_article","abstract":[{"text":"<jats:title>Abstract</jats:title><jats:sec>\r\n              <jats:title>Background/objectives</jats:title>\r\n              <jats:p>Adolescence is a critical period for both the development of overweight and the transition toward a later chronotype, often accompanied by an increase in social jetlag. This study assessed whether changes in chronotype and social jetlag, are linked to changes in body composition during adolescence.</jats:p>\r\n            </jats:sec><jats:sec>\r\n              <jats:title>Subjects/methods</jats:title>\r\n              <jats:p>We used data from the DONALD open cohort study, collected between 2014 and 2019, from 213 adolescents (9–17 years at baseline, 45% females) having at least two measures of chronotype and anthropometry (<jats:italic>N</jats:italic> = 572). Chronotype was assessed with the Munich Chronotype Questionnaire and defined as: midpoint of sleep corrected for sleep-debt (MSFsc) accumulated over the week (later MSFsc represents later chronotype). Social jetlag (SJL) defines the difference between midpoint of sleep during week and weekend. Calculations for Fat Free Mass Index (FFMI [kg/m<jats:sup>2</jats:sup>)]) and Fat Mass Index (FMI) [kg/m<jats:sup>2</jats:sup>)]) were based on body fat percentage, weight, and height. To analyze the associations, we used linear mixed-effect regression models. Finally, the total cohort was split into three biologically relevant age groups (cut-off set at &lt;12 years, ≥12 to ≤15 years and &gt;15 years).</jats:p>\r\n            </jats:sec><jats:sec>\r\n              <jats:title>Results</jats:title>\r\n              <jats:p>Median follow-up was 2.1 years. Overall, change toward a later chronotype was significantly related with an increase in FMI (ß: 0.05, 95% CI: 0.01–0.08). A 1 h increase in social jetlag predicted an increase in BMI-SDS of 0.08 SDS units (95% CI: 0.01–0.14) and in FMI of 0.04 kg/m2 (95% CI: 0.003–0.08). Associations were stronger for the age group ≥12 to ≤15 years (<jats:italic>p</jats:italic> for interaction: &lt;0.001). No relationship was found with FFMI.</jats:p>\r\n            </jats:sec><jats:sec>\r\n              <jats:title>Conclusions</jats:title>\r\n              <jats:p>Changes in MSFsc and SJL during adolescence were associated with concurrent changes in BMI-SDS and FMI. The age ≥12 to ≤15 years appears to be a sensitive period in which chronobiological changes were clearly associated with increasing body fatness.</jats:p>\r\n            </jats:sec>","lang":"eng"}],"status":"public","_id":"27114","department":[{"_id":"35"},{"_id":"22"},{"_id":"571"}],"user_id":"49428","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0954-3007","1476-5640"]},"publication_status":"published","year":"2021","citation":{"chicago":"Jankovic, Nicole, Sarah Schmitting, Bettina Krüger, Ute Nöthlings, Anette E. Buyken, and Ute Alexy. “Changes in Chronotype and Social Jetlag during Adolescence and Their Association with Concurrent Changes in BMI-SDS and Body Composition, in the DONALD Study.” <i>European Journal of Clinical Nutrition</i>, 2021. <a href=\"https://doi.org/10.1038/s41430-021-01024-y\">https://doi.org/10.1038/s41430-021-01024-y</a>.","ieee":"N. Jankovic, S. Schmitting, B. Krüger, U. Nöthlings, A. E. Buyken, and U. Alexy, “Changes in chronotype and social jetlag during adolescence and their association with concurrent changes in BMI-SDS and body composition, in the DONALD Study,” <i>European Journal of Clinical Nutrition</i>, 2021, doi: <a href=\"https://doi.org/10.1038/s41430-021-01024-y\">10.1038/s41430-021-01024-y</a>.","ama":"Jankovic N, Schmitting S, Krüger B, Nöthlings U, Buyken AE, Alexy U. Changes in chronotype and social jetlag during adolescence and their association with concurrent changes in BMI-SDS and body composition, in the DONALD Study. <i>European Journal of Clinical Nutrition</i>. Published online 2021. doi:<a href=\"https://doi.org/10.1038/s41430-021-01024-y\">10.1038/s41430-021-01024-y</a>","bibtex":"@article{Jankovic_Schmitting_Krüger_Nöthlings_Buyken_Alexy_2021, title={Changes in chronotype and social jetlag during adolescence and their association with concurrent changes in BMI-SDS and body composition, in the DONALD Study}, DOI={<a href=\"https://doi.org/10.1038/s41430-021-01024-y\">10.1038/s41430-021-01024-y</a>}, journal={European Journal of Clinical Nutrition}, author={Jankovic, Nicole and Schmitting, Sarah and Krüger, Bettina and Nöthlings, Ute and Buyken, Anette E. and Alexy, Ute}, year={2021} }","short":"N. Jankovic, S. Schmitting, B. Krüger, U. Nöthlings, A.E. Buyken, U. Alexy, European Journal of Clinical Nutrition (2021).","mla":"Jankovic, Nicole, et al. “Changes in Chronotype and Social Jetlag during Adolescence and Their Association with Concurrent Changes in BMI-SDS and Body Composition, in the DONALD Study.” <i>European Journal of Clinical Nutrition</i>, 2021, doi:<a href=\"https://doi.org/10.1038/s41430-021-01024-y\">10.1038/s41430-021-01024-y</a>.","apa":"Jankovic, N., Schmitting, S., Krüger, B., Nöthlings, U., Buyken, A. E., &#38; Alexy, U. (2021). Changes in chronotype and social jetlag during adolescence and their association with concurrent changes in BMI-SDS and body composition, in the DONALD Study. <i>European Journal of Clinical Nutrition</i>. <a href=\"https://doi.org/10.1038/s41430-021-01024-y\">https://doi.org/10.1038/s41430-021-01024-y</a>"},"date_updated":"2022-01-06T06:57:35Z","date_created":"2021-11-03T12:57:29Z","author":[{"full_name":"Jankovic, Nicole","last_name":"Jankovic","first_name":"Nicole"},{"first_name":"Sarah","last_name":"Schmitting","full_name":"Schmitting, Sarah"},{"last_name":"Krüger","orcid":"0000-0001-5351-1785","full_name":"Krüger, Bettina","id":"49428","first_name":"Bettina"},{"first_name":"Ute","last_name":"Nöthlings","full_name":"Nöthlings, Ute"},{"first_name":"Anette E.","last_name":"Buyken","full_name":"Buyken, Anette E.","id":"65985"},{"full_name":"Alexy, Ute","last_name":"Alexy","first_name":"Ute"}],"title":"Changes in chronotype and social jetlag during adolescence and their association with concurrent changes in BMI-SDS and body composition, in the DONALD Study","doi":"10.1038/s41430-021-01024-y"},{"date_updated":"2024-06-30T13:43:39Z","publisher":"Springer","date_created":"2024-06-30T13:43:17Z","author":[{"id":"49428","full_name":"Krueger, Bettina","orcid":"0000-0001-5351-1785","last_name":"Krueger","first_name":"Bettina"},{"last_name":"Yang","full_name":"Yang, Limin","first_name":"Limin"},{"last_name":"Korbmacher","full_name":"Korbmacher, Christoph","first_name":"Christoph"},{"full_name":"Rauh, Robert","last_name":"Rauh","first_name":"Robert"}],"volume":470,"title":"The phosphorylation site T613 in the $\\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates channel inhibition by Nedd4-2","doi":"10.1007/s00424-018-2115-2","issue":"4","year":"2018","citation":{"ama":"Krueger B, Yang L, Korbmacher C, Rauh R. The phosphorylation site T613 in the $\\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates channel inhibition by Nedd4-2. <i>Pflügers Archiv - European Journal of Physiology</i>. 2018;470(4):649–660. doi:<a href=\"https://doi.org/10.1007/s00424-018-2115-2\">10.1007/s00424-018-2115-2</a>","chicago":"Krueger, Bettina, Limin Yang, Christoph Korbmacher, and Robert Rauh. “The Phosphorylation Site T613 in the $\\beta$-Subunit of Rat Epithelial Na+ Channel (ENaC) Modulates Channel Inhibition by Nedd4-2.” <i>Pflügers Archiv - European Journal of Physiology</i> 470, no. 4 (2018): 649–660. <a href=\"https://doi.org/10.1007/s00424-018-2115-2\">https://doi.org/10.1007/s00424-018-2115-2</a>.","ieee":"B. Krueger, L. Yang, C. Korbmacher, and R. Rauh, “The phosphorylation site T613 in the $\\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates channel inhibition by Nedd4-2,” <i>Pflügers Archiv - European Journal of Physiology</i>, vol. 470, no. 4, pp. 649–660, 2018, doi: <a href=\"https://doi.org/10.1007/s00424-018-2115-2\">10.1007/s00424-018-2115-2</a>.","apa":"Krueger, B., Yang, L., Korbmacher, C., &#38; Rauh, R. (2018). The phosphorylation site T613 in the $\\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates channel inhibition by Nedd4-2. <i>Pflügers Archiv - European Journal of Physiology</i>, <i>470</i>(4), 649–660. <a href=\"https://doi.org/10.1007/s00424-018-2115-2\">https://doi.org/10.1007/s00424-018-2115-2</a>","short":"B. Krueger, L. Yang, C. Korbmacher, R. Rauh, Pflügers Archiv - European Journal of Physiology 470 (2018) 649–660.","bibtex":"@article{Krueger_Yang_Korbmacher_Rauh_2018, title={The phosphorylation site T613 in the $\\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates channel inhibition by Nedd4-2}, volume={470}, DOI={<a href=\"https://doi.org/10.1007/s00424-018-2115-2\">10.1007/s00424-018-2115-2</a>}, number={4}, journal={Pflügers Archiv - European Journal of Physiology}, publisher={Springer}, author={Krueger, Bettina and Yang, Limin and Korbmacher, Christoph and Rauh, Robert}, year={2018}, pages={649–660} }","mla":"Krueger, Bettina, et al. “The Phosphorylation Site T613 in the $\\beta$-Subunit of Rat Epithelial Na+ Channel (ENaC) Modulates Channel Inhibition by Nedd4-2.” <i>Pflügers Archiv - European Journal of Physiology</i>, vol. 470, no. 4, Springer, 2018, pp. 649–660, doi:<a href=\"https://doi.org/10.1007/s00424-018-2115-2\">10.1007/s00424-018-2115-2</a>."},"intvolume":"       470","page":"649–660","_id":"54928","user_id":"49428","department":[{"_id":"35"},{"_id":"22"}],"language":[{"iso":"eng"}],"type":"journal_article","publication":"Pflügers Archiv - European Journal of Physiology","abstract":[{"text":"The epithelial Na+ channel (ENaC) is a heteromeric channel composed of three subunits ($\\alpha$, $\\beta$, $\\gamma$). At the C-terminus of each subunit, a PY-motif allows binding of the ubiquitin ligase Nedd4-2 which plays a key role in promoting ENaC retrieval from the plasma membrane. Phosphorylation of Nedd4-2 by the serum and glucocorticoid-inducible kinase 1 (Sgk1) reduces Nedd4-2 binding to the PY-motifs. In $\\beta$ and $\\gamma$ENaC, threonine residues ($\\beta$T613, $\\gamma$T623) belong to an extracellular signal-regulated kinase (ERK) motif and directly precede the PY-motifs. Thus, phosphorylation of these residues may modulate the interaction of their adjacent PY-motifs with Nedd4-2. In this study, a phosphospecific antibody was used to demonstrate phosphorylation of $\\beta$T613 in Xenopus laevis oocytes heterologously expressing rat $\\alpha$$\\beta$$\\gamma$ENaC. Treating the oocytes with progesterone to stimulate ERK increased phosphorylation of $\\beta$T613. Inactivation of the putative phosphorylation sites by mutating both threonine residues to alanine ($\\beta$T613A/$\\gamma$T623A) increased ENaC-mediated amiloride-sensitive whole-cell currents ($\\Delta$Iami) and expression of $\\beta$ENaC at the cell surface. Co-expression of Nedd4-2 largely reduced $\\Delta$Iami in oocytes expressing $\\alpha$$\\beta$$\\gamma$ENaC or channels with mutated PY-motifs in $\\alpha$ and $\\gamma$ENaC or in $\\alpha$ and $\\beta$ENaC. Importantly, the inhibitory effect of co-expressed Nedd4-2 was largely reduced in channels with mutated PY-motifs in $\\alpha$ and $\\gamma$ENaC when combined with the $\\beta$T613A mutation but conserved in channels with mutated PY-motifs in $\\alpha$ and $\\beta$ENaC combined with the $\\gamma$T623A mutation. These results suggest that phosphorylation and dephosphorylation of $\\beta$T613 play a prominent role in regulating Nedd4-2-mediated ENaC retrieval from the plasma membrane.","lang":"eng"}],"status":"public"},{"language":[{"iso":"eng"}],"department":[{"_id":"35"},{"_id":"22"}],"user_id":"49428","_id":"54929","status":"public","abstract":[{"text":"The epithelial sodium channel (ENaC) is rate limiting for Na(+) absorption in the aldosterone-sensitive distal nephron comprising the late distal convoluted tubule (DCT2), the connecting tubule (CNT), and the entire collecting duct. Liddle syndrome (pseudohyperaldosteronism), a severe form of salt-sensitive hypertension, is caused by gain-of-function mutations of ENaC, but the precise tubular site of increased ENaC function is unknown. In the cortical collecting duct (CCD), ENaC is known to be regulated by aldosterone. In contrast, we recently reported aldosterone-independent ENaC regulation in the early part of the aldosterone-sensitive distal nephron. Here, we investigated ENaC function in the transition zone of DCT2/CNT or CNT/CCD microdissected from mice homozygous for Liddle syndrome mutation or from wild-type control mice. Whole-cell patch-clamp recordings were used to measure amiloride-sensitive ENaC currents in nephron fragments from mice maintained on different sodium diets to vary plasma aldosterone levels. Our data indicate that in mice with Liddle syndrome, the primary site of increased Na(+) reabsorption is the DCT2/CNT. In addition, increased aldosterone responsiveness of ENaC in CNT/CCD may contribute to salt-sensitive hypertension in Liddle syndrome. Single channel properties of ENaC were similar in Liddle syndrome mutation and wild-type mice, but ENaC expression at the apical membrane was increased in Liddle syndrome mutation when compared with wild-type mice, in particular, in animals maintained on a high salt diet. Our findings highlight the importance of ENaC function and regulation in the early part of the aldosterone-sensitive distal nephron for the maintenance of sodium balance and blood pressure control.","lang":"eng"}],"publication":"Hypertension","type":"journal_article","doi":"10.1161/hypertensionaha.115.07061","title":"In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron","volume":67,"author":[{"full_name":"Nesterov, Viatcheslav","last_name":"Nesterov","first_name":"Viatcheslav"},{"id":"49428","full_name":"Krueger, Bettina","last_name":"Krueger","orcid":"0000-0001-5351-1785","first_name":"Bettina"},{"first_name":"Marko","last_name":"Bertog","full_name":"Bertog, Marko"},{"last_name":"Dahlmann","full_name":"Dahlmann, Anke","first_name":"Anke"},{"first_name":"Ralf","full_name":"Palmisano, Ralf","last_name":"Palmisano"},{"full_name":"Korbmacher, Christoph","last_name":"Korbmacher","first_name":"Christoph"}],"date_created":"2024-06-30T13:44:27Z","date_updated":"2024-06-30T13:44:45Z","publisher":"Ovid Technologies (Wolters Kluwer Health)","page":"1256–1262","intvolume":"        67","citation":{"ama":"Nesterov V, Krueger B, Bertog M, Dahlmann A, Palmisano R, Korbmacher C. In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron. <i>Hypertension</i>. 2016;67(6):1256–1262. doi:<a href=\"https://doi.org/10.1161/hypertensionaha.115.07061\">10.1161/hypertensionaha.115.07061</a>","ieee":"V. Nesterov, B. Krueger, M. Bertog, A. Dahlmann, R. Palmisano, and C. Korbmacher, “In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron,” <i>Hypertension</i>, vol. 67, no. 6, pp. 1256–1262, 2016, doi: <a href=\"https://doi.org/10.1161/hypertensionaha.115.07061\">10.1161/hypertensionaha.115.07061</a>.","chicago":"Nesterov, Viatcheslav, Bettina Krueger, Marko Bertog, Anke Dahlmann, Ralf Palmisano, and Christoph Korbmacher. “In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron.” <i>Hypertension</i> 67, no. 6 (2016): 1256–1262. <a href=\"https://doi.org/10.1161/hypertensionaha.115.07061\">https://doi.org/10.1161/hypertensionaha.115.07061</a>.","apa":"Nesterov, V., Krueger, B., Bertog, M., Dahlmann, A., Palmisano, R., &#38; Korbmacher, C. (2016). In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron. <i>Hypertension</i>, <i>67</i>(6), 1256–1262. <a href=\"https://doi.org/10.1161/hypertensionaha.115.07061\">https://doi.org/10.1161/hypertensionaha.115.07061</a>","short":"V. Nesterov, B. Krueger, M. Bertog, A. Dahlmann, R. Palmisano, C. Korbmacher, Hypertension 67 (2016) 1256–1262.","bibtex":"@article{Nesterov_Krueger_Bertog_Dahlmann_Palmisano_Korbmacher_2016, title={In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron}, volume={67}, DOI={<a href=\"https://doi.org/10.1161/hypertensionaha.115.07061\">10.1161/hypertensionaha.115.07061</a>}, number={6}, journal={Hypertension}, publisher={Ovid Technologies (Wolters Kluwer Health)}, author={Nesterov, Viatcheslav and Krueger, Bettina and Bertog, Marko and Dahlmann, Anke and Palmisano, Ralf and Korbmacher, Christoph}, year={2016}, pages={1256–1262} }","mla":"Nesterov, Viatcheslav, et al. “In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron.” <i>Hypertension</i>, vol. 67, no. 6, Ovid Technologies (Wolters Kluwer Health), 2016, pp. 1256–1262, doi:<a href=\"https://doi.org/10.1161/hypertensionaha.115.07061\">10.1161/hypertensionaha.115.07061</a>."},"year":"2016","issue":"6"},{"issue":"27","citation":{"apa":"Haerteis, S., Krappitz, A., Krappitz, M., Murphy, J. E., Bertog, M., Krueger, B., Nacken, R., Chung, H., Hollenberg, M. D., Knecht, W., Bunnett, N. W., &#38; Korbmacher, C. (2014). Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites. <i>Journal of Biological Chemistry</i>, <i>289</i>(27), 19067–19078. <a href=\"https://doi.org/10.1074/jbc.m113.538470\">https://doi.org/10.1074/jbc.m113.538470</a>","bibtex":"@article{Haerteis_Krappitz_Krappitz_Murphy_Bertog_Krueger_Nacken_Chung_Hollenberg_Knecht_et al._2014, title={Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites}, volume={289}, DOI={<a href=\"https://doi.org/10.1074/jbc.m113.538470\">10.1074/jbc.m113.538470</a>}, number={27}, journal={Journal of Biological Chemistry}, publisher={Elsevier}, author={Haerteis, Silke and Krappitz, Annabel and Krappitz, Matteus and Murphy, Jane E. and Bertog, Marko and Krueger, Bettina and Nacken, Regina and Chung, Hyunjae and Hollenberg, Morley D. and Knecht, Wolfgang and et al.}, year={2014}, pages={19067–19078} }","mla":"Haerteis, Silke, et al. “Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites.” <i>Journal of Biological Chemistry</i>, vol. 289, no. 27, Elsevier, 2014, pp. 19067–19078, doi:<a href=\"https://doi.org/10.1074/jbc.m113.538470\">10.1074/jbc.m113.538470</a>.","short":"S. Haerteis, A. Krappitz, M. Krappitz, J.E. Murphy, M. Bertog, B. Krueger, R. Nacken, H. Chung, M.D. Hollenberg, W. Knecht, N.W. Bunnett, C. Korbmacher, Journal of Biological Chemistry 289 (2014) 19067–19078.","chicago":"Haerteis, Silke, Annabel Krappitz, Matteus Krappitz, Jane E. Murphy, Marko Bertog, Bettina Krueger, Regina Nacken, et al. “Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites.” <i>Journal of Biological Chemistry</i> 289, no. 27 (2014): 19067–19078. <a href=\"https://doi.org/10.1074/jbc.m113.538470\">https://doi.org/10.1074/jbc.m113.538470</a>.","ieee":"S. Haerteis <i>et al.</i>, “Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites,” <i>Journal of Biological Chemistry</i>, vol. 289, no. 27, pp. 19067–19078, 2014, doi: <a href=\"https://doi.org/10.1074/jbc.m113.538470\">10.1074/jbc.m113.538470</a>.","ama":"Haerteis S, Krappitz A, Krappitz M, et al. Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites. <i>Journal of Biological Chemistry</i>. 2014;289(27):19067–19078. doi:<a href=\"https://doi.org/10.1074/jbc.m113.538470\">10.1074/jbc.m113.538470</a>"},"page":"19067–19078","intvolume":"       289","year":"2014","date_created":"2024-06-30T13:57:24Z","author":[{"first_name":"Silke","last_name":"Haerteis","full_name":"Haerteis, Silke"},{"last_name":"Krappitz","full_name":"Krappitz, Annabel","first_name":"Annabel"},{"first_name":"Matteus","last_name":"Krappitz","full_name":"Krappitz, Matteus"},{"first_name":"Jane E.","last_name":"Murphy","full_name":"Murphy, Jane E."},{"full_name":"Bertog, Marko","last_name":"Bertog","first_name":"Marko"},{"id":"49428","full_name":"Krueger, Bettina","orcid":"0000-0001-5351-1785","last_name":"Krueger","first_name":"Bettina"},{"first_name":"Regina","full_name":"Nacken, Regina","last_name":"Nacken"},{"first_name":"Hyunjae","full_name":"Chung, Hyunjae","last_name":"Chung"},{"first_name":"Morley D.","last_name":"Hollenberg","full_name":"Hollenberg, Morley D."},{"last_name":"Knecht","full_name":"Knecht, Wolfgang","first_name":"Wolfgang"},{"full_name":"Bunnett, Nigel W.","last_name":"Bunnett","first_name":"Nigel W."},{"first_name":"Christoph","full_name":"Korbmacher, Christoph","last_name":"Korbmacher"}],"volume":289,"date_updated":"2024-06-30T13:57:37Z","publisher":"Elsevier","doi":"10.1074/jbc.m113.538470","title":"Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites","type":"journal_article","publication":"Journal of Biological Chemistry","status":"public","abstract":[{"text":"Proteolytic activation is a unique feature of the epithelial sodium channel (ENaC). However, the underlying molecular mechanisms and the physiologically relevant proteases remain to be identified. The serine protease trypsin I can activate ENaC in vitro but is unlikely to be the physiologically relevant activating protease in ENaC-expressing tissues in vivo. Herein, we investigated whether human trypsin IV, a form of trypsin that is co-expressed in several extrapancreatic epithelial cells with ENaC, can activate human ENaC. In Xenopus laevis oocytes, we monitored proteolytic activation of ENaC currents and the appearance of $\\gamma$ENaC cleavage products at the cell surface. We demonstrated that trypsin IV and trypsin I can stimulate ENaC heterologously expressed in oocytes. ENaC cleavage and activation by trypsin IV but not by trypsin I required a critical cleavage site (Lys-189) in the extracellular domain of the $\\gamma$-subunit. In contrast, channel activation by trypsin I was prevented by mutating three putative cleavage sites (Lys-168, Lys-170, and Arg-172) in addition to mutating previously described prostasin (RKRK(178)), plasmin (Lys-189), and neutrophil elastase (Val-182 and Val-193) sites. Moreover, we found that trypsin IV is expressed in human renal epithelial cells and can increase ENaC-mediated sodium transport in cultured human airway epithelial cells. Thus, trypsin IV may regulate ENaC function in epithelial tissues. Our results show, for the first time, that trypsin IV can stimulate ENaC and that trypsin IV and trypsin I activate ENaC by cleavage at distinct sites. The presence of distinct cleavage sites may be important for ENaC regulation by tissue-specific proteases.","lang":"eng"}],"user_id":"49428","department":[{"_id":"35"},{"_id":"22"}],"_id":"54943","language":[{"iso":"eng"}]},{"year":"2013","citation":{"ama":"Rauh R, Soell D, Haerteis S, et al. A mutation in the $\\beta$-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect. <i>American Journal of Physiology-Lung Cellular and Molecular Physiology</i>. 2013;304(1):L43–L55. doi:<a href=\"https://doi.org/10.1152/ajplung.00093.2012\">10.1152/ajplung.00093.2012</a>","chicago":"Rauh, Robert, Daniel Soell, Silke Haerteis, Alexei Diakov, Viatcheslav Nesterov, Bettina Krueger, Heinrich Sticht, and Christoph Korbmacher. “A Mutation in the $\\beta$-Subunit of ENaC Identified in a Patient with Cystic Fibrosis-like Symptoms Has a Gain-of-Function Effect.” <i>American Journal of Physiology-Lung Cellular and Molecular Physiology</i> 304, no. 1 (2013): L43–L55. <a href=\"https://doi.org/10.1152/ajplung.00093.2012\">https://doi.org/10.1152/ajplung.00093.2012</a>.","ieee":"R. Rauh <i>et al.</i>, “A mutation in the $\\beta$-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect,” <i>American Journal of Physiology-Lung Cellular and Molecular Physiology</i>, vol. 304, no. 1, pp. L43–L55, 2013, doi: <a href=\"https://doi.org/10.1152/ajplung.00093.2012\">10.1152/ajplung.00093.2012</a>.","mla":"Rauh, Robert, et al. “A Mutation in the $\\beta$-Subunit of ENaC Identified in a Patient with Cystic Fibrosis-like Symptoms Has a Gain-of-Function Effect.” <i>American Journal of Physiology-Lung Cellular and Molecular Physiology</i>, vol. 304, no. 1, American Physiological Society, 2013, pp. L43–L55, doi:<a href=\"https://doi.org/10.1152/ajplung.00093.2012\">10.1152/ajplung.00093.2012</a>.","short":"R. Rauh, D. Soell, S. Haerteis, A. Diakov, V. Nesterov, B. Krueger, H. Sticht, C. Korbmacher, American Journal of Physiology-Lung Cellular and Molecular Physiology 304 (2013) L43–L55.","bibtex":"@article{Rauh_Soell_Haerteis_Diakov_Nesterov_Krueger_Sticht_Korbmacher_2013, title={A mutation in the $\\beta$-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect}, volume={304}, DOI={<a href=\"https://doi.org/10.1152/ajplung.00093.2012\">10.1152/ajplung.00093.2012</a>}, number={1}, journal={American Journal of Physiology-Lung Cellular and Molecular Physiology}, publisher={American Physiological Society}, author={Rauh, Robert and Soell, Daniel and Haerteis, Silke and Diakov, Alexei and Nesterov, Viatcheslav and Krueger, Bettina and Sticht, Heinrich and Korbmacher, Christoph}, year={2013}, pages={L43–L55} }","apa":"Rauh, R., Soell, D., Haerteis, S., Diakov, A., Nesterov, V., Krueger, B., Sticht, H., &#38; Korbmacher, C. (2013). A mutation in the $\\beta$-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect. <i>American Journal of Physiology-Lung Cellular and Molecular Physiology</i>, <i>304</i>(1), L43–L55. <a href=\"https://doi.org/10.1152/ajplung.00093.2012\">https://doi.org/10.1152/ajplung.00093.2012</a>"},"page":"L43–L55","intvolume":"       304","issue":"1","title":"A mutation in the $\\beta$-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect","doi":"10.1152/ajplung.00093.2012","publisher":"American Physiological Society","date_updated":"2024-06-30T13:47:56Z","author":[{"full_name":"Rauh, Robert","last_name":"Rauh","first_name":"Robert"},{"last_name":"Soell","full_name":"Soell, Daniel","first_name":"Daniel"},{"last_name":"Haerteis","full_name":"Haerteis, Silke","first_name":"Silke"},{"first_name":"Alexei","full_name":"Diakov, Alexei","last_name":"Diakov"},{"last_name":"Nesterov","full_name":"Nesterov, Viatcheslav","first_name":"Viatcheslav"},{"orcid":"0000-0001-5351-1785","last_name":"Krueger","full_name":"Krueger, Bettina","id":"49428","first_name":"Bettina"},{"full_name":"Sticht, Heinrich","last_name":"Sticht","first_name":"Heinrich"},{"full_name":"Korbmacher, Christoph","last_name":"Korbmacher","first_name":"Christoph"}],"date_created":"2024-06-30T13:47:44Z","volume":304,"abstract":[{"text":"In some patients with atypical cystic fibrosis (CF), only one allele of the CF transmembrane conductance regulator (CFTR) gene is affected. Mutations of the epithelial sodium channel (ENaC) may contribute to the pathophysiology of the disease in these patients. To functionally characterize a mutation in the $\\beta$-subunit of ENaC ($\\beta$V348M) recently identified in a patient with severe CF-like symptoms (Mutesa et al. 2009), we expressed wild-type (wt) $\\alpha$$\\beta$$\\gamma$ENaC or mutant $\\alpha$$\\beta$V348M$\\gamma$ENaC in Xenopus laevis oocytes. The $\\beta$V348M mutation stimulated amiloride-sensitive whole-cell current ($\\Delta$I(ami)) by $\\sim$40% but had no effect on surface expression or single-channel conductance of ENaC. Instead the mutation increased channel open probability (P(o)). Proteolytic activation of mutant ENaC by chymotrypsin was reduced compared with that of wt ENaC ($\\sim$3.0-fold vs. $\\sim$4.2-fold), which is consistent with the increased baseline P(o) of mutant ENaC. Similarly, the ENaC activator S3969 stimulated mutant ENaC currents to a lesser degree (by $\\sim$2.6-fold) than wt ENaC currents (by $\\sim$3.5-fold). The gain-of-function effect of the $\\beta$V348M mutation was confirmed by whole-cell current measurements in HEK293 cells transiently transfected with wt or mutant ENaC. Computational channel modeling in combination with functional expression of different $\\beta$V348 mutants in oocytes suggests that the $\\beta$V348M mutation increases channel P(o) by destabilizing the closed channel state. Our findings indicate that the gain-of-function effect of the $\\beta$V348M mutation may contribute to CF pathophysiology by inappropriately increasing sodium and fluid absorption in the respiratory tract.","lang":"eng"}],"status":"public","type":"journal_article","publication":"American Journal of Physiology-Lung Cellular and Molecular Physiology","language":[{"iso":"eng"}],"_id":"54933","user_id":"49428","department":[{"_id":"35"},{"_id":"22"}]},{"language":[{"iso":"eng"}],"department":[{"_id":"35"},{"_id":"22"}],"user_id":"49428","_id":"54937","status":"public","abstract":[{"lang":"eng","text":"Purpose: The epithelial sodium channel (ENaC) is typically expressed in sodium-absorbing epithelia. Several reports suggest that ENaC is also expressed in ocular tissues and may play a role in aqueous humor secretion and glaucoma. However, the precise localization of ENaC in the human eye is still unclear. Here, the authors studied ENaC expression in 12 normal human donor eyes and in six eyes of patients with glaucoma. Methods: Quantitative real-time PCR was used to investigate the expression of $\\alpha$-, $\\beta$-, $\\gamma$-, and $\\delta$-ENaC transcripts in ocular tissues. In addition, the authors performed immunohistochemical studies using recently generated antibodies against human $\\beta$- and $\\gamma$-ENaC. Results: At the mRNA level, all four ENaC subunits were found to be expressed in a wide range of ocular tissues from normal and glaucomatous human eyes, with the cornea, ciliary body, iris, and retina showing the highest expression levels. At the protein level, $\\beta$- and $\\gamma$-ENaC subunits showed distinct distribution patterns and could be immunolocalized primarily to the cell membranes of epithelial cells of the cornea and to the conjunctiva, iris, ciliary body, lens, and retinal pigment epithelium but also to vascular endothelial cells, smooth muscle cells, stromal cells, and retinal neurons. The authors found no altered mRNA level of any subunit in glaucomatous eyes. Conclusions: All four ENaC subunits ($\\alpha$$\\beta$$\\gamma$$\\delta$) are expressed in the normal human eye, with distinct localization of subunits possibly reflecting different functional states of the channel. The (patho-)physiological roles of ENaC in the various localizations in the eye remain to be determined."}],"publication":"Investigative Opthalmology & Visual Science","type":"journal_article","doi":"10.1167/iovs.11-8581","title":"Four Subunits ($\\alpha$$\\beta$$\\gamma$$\\delta$) of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations","volume":53,"author":[{"orcid":"0000-0001-5351-1785","last_name":"Krueger","full_name":"Krueger, Bettina","id":"49428","first_name":"Bettina"},{"full_name":"Schlötzer-Schrehardt, Ursula","last_name":"Schlötzer-Schrehardt","first_name":"Ursula"},{"full_name":"Haerteis, Silke","last_name":"Haerteis","first_name":"Silke"},{"last_name":"Zenkel","full_name":"Zenkel, Matthias","first_name":"Matthias"},{"first_name":"Verena E.","last_name":"Chankiewitz","full_name":"Chankiewitz, Verena E."},{"full_name":"Amann, Kerstin U.","last_name":"Amann","first_name":"Kerstin U."},{"first_name":"Friedrich E.","full_name":"Kruse, Friedrich E.","last_name":"Kruse"},{"full_name":"Korbmacher, Christoph","last_name":"Korbmacher","first_name":"Christoph"}],"date_created":"2024-06-30T13:51:35Z","publisher":"Association for Research in Vision and Ophthalmology (ARVO)","date_updated":"2024-06-30T13:52:14Z","page":"596–604","intvolume":"        53","citation":{"apa":"Krueger, B., Schlötzer-Schrehardt, U., Haerteis, S., Zenkel, M., Chankiewitz, V. E., Amann, K. U., Kruse, F. E., &#38; Korbmacher, C. (2012). Four Subunits ($\\alpha$$\\beta$$\\gamma$$\\delta$) of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations. <i>Investigative Opthalmology &#38; Visual Science</i>, <i>53</i>(2), 596–604. <a href=\"https://doi.org/10.1167/iovs.11-8581\">https://doi.org/10.1167/iovs.11-8581</a>","short":"B. Krueger, U. Schlötzer-Schrehardt, S. Haerteis, M. Zenkel, V.E. Chankiewitz, K.U. Amann, F.E. Kruse, C. Korbmacher, Investigative Opthalmology &#38; Visual Science 53 (2012) 596–604.","bibtex":"@article{Krueger_Schlötzer-Schrehardt_Haerteis_Zenkel_Chankiewitz_Amann_Kruse_Korbmacher_2012, title={Four Subunits ($\\alpha$$\\beta$$\\gamma$$\\delta$) of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations}, volume={53}, DOI={<a href=\"https://doi.org/10.1167/iovs.11-8581\">10.1167/iovs.11-8581</a>}, number={2}, journal={Investigative Opthalmology &#38; Visual Science}, publisher={Association for Research in Vision and Ophthalmology (ARVO)}, author={Krueger, Bettina and Schlötzer-Schrehardt, Ursula and Haerteis, Silke and Zenkel, Matthias and Chankiewitz, Verena E. and Amann, Kerstin U. and Kruse, Friedrich E. and Korbmacher, Christoph}, year={2012}, pages={596–604} }","mla":"Krueger, Bettina, et al. “Four Subunits ($\\alpha$$\\beta$$\\gamma$$\\delta$) of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations.” <i>Investigative Opthalmology &#38; Visual Science</i>, vol. 53, no. 2, Association for Research in Vision and Ophthalmology (ARVO), 2012, pp. 596–604, doi:<a href=\"https://doi.org/10.1167/iovs.11-8581\">10.1167/iovs.11-8581</a>.","ama":"Krueger B, Schlötzer-Schrehardt U, Haerteis S, et al. Four Subunits ($\\alpha$$\\beta$$\\gamma$$\\delta$) of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations. <i>Investigative Opthalmology &#38; Visual Science</i>. 2012;53(2):596–604. doi:<a href=\"https://doi.org/10.1167/iovs.11-8581\">10.1167/iovs.11-8581</a>","ieee":"B. Krueger <i>et al.</i>, “Four Subunits ($\\alpha$$\\beta$$\\gamma$$\\delta$) of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations,” <i>Investigative Opthalmology &#38; Visual Science</i>, vol. 53, no. 2, pp. 596–604, 2012, doi: <a href=\"https://doi.org/10.1167/iovs.11-8581\">10.1167/iovs.11-8581</a>.","chicago":"Krueger, Bettina, Ursula Schlötzer-Schrehardt, Silke Haerteis, Matthias Zenkel, Verena E. Chankiewitz, Kerstin U. Amann, Friedrich E. Kruse, and Christoph Korbmacher. “Four Subunits ($\\alpha$$\\beta$$\\gamma$$\\delta$) of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations.” <i>Investigative Opthalmology &#38; Visual Science</i> 53, no. 2 (2012): 596–604. <a href=\"https://doi.org/10.1167/iovs.11-8581\">https://doi.org/10.1167/iovs.11-8581</a>."},"year":"2012","issue":"2"},{"language":[{"iso":"eng"}],"user_id":"49428","department":[{"_id":"35"},{"_id":"22"}],"_id":"54930","status":"public","abstract":[{"lang":"eng","text":"Background: Increased expression of the pro-fibrotic protein connective tissue growth factor (CTGF) has been detected in injured kidneys and elevated urinary levels of CTGF are discussed as prognostic marker of chronic kidney disease. There is evidence that epithelial cells lining the renal tubular system contribute to uptake and secretion of CTGF. However, the role of different types of tubular epithelial cells in these processes so far has not been addressed in primary cultures of human cells. Results: Tubular epithelial cells of proximal and distal origin were isolated from human kidneys and cultured as polarized cells in insert wells. The pro-fibrotic stimuli lysophosphatidic acid (LPA) and transforming growth factor $\\beta$ (TGF-$\\beta$) were used to induce CTGF secretion.LPA activated CTGF secretion in proximal tubular cells when applied from either the apical or the basolateral side as shown by immunocytochemistry. CTGF was secreted exclusively to the apical side. Signaling pathways activated by LPA included MAP kinase and Rho kinase signaling. TGF-$\\beta$ applied from either side also stimulated CTGF secretion primarily to the apical side with little basolateral release.Interestingly, TGF-$\\beta$ activation induced different signaling pathways depending on the side of TGF-$\\beta$ application. Smad signaling was almost exclusively activated from the basolateral side most prominently in cells of distal origin. Only part of these cells also synthesized CTGF indicating that Smad activation alone was not sufficient for CTGF induction. MAP kinases were involved in apical TGF-$\\beta$-mediated activation of CTGF synthesis in proximal cells and a subset of epithelial cells of distal origin. This subpopulation of distal tubular cells was also able to internalize recombinant apical CTGF, in addition to proximal cells which were the main cells to take up exogenous CTGF. Conclusions: Analysis of polarized human primary renal epithelial cells in a transwell system shows that vectorial secretion of the pro-fibrotic protein CTGF depends on the cell type, the stimulus and the signaling pathway activated. In all conditions, CTGF was secreted mainly to the apical side upon TGF-$\\beta$ and LPA treatment and therefore, likely contributes to increased urinary CTGF levels in vivo. Moreover, CTGF secreted basolaterally may be active as paracrine pro-fibrotic mediator."}],"type":"journal_article","publication":"Cell Communication and Signaling","doi":"10.1186/1478-811x-10-25","title":"Vectorial secretion of CTGF as a cell-type specific response to LPA and TGF-$\\beta$ in human tubular epithelial cells","author":[{"first_name":"Jonathan","full_name":"Zuehlke, Jonathan","last_name":"Zuehlke"},{"full_name":"Ebenau, Astrid","last_name":"Ebenau","first_name":"Astrid"},{"first_name":"Bettina","id":"49428","full_name":"Krueger, Bettina","last_name":"Krueger","orcid":"0000-0001-5351-1785"},{"full_name":"Goppelt-Struebe, Margarete","last_name":"Goppelt-Struebe","first_name":"Margarete"}],"date_created":"2024-06-30T13:45:36Z","volume":10,"date_updated":"2024-06-30T13:45:48Z","publisher":"Springer","citation":{"apa":"Zuehlke, J., Ebenau, A., Krueger, B., &#38; Goppelt-Struebe, M. (2012). Vectorial secretion of CTGF as a cell-type specific response to LPA and TGF-$\\beta$ in human tubular epithelial cells. <i>Cell Communication and Signaling</i>, <i>10</i>(1). <a href=\"https://doi.org/10.1186/1478-811x-10-25\">https://doi.org/10.1186/1478-811x-10-25</a>","short":"J. Zuehlke, A. Ebenau, B. Krueger, M. Goppelt-Struebe, Cell Communication and Signaling 10 (2012).","mla":"Zuehlke, Jonathan, et al. “Vectorial Secretion of CTGF as a Cell-Type Specific Response to LPA and TGF-$\\beta$ in Human Tubular Epithelial Cells.” <i>Cell Communication and Signaling</i>, vol. 10, no. 1, Springer, 2012, doi:<a href=\"https://doi.org/10.1186/1478-811x-10-25\">10.1186/1478-811x-10-25</a>.","bibtex":"@article{Zuehlke_Ebenau_Krueger_Goppelt-Struebe_2012, title={Vectorial secretion of CTGF as a cell-type specific response to LPA and TGF-$\\beta$ in human tubular epithelial cells}, volume={10}, DOI={<a href=\"https://doi.org/10.1186/1478-811x-10-25\">10.1186/1478-811x-10-25</a>}, number={1}, journal={Cell Communication and Signaling}, publisher={Springer}, author={Zuehlke, Jonathan and Ebenau, Astrid and Krueger, Bettina and Goppelt-Struebe, Margarete}, year={2012} }","chicago":"Zuehlke, Jonathan, Astrid Ebenau, Bettina Krueger, and Margarete Goppelt-Struebe. “Vectorial Secretion of CTGF as a Cell-Type Specific Response to LPA and TGF-$\\beta$ in Human Tubular Epithelial Cells.” <i>Cell Communication and Signaling</i> 10, no. 1 (2012). <a href=\"https://doi.org/10.1186/1478-811x-10-25\">https://doi.org/10.1186/1478-811x-10-25</a>.","ieee":"J. Zuehlke, A. Ebenau, B. Krueger, and M. Goppelt-Struebe, “Vectorial secretion of CTGF as a cell-type specific response to LPA and TGF-$\\beta$ in human tubular epithelial cells,” <i>Cell Communication and Signaling</i>, vol. 10, no. 1, 2012, doi: <a href=\"https://doi.org/10.1186/1478-811x-10-25\">10.1186/1478-811x-10-25</a>.","ama":"Zuehlke J, Ebenau A, Krueger B, Goppelt-Struebe M. Vectorial secretion of CTGF as a cell-type specific response to LPA and TGF-$\\beta$ in human tubular epithelial cells. <i>Cell Communication and Signaling</i>. 2012;10(1). doi:<a href=\"https://doi.org/10.1186/1478-811x-10-25\">10.1186/1478-811x-10-25</a>"},"intvolume":"        10","year":"2012","issue":"1"},{"abstract":[{"lang":"eng","text":"Aldosterone is thought to be the main hormone to stimulate the epithelial sodium channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) comprising the late distal convoluted tubule (DCT2), the connecting tubule (CNT) and the entire collecting duct (CD). There is immunohistochemical evidence for an axial gradient of ENaC expression along the ASDN with highest expression in the DCT2 and CNT. However, most of our knowledge about renal ENaC function stems from studies in the cortical collecting duct (CCD). Here we investigated ENaC function in the transition zone of DCT2/CNT or CNT/CCD microdissected from mice maintained on different sodium diets to vary plasma aldosterone levels. Single-channel recordings demonstrated amiloride-sensitive Na(+) channels in DCT2/CNT with biophysical properties typical for ENaC previously described in CNT/CCD. In animals maintained on a standard salt diet, the average ENaC-mediated whole cell current ($\\Delta$I(ami)) was higher in DCT2/CNT than in CNT/CCD. A low salt diet increased $\\Delta$I(ami) in CNT/CCD but had little effect on $\\Delta$I(ami) in DCT2/CNT. To investigate whether aldosterone is necessary for ENaC activity in the DCT2/CNT, we used aldosterone synthase knockout (AS(-/-)) mice that lack aldosterone. In CNT/CCD of AS(-/-) mice, $\\Delta$I(ami) was lower than that in wild-type (WT) animals and was not stimulated by a low salt diet. In contrast, in DCT2/CNT of AS(-/-) mice, $\\Delta$I(ami) was similar to that in DCT2/CNT of WT animals both on a standard and on a low salt diet. We conclude that ENaC function in the DCT2/CNT is largely independent of aldosterone which is in contrast to its known aldosterone sensitivity in CNT/CCD."}],"status":"public","type":"journal_article","publication":"American Journal of Physiology-Renal Physiology","language":[{"iso":"eng"}],"_id":"54934","user_id":"49428","department":[{"_id":"35"},{"_id":"22"}],"year":"2012","citation":{"chicago":"Nesterov, Viatcheslav, Anke Dahlmann, Bettina Krueger, Marko Bertog, Johannes Loffing, and Christoph Korbmacher. “Aldosterone-Dependent and -Independent Regulation of the Epithelial Sodium Channel (ENaC) in Mouse Distal Nephron.” <i>American Journal of Physiology-Renal Physiology</i> 303, no. 9 (2012): F1289–F1299. <a href=\"https://doi.org/10.1152/ajprenal.00247.2012\">https://doi.org/10.1152/ajprenal.00247.2012</a>.","ieee":"V. Nesterov, A. Dahlmann, B. Krueger, M. Bertog, J. Loffing, and C. Korbmacher, “Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron,” <i>American Journal of Physiology-Renal Physiology</i>, vol. 303, no. 9, pp. F1289–F1299, 2012, doi: <a href=\"https://doi.org/10.1152/ajprenal.00247.2012\">10.1152/ajprenal.00247.2012</a>.","ama":"Nesterov V, Dahlmann A, Krueger B, Bertog M, Loffing J, Korbmacher C. Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron. <i>American Journal of Physiology-Renal Physiology</i>. 2012;303(9):F1289–F1299. doi:<a href=\"https://doi.org/10.1152/ajprenal.00247.2012\">10.1152/ajprenal.00247.2012</a>","apa":"Nesterov, V., Dahlmann, A., Krueger, B., Bertog, M., Loffing, J., &#38; Korbmacher, C. (2012). Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron. <i>American Journal of Physiology-Renal Physiology</i>, <i>303</i>(9), F1289–F1299. <a href=\"https://doi.org/10.1152/ajprenal.00247.2012\">https://doi.org/10.1152/ajprenal.00247.2012</a>","bibtex":"@article{Nesterov_Dahlmann_Krueger_Bertog_Loffing_Korbmacher_2012, title={Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron}, volume={303}, DOI={<a href=\"https://doi.org/10.1152/ajprenal.00247.2012\">10.1152/ajprenal.00247.2012</a>}, number={9}, journal={American Journal of Physiology-Renal Physiology}, publisher={American Physiological Society}, author={Nesterov, Viatcheslav and Dahlmann, Anke and Krueger, Bettina and Bertog, Marko and Loffing, Johannes and Korbmacher, Christoph}, year={2012}, pages={F1289–F1299} }","short":"V. Nesterov, A. Dahlmann, B. Krueger, M. Bertog, J. Loffing, C. Korbmacher, American Journal of Physiology-Renal Physiology 303 (2012) F1289–F1299.","mla":"Nesterov, Viatcheslav, et al. “Aldosterone-Dependent and -Independent Regulation of the Epithelial Sodium Channel (ENaC) in Mouse Distal Nephron.” <i>American Journal of Physiology-Renal Physiology</i>, vol. 303, no. 9, American Physiological Society, 2012, pp. F1289–F1299, doi:<a href=\"https://doi.org/10.1152/ajprenal.00247.2012\">10.1152/ajprenal.00247.2012</a>."},"page":"F1289–F1299","intvolume":"       303","issue":"9","title":"Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron","doi":"10.1152/ajprenal.00247.2012","publisher":"American Physiological Society","date_updated":"2024-06-30T13:49:30Z","author":[{"last_name":"Nesterov","full_name":"Nesterov, Viatcheslav","first_name":"Viatcheslav"},{"first_name":"Anke","full_name":"Dahlmann, Anke","last_name":"Dahlmann"},{"first_name":"Bettina","full_name":"Krueger, Bettina","id":"49428","last_name":"Krueger","orcid":"0000-0001-5351-1785"},{"first_name":"Marko","last_name":"Bertog","full_name":"Bertog, Marko"},{"first_name":"Johannes","last_name":"Loffing","full_name":"Loffing, Johannes"},{"first_name":"Christoph","last_name":"Korbmacher","full_name":"Korbmacher, Christoph"}],"date_created":"2024-06-30T13:49:18Z","volume":303},{"_id":"54939","department":[{"_id":"35"},{"_id":"22"}],"user_id":"49428","language":[{"iso":"eng"}],"publication":"PLOS ONE","type":"journal_article","abstract":[{"lang":"eng","text":"Background: Renal tubular epithelial cells of proximal and distal origin differ markedly in their physiological functions. Therefore, we hypothesized that they also differ in their capacity to undergo epithelial to mesenchymal alterations. Results: We used cultures of freshly isolated primary human tubular cells. To distinguish cells of different tubular origin we took advantage of the fact that human proximal epithelial cells uniquely express N-cadherin instead of E-cadherin as major cell-cell adhesion molecule. To provoke mesenchymal alteration we treated these cocultures with TGF-$\\beta$ for up to 6 days. Within this time period, the morphology of distal tubular cells was barely altered. In contrast to tubular cell lines, E-cadherin was not down-regulated by TGF-$\\beta$, even though TGF-$\\beta$ signal transduction was initiated as demonstrated by nuclear localization of Smad2/3. Analysis of transcription factors and miRNAs possibly involved in E-cadherin regulation revealed high levels of miRNAs of the miR200-family, which may contribute to the stability of E-cadherin expression in human distal tubular epithelial cells. By contrast, proximal tubular epithelial cells altered their phenotype when treated with TGF-$\\beta$. They became elongated and formed three-dimensional structures. Rho-kinases were identified as modulators of TGF-$\\beta$-induced morphological alterations. Non-specific inhibition of Rho-kinases resulted in stabilization of the epithelial phenotype, while partial effects were observed upon downregulation of Rho-kinase isoforms ROCK1 and ROCK2. The distinct reactivity of proximal and distal cells was retained when the cells were cultured as polarized cells. Conclusions: Interference with Rho-kinase signaling provides a target to counteract TGF-$\\beta$-mediated mesenchymal alterations of epithelial cells, particularly in proximal tubular epithelial cells. Furthermore, primary distal tubular cells differed from cell lines by their high phenotypic stability which included constant expression of E-cadherin. Our cell culture system of primary epithelial cells is thus suitable to understand and modulate cellular remodeling processes of distinct tubular cells relevant for human renal disease."}],"status":"public","publisher":"Public Library of Science","date_updated":"2024-06-30T13:53:30Z","volume":7,"date_created":"2024-06-30T13:53:18Z","author":[{"full_name":"Keller, Christof","last_name":"Keller","first_name":"Christof"},{"full_name":"Kroening, Sven","last_name":"Kroening","first_name":"Sven"},{"first_name":"Jonathan","last_name":"Zuehlke","full_name":"Zuehlke, Jonathan"},{"first_name":"Frank","full_name":"Kunath, Frank","last_name":"Kunath"},{"full_name":"Krueger, Bettina","id":"49428","orcid":"0000-0001-5351-1785","last_name":"Krueger","first_name":"Bettina"},{"full_name":"Goppelt-Struebe, Margarete","last_name":"Goppelt-Struebe","first_name":"Margarete"}],"title":"Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial Cells","doi":"10.1371/journal.pone.0043584","publication_identifier":{"issn":["1932-6203"]},"issue":"8","year":"2012","intvolume":"         7","page":"e43584","citation":{"apa":"Keller, C., Kroening, S., Zuehlke, J., Kunath, F., Krueger, B., &#38; Goppelt-Struebe, M. (2012). Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial Cells. <i>PLOS ONE</i>, <i>7</i>(8), e43584. <a href=\"https://doi.org/10.1371/journal.pone.0043584\">https://doi.org/10.1371/journal.pone.0043584</a>","mla":"Keller, Christof, et al. “Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial Cells.” <i>PLOS ONE</i>, vol. 7, no. 8, Public Library of Science, 2012, p. e43584, doi:<a href=\"https://doi.org/10.1371/journal.pone.0043584\">10.1371/journal.pone.0043584</a>.","short":"C. Keller, S. Kroening, J. Zuehlke, F. Kunath, B. Krueger, M. Goppelt-Struebe, PLOS ONE 7 (2012) e43584.","bibtex":"@article{Keller_Kroening_Zuehlke_Kunath_Krueger_Goppelt-Struebe_2012, title={Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial Cells}, volume={7}, DOI={<a href=\"https://doi.org/10.1371/journal.pone.0043584\">10.1371/journal.pone.0043584</a>}, number={8}, journal={PLOS ONE}, publisher={Public Library of Science}, author={Keller, Christof and Kroening, Sven and Zuehlke, Jonathan and Kunath, Frank and Krueger, Bettina and Goppelt-Struebe, Margarete}, year={2012}, pages={e43584} }","ieee":"C. Keller, S. Kroening, J. Zuehlke, F. Kunath, B. Krueger, and M. Goppelt-Struebe, “Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial Cells,” <i>PLOS ONE</i>, vol. 7, no. 8, p. e43584, 2012, doi: <a href=\"https://doi.org/10.1371/journal.pone.0043584\">10.1371/journal.pone.0043584</a>.","chicago":"Keller, Christof, Sven Kroening, Jonathan Zuehlke, Frank Kunath, Bettina Krueger, and Margarete Goppelt-Struebe. “Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial Cells.” <i>PLOS ONE</i> 7, no. 8 (2012): e43584. <a href=\"https://doi.org/10.1371/journal.pone.0043584\">https://doi.org/10.1371/journal.pone.0043584</a>.","ama":"Keller C, Kroening S, Zuehlke J, Kunath F, Krueger B, Goppelt-Struebe M. Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial Cells. <i>PLOS ONE</i>. 2012;7(8):e43584. doi:<a href=\"https://doi.org/10.1371/journal.pone.0043584\">10.1371/journal.pone.0043584</a>"}},{"type":"journal_article","publication":"Cellular Physiology and Biochemistry","status":"public","abstract":[{"lang":"eng","text":"Loss-of-function mutations of the epithelial sodium channel (ENaC) may contribute to pulmonary symptoms resembling those of patients with atypical cystic fibrosis (CF). Recently, we identified a loss-of-function mutation in the alpha-subunit of ENaC (alphaF61L) in an atypical CF patient without mutations in CFTR. To investigate the functional effect of this mutation, we expressed human wild-type alpha beta gamma-ENaC or mutant alpha(F61L) beta gamma-ENaC in Xenopus laevis oocytes. The alphaF61L mutation reduced the ENaC mediated whole-cell currents by approximately 90%. In contrast, the mutation decreased channel surface expression only by approximately 40% and did not alter the single-channel conductance. These findings indicate that the major effect of the mutation is a reduction of the average channel open probability (P(o)). This was confirmed by experiments using the betaS520C mutant ENaC which can be converted to a channel with a P(o) of nearly one, and by experiments using chymotrypsin to proteolytically activate the channel. These experiments revealed that the mutation reduced the average P(o) of ENaC by approximately 75%. Na(+) self inhibition of the mutant channel was significantly enhanced, but the observed effect was too small to account for the large reduction in average channel P(o). The ENaC-activator S3969 partially rescued the loss-of-function phenotype of the alphaF61L mutation. We conclude that the alphaF61L mutation may contribute to respiratory symptoms in atypical CF patients."}],"user_id":"49428","department":[{"_id":"35"},{"_id":"22"}],"_id":"54942","language":[{"iso":"eng"}],"issue":"001","citation":{"short":"R. Huber, B. Krueger, A. Diakov, J. Korbmacher, S. Haerteis, J. Einsiedel, P. Gmeiner, A. Azad, H. Cuppens, J.-J. Cassiman, C. Korbmacher, R. Rauh, Cellular Physiology and Biochemistry 25 (2010) 145–158.","mla":"Huber, Regina, et al. “Functional Characterization of a Partial Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis.” <i>Cellular Physiology and Biochemistry</i>, vol. 25, no. 001, S. Karger AG, 2010, pp. 145–158, doi:<a href=\"https://doi.org/10.1159/000272059\">10.1159/000272059</a>.","bibtex":"@article{Huber_Krueger_Diakov_Korbmacher_Haerteis_Einsiedel_Gmeiner_Azad_Cuppens_Cassiman_et al._2010, title={Functional Characterization of a Partial Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis}, volume={25}, DOI={<a href=\"https://doi.org/10.1159/000272059\">10.1159/000272059</a>}, number={001}, journal={Cellular Physiology and Biochemistry}, publisher={S. Karger AG}, author={Huber, Regina and Krueger, Bettina and Diakov, Alexei and Korbmacher, Judit and Haerteis, Silke and Einsiedel, Jürgen and Gmeiner, Peter and Azad, Abul and Cuppens, Harry and Cassiman, Jean-Jaques and et al.}, year={2010}, pages={145–158} }","apa":"Huber, R., Krueger, B., Diakov, A., Korbmacher, J., Haerteis, S., Einsiedel, J., Gmeiner, P., Azad, A., Cuppens, H., Cassiman, J.-J., Korbmacher, C., &#38; Rauh, R. (2010). Functional Characterization of a Partial Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis. <i>Cellular Physiology and Biochemistry</i>, <i>25</i>(001), 145–158. <a href=\"https://doi.org/10.1159/000272059\">https://doi.org/10.1159/000272059</a>","ama":"Huber R, Krueger B, Diakov A, et al. Functional Characterization of a Partial Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis. <i>Cellular Physiology and Biochemistry</i>. 2010;25(001):145–158. doi:<a href=\"https://doi.org/10.1159/000272059\">10.1159/000272059</a>","ieee":"R. Huber <i>et al.</i>, “Functional Characterization of a Partial Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis,” <i>Cellular Physiology and Biochemistry</i>, vol. 25, no. 001, pp. 145–158, 2010, doi: <a href=\"https://doi.org/10.1159/000272059\">10.1159/000272059</a>.","chicago":"Huber, Regina, Bettina Krueger, Alexei Diakov, Judit Korbmacher, Silke Haerteis, Jürgen Einsiedel, Peter Gmeiner, et al. “Functional Characterization of a Partial Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis.” <i>Cellular Physiology and Biochemistry</i> 25, no. 001 (2010): 145–158. <a href=\"https://doi.org/10.1159/000272059\">https://doi.org/10.1159/000272059</a>."},"intvolume":"        25","page":"145–158","year":"2010","author":[{"first_name":"Regina","last_name":"Huber","full_name":"Huber, Regina"},{"full_name":"Krueger, Bettina","id":"49428","last_name":"Krueger","orcid":"0000-0001-5351-1785","first_name":"Bettina"},{"full_name":"Diakov, Alexei","last_name":"Diakov","first_name":"Alexei"},{"first_name":"Judit","last_name":"Korbmacher","full_name":"Korbmacher, Judit"},{"first_name":"Silke","full_name":"Haerteis, Silke","last_name":"Haerteis"},{"first_name":"Jürgen","last_name":"Einsiedel","full_name":"Einsiedel, Jürgen"},{"first_name":"Peter","full_name":"Gmeiner, Peter","last_name":"Gmeiner"},{"first_name":"Abul","last_name":"Azad","full_name":"Azad, Abul"},{"first_name":"Harry","last_name":"Cuppens","full_name":"Cuppens, Harry"},{"last_name":"Cassiman","full_name":"Cassiman, Jean-Jaques","first_name":"Jean-Jaques"},{"full_name":"Korbmacher, Christoph","last_name":"Korbmacher","first_name":"Christoph"},{"first_name":"Robert","full_name":"Rauh, Robert","last_name":"Rauh"}],"date_created":"2024-06-30T13:56:57Z","volume":25,"date_updated":"2024-06-30T13:57:07Z","publisher":"S. Karger AG","doi":"10.1159/000272059","title":"Functional Characterization of a Partial Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis"},{"_id":"54931","user_id":"49428","department":[{"_id":"35"},{"_id":"22"}],"language":[{"iso":"eng"}],"type":"journal_article","publication":"Journal of the American Society of Nephrology","abstract":[{"lang":"eng","text":"Proteinuria and increased renal reabsorption of NaCl characterize the nephrotic syndrome. Here, we show that protein-rich urine from nephrotic rats and from patients with nephrotic syndrome activate the epithelial sodium channel (ENaC) in cultured M-1 mouse collecting duct cells and in Xenopus laevis oocytes heterologously expressing ENaC. The activation depended on urinary serine protease activity. We identified plasmin as a urinary serine protease by matrix-assisted laser desorption/ionization time of-flight mass spectrometry. Purified plasmin activated ENaC currents, and inhibitors of plasmin abolished urinary protease activity and the ability to activate ENaC. In nephrotic syndrome, tubular urokinase-type plasminogen activator likely converts filtered plasminogen to plasmin. Consistent with this, the combined application of urokinase-type plasminogen activator and plasminogen stimulated amiloride-sensitive transepithelial sodium transport in M-1 cells and increased amiloride-sensitive whole-cell currents in Xenopus laevis oocytes heterologously expressing ENaC. Activation of ENaC by plasmin involved cleavage and release of an inhibitory peptide from the ENaC gamma subunit ectodomain. These data suggest that a defective glomerular filtration barrier allows passage of proteolytic enzymes that have the ability to activate ENaC."}],"status":"public","date_updated":"2024-06-30T13:46:44Z","publisher":"Ovid Technologies (Wolters Kluwer Health)","author":[{"last_name":"Svenningsen","full_name":"Svenningsen, Per","first_name":"Per"},{"first_name":"Claus","last_name":"Bistrup","full_name":"Bistrup, Claus"},{"last_name":"Friis","full_name":"Friis, Ulla G.","first_name":"Ulla G."},{"first_name":"Marko","last_name":"Bertog","full_name":"Bertog, Marko"},{"first_name":"Silke","full_name":"Haerteis, Silke","last_name":"Haerteis"},{"first_name":"Bettina","orcid":"0000-0001-5351-1785","last_name":"Krueger","id":"49428","full_name":"Krueger, Bettina"},{"full_name":"Stubbe, Jane","last_name":"Stubbe","first_name":"Jane"},{"last_name":"Jensen","full_name":"Jensen, Ole Nørregaard","first_name":"Ole Nørregaard"},{"first_name":"Helle C.","full_name":"Thiesson, Helle C.","last_name":"Thiesson"},{"full_name":"Uhrenholt, Torben R.","last_name":"Uhrenholt","first_name":"Torben R."},{"first_name":"Bente","full_name":"Jespersen, Bente","last_name":"Jespersen"},{"first_name":"Boye L.","full_name":"Jensen, Boye L.","last_name":"Jensen"},{"full_name":"Korbmacher, Christoph","last_name":"Korbmacher","first_name":"Christoph"},{"full_name":"Skøtt, Ole","last_name":"Skøtt","first_name":"Ole"}],"date_created":"2024-06-30T13:46:31Z","volume":20,"title":"Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel","doi":"10.1681/asn.2008040364","issue":"2","year":"2009","citation":{"ama":"Svenningsen P, Bistrup C, Friis UG, et al. Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel. <i>Journal of the American Society of Nephrology</i>. 2009;20(2):299–310. doi:<a href=\"https://doi.org/10.1681/asn.2008040364\">10.1681/asn.2008040364</a>","chicago":"Svenningsen, Per, Claus Bistrup, Ulla G. Friis, Marko Bertog, Silke Haerteis, Bettina Krueger, Jane Stubbe, et al. “Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel.” <i>Journal of the American Society of Nephrology</i> 20, no. 2 (2009): 299–310. <a href=\"https://doi.org/10.1681/asn.2008040364\">https://doi.org/10.1681/asn.2008040364</a>.","ieee":"P. Svenningsen <i>et al.</i>, “Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel,” <i>Journal of the American Society of Nephrology</i>, vol. 20, no. 2, pp. 299–310, 2009, doi: <a href=\"https://doi.org/10.1681/asn.2008040364\">10.1681/asn.2008040364</a>.","short":"P. Svenningsen, C. Bistrup, U.G. Friis, M. Bertog, S. Haerteis, B. Krueger, J. Stubbe, O.N. Jensen, H.C. Thiesson, T.R. Uhrenholt, B. Jespersen, B.L. Jensen, C. Korbmacher, O. Skøtt, Journal of the American Society of Nephrology 20 (2009) 299–310.","bibtex":"@article{Svenningsen_Bistrup_Friis_Bertog_Haerteis_Krueger_Stubbe_Jensen_Thiesson_Uhrenholt_et al._2009, title={Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel}, volume={20}, DOI={<a href=\"https://doi.org/10.1681/asn.2008040364\">10.1681/asn.2008040364</a>}, number={2}, journal={Journal of the American Society of Nephrology}, publisher={Ovid Technologies (Wolters Kluwer Health)}, author={Svenningsen, Per and Bistrup, Claus and Friis, Ulla G. and Bertog, Marko and Haerteis, Silke and Krueger, Bettina and Stubbe, Jane and Jensen, Ole Nørregaard and Thiesson, Helle C. and Uhrenholt, Torben R. and et al.}, year={2009}, pages={299–310} }","mla":"Svenningsen, Per, et al. “Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel.” <i>Journal of the American Society of Nephrology</i>, vol. 20, no. 2, Ovid Technologies (Wolters Kluwer Health), 2009, pp. 299–310, doi:<a href=\"https://doi.org/10.1681/asn.2008040364\">10.1681/asn.2008040364</a>.","apa":"Svenningsen, P., Bistrup, C., Friis, U. G., Bertog, M., Haerteis, S., Krueger, B., Stubbe, J., Jensen, O. N., Thiesson, H. C., Uhrenholt, T. R., Jespersen, B., Jensen, B. L., Korbmacher, C., &#38; Skøtt, O. (2009). Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel. <i>Journal of the American Society of Nephrology</i>, <i>20</i>(2), 299–310. <a href=\"https://doi.org/10.1681/asn.2008040364\">https://doi.org/10.1681/asn.2008040364</a>"},"page":"299–310","intvolume":"        20"},{"user_id":"49428","department":[{"_id":"35"},{"_id":"22"}],"_id":"54932","language":[{"iso":"eng"}],"type":"journal_article","publication":"Molecular Cancer Research","status":"public","abstract":[{"text":"Incubation of microvascular endothelial cells with combretastatin A-4 phosphate (CA-4P), a microtubule-destabilizing compound that preferentially targets tumor vessels, altered cell morphology and induced scattering of Golgi stacks. Concomitantly, CA-4P up-regulated connective tissue growth factor (CTGF/CCN2), a pleiotropic factor with antiangiogenic properties. In contrast to the effects of other microtubule-targeting agents such as colchicine or nocodazole, up-regulation of CTGF was only detectable in sparse cells, which were not embedded in a cell monolayer. Furthermore, CA-4P induced CTGF expression in endothelial cells, forming tube-like structures on basement membrane gels. Up-regulation of CTGF by CA-4P was dependent on Rho kinase signaling and was increased when p42/44 mitogen-activated protein kinase was inhibited. Additionally, FoxO transcription factors were identified as potent regulators of CTGF expression in endothelial cells. Activation of FoxO transcription factors by inhibition of phosphatidylinositol 3-kinase/AKT signaling resulted in a synergistic increase in CA-4P-mediated CTGF induction. CA-4P-mediated expression of CTGF was thus potentiated by the inhibition of kinase pathways, which are targets of novel antineoplastic drugs. Up-regulation of CTGF by low concentrations of CA-4P may thus occur in newly formed tumor vessels and contribute to the microvessel destabilization and antiangiogenic effects of CA-4P observed in vivo.","lang":"eng"}],"date_created":"2024-06-30T13:47:10Z","author":[{"full_name":"Samarin, Jana","last_name":"Samarin","first_name":"Jana"},{"first_name":"Margot","full_name":"Rehm, Margot","last_name":"Rehm"},{"last_name":"Krueger","orcid":"0000-0001-5351-1785","full_name":"Krueger, Bettina","id":"49428","first_name":"Bettina"},{"first_name":"Jens","last_name":"Waschke","full_name":"Waschke, Jens"},{"first_name":"Margarete","last_name":"Goppelt-Struebe","full_name":"Goppelt-Struebe, Margarete"}],"volume":7,"publisher":"American Association for Cancer Research (AACR)","date_updated":"2024-06-30T13:47:22Z","doi":"10.1158/1541-7786.mcr-08-0292","title":"Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4","issue":"2","citation":{"chicago":"Samarin, Jana, Margot Rehm, Bettina Krueger, Jens Waschke, and Margarete Goppelt-Struebe. “Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4.” <i>Molecular Cancer Research</i> 7, no. 2 (2009): 180–188. <a href=\"https://doi.org/10.1158/1541-7786.mcr-08-0292\">https://doi.org/10.1158/1541-7786.mcr-08-0292</a>.","ieee":"J. Samarin, M. Rehm, B. Krueger, J. Waschke, and M. Goppelt-Struebe, “Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4,” <i>Molecular Cancer Research</i>, vol. 7, no. 2, pp. 180–188, 2009, doi: <a href=\"https://doi.org/10.1158/1541-7786.mcr-08-0292\">10.1158/1541-7786.mcr-08-0292</a>.","ama":"Samarin J, Rehm M, Krueger B, Waschke J, Goppelt-Struebe M. Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4. <i>Molecular Cancer Research</i>. 2009;7(2):180–188. doi:<a href=\"https://doi.org/10.1158/1541-7786.mcr-08-0292\">10.1158/1541-7786.mcr-08-0292</a>","bibtex":"@article{Samarin_Rehm_Krueger_Waschke_Goppelt-Struebe_2009, title={Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4}, volume={7}, DOI={<a href=\"https://doi.org/10.1158/1541-7786.mcr-08-0292\">10.1158/1541-7786.mcr-08-0292</a>}, number={2}, journal={Molecular Cancer Research}, publisher={American Association for Cancer Research (AACR)}, author={Samarin, Jana and Rehm, Margot and Krueger, Bettina and Waschke, Jens and Goppelt-Struebe, Margarete}, year={2009}, pages={180–188} }","mla":"Samarin, Jana, et al. “Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4.” <i>Molecular Cancer Research</i>, vol. 7, no. 2, American Association for Cancer Research (AACR), 2009, pp. 180–188, doi:<a href=\"https://doi.org/10.1158/1541-7786.mcr-08-0292\">10.1158/1541-7786.mcr-08-0292</a>.","short":"J. Samarin, M. Rehm, B. Krueger, J. Waschke, M. Goppelt-Struebe, Molecular Cancer Research 7 (2009) 180–188.","apa":"Samarin, J., Rehm, M., Krueger, B., Waschke, J., &#38; Goppelt-Struebe, M. (2009). Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4. <i>Molecular Cancer Research</i>, <i>7</i>(2), 180–188. <a href=\"https://doi.org/10.1158/1541-7786.mcr-08-0292\">https://doi.org/10.1158/1541-7786.mcr-08-0292</a>"},"intvolume":"         7","page":"180–188","year":"2009"}]