Zobrazeno 1 - 10
of 24
pro vyhledávání: '"Christopher H Emfinger"'
Autor:
Christopher H Emfinger, Lauren E Clark, Brian Yandell, Kathryn L Schueler, Shane P Simonett, Donnie S Stapleton, Kelly A Mitok, Matthew J Merrins, Mark P Keller, Alan D Attie
Publikováno v:
eLife, Vol 12 (2023)
Insufficient insulin secretion to meet metabolic demand results in diabetes. The intracellular flux of Ca2+ into β-cells triggers insulin release. Since genetics strongly influences variation in islet secretory responses, we surveyed islet Ca2+ dyna
Externí odkaz:
https://doaj.org/article/de0ff10cf88640b2b8b46a53e15528a6
Autor:
Christopher H. Emfinger, Eleonora de Klerk, Kathryn L. Schueler, Mary E. Rabaglia, Donnie S. Stapleton, Shane P. Simonett, Kelly A. Mitok, Ziyue Wang, Xinyue Liu, Joao A. Paulo, Qinq Yu, Rebecca L. Cardone, Hannah R. Foster, Sophie L. Lewandowski, José C. Perales, Christina M. Kendziorski, Steven P. Gygi, Richard G. Kibbey, Mark P. Keller, Matthias Hebrok, Matthew J. Merrins, Alan D. Attie
Publikováno v:
JCI Insight, Vol 7, Iss 10 (2022)
Insulin secretion from pancreatic β cells is essential for glucose homeostasis. An insufficient response to the demand for insulin results in diabetes. We previously showed that β cell–specific deletion of Zfp148 (β-Zfp148KO) improves glucose to
Externí odkaz:
https://doaj.org/article/89940b8a0be241239ae78674f9a31df7
Autor:
Christopher H. Emfinger, Réka Lőrincz, Yixi Wang, Nathaniel W. York, Soma S. Singareddy, Jennifer M. Ikle, Robert C. Tryon, Conor McClenaghan, Zeenat A. Shyr, Yan Huang, Christopher A. Reissaus, Dirk Meyer, David W. Piston, Krzysztof Hyrc, Maria S. Remedi, Colin G. Nichols
Publikováno v:
Physiological Reports, Vol 7, Iss 11, Pp n/a-n/a (2019)
Abstract Islet β‐cell membrane excitability is a well‐established regulator of mammalian insulin secretion, and defects in β‐cell excitability are linked to multiple forms of diabetes. Evolutionary conservation of islet excitability in lower
Externí odkaz:
https://doaj.org/article/a0d6372c22d44973a78da986fad96465
Novel regulators of islet function identified from genetic variation in mouse islet Ca2+oscillations
Autor:
Christopher H. Emfinger, Lauren E. Clark, Brian Yandell, Kathryn L. Schueler, Shane P. Simonett, Donnie S. Stapleton, Kelly A. Mitok, Matthew J. Merrins, Mark P. Keller, Alan D. Attie
Insufficient insulin secretion to meet metabolic demand results in diabetes. The intracellular flux of Ca2+into β-cells triggers insulin release. Since genetics strongly influences variation in islet secretory responses, we surveyed islet Ca2+dynami
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::1df50c6b59c07f51672ceb5e0a7726fb
https://doi.org/10.1101/2022.11.26.517741
https://doi.org/10.1101/2022.11.26.517741
Autor:
Christopher H. Emfinger, Alecia Welscher, Zihan Yan, Yixi Wang, Hannah Conway, Jennifer B. Moss, Larry G. Moss, Maria S. Remedi, Colin G. Nichols
Publikováno v:
Royal Society Open Science, Vol 4, Iss 2 (2017)
ATP-sensitive potassium channels (KATP channels) are critical nutrient sensors in many mammalian tissues. In the pancreas, KATP channels are essential for coupling glucose metabolism to insulin secretion. While orthologous genes for many components o
Externí odkaz:
https://doaj.org/article/185531efc05b409bbfdf3c11b18bfdc6
Autor:
Melissa N. Martinez, Christopher H. Emfinger, Matthew Overton, Salisha Hill, Tara S. Ramaswamy, David A. Cappel, Ke Wu, Sergio Fazio, W. Hayes McDonald, David L. Hachey, David L. Tabb, John M. Stafford
Publikováno v:
Journal of Lipid Research, Vol 53, Iss 3, Pp 379-389 (2012)
Mechanisms underlying changes in HDL composition caused by obesity are poorly defined, partly because mice lack expression of cholesteryl ester transfer protein (CETP), which shuttles triglyceride and cholesteryl ester between lipoproteins. Because m
Externí odkaz:
https://doaj.org/article/be230677c69d40ba923e39e0de70e324
Autor:
Christopher H. Emfinger, Eleonora de Klerk, Kathryn L. Schueler, Mary E. Rabaglia, Donnie S. Stapleton, Shane P. Simonett, Kelly A. Mitok, Ziyue Wang, Xinyue Liu, Joao A. Paulo, Qinq Yu, Rebecca L. Cardone, Hannah R. Foster, Sophie L. Lewandowski, José C. Perales, Christina M. Kendziorski, Steven P. Gygi, Richard G. Kibbey, Mark P. Keller, Matthias Hebrok, Matthew J. Merrins, Alan D. Attie
Publikováno v:
JCI insight. 7(10)
Insulin secretion from pancreatic β cells is essential for glucose homeostasis. An insufficient response to the demand for insulin results in diabetes. We previously showed that β cell-specific deletion of Zfp148 (β-Zfp148KO) improves glucose tole
Autor:
Daniel M. Gatti, Rahul Das, Brian S. Yandell, Kelly A. Mitok, Ziyue Wang, Mark P. Keller, Donnie S. Stapleton, Matthew Vincent, Karl W. Broman, Kathryn L. Schueler, Shane P Simonett, Takanao Ishimura, Alan D. Attie, Mary E. Rabaglia, Gary A. Churchill, Christopher H. Emfinger, Tim Beck, Christina Kendziorski
Publikováno v:
J Clin Invest
Genetic susceptibility to type 2 diabetes is primarily due to β cell dysfunction. However, a genetic study to directly interrogate β cell function ex vivo has never been previously performed. We isolated 233,447 islets from 483 Diversity Outbred (D
Autor:
G. Schuyler Brown, Theresa M. Harter, Atilla Kovacs, Alex Hanson, Robert P. Mecham, Haixia Zhang, Paige E. Cooper, Colin G. Nichols, Blanche Schwappach, Christopher H. Emfinger, Carmen M. Halabi, Zihan Yan, Tobias Scherf de Almeida, Conor McClenaghan, Maria S. Remedi, Eric C. Arakel
Publikováno v:
JCI Insight, Vol 6, Iss 5 (2021)
JCI Insight
JCI Insight
Cantu syndrome (CS) is caused by gain-of-function (GOF) mutations in pore-forming (Kir6.1, KCNJ8) and accessory (SUR2, ABCC9) ATP-sensitive potassium (KATP) channel subunits, the most common mutations being SUR2[R1154Q] and SUR2[R1154W], carried by a
Autor:
Peter Hung, William McAllister, Alecia Welscher, Maria S. Remedi, Paul W. Hruz, Christopher H. Emfinger, Colin G. Nichols, Zihan Yan
Publikováno v:
American Journal of Physiology-Endocrinology and Metabolism. 315:E1121-E1132
Gain-of-function (GOF) mutations in the ATP-sensitive potassium (KATP) channels cause neonatal diabetes. Despite the well-established genetic root of the disease, pathways modulating disease severity and treatment effectiveness remain poorly understo