Zobrazeno 1 - 10
of 14
pro vyhledávání: '"Michael J. Litt"'
Publikováno v:
Vascular Health and Risk Management. 19:211-221
Autor:
Işın Çakır, Colleen K. Hadley, Pauline Lining Pan, Rushita A. Bagchi, Masoud Ghamari-Langroudi, Danielle T. Porter, Qiuyu Wang, Michael J. Litt, Somnath Jana, Susan Hagen, Pil Lee, Andrew White, Jiandie D. Lin, Timothy A. McKinsey, Roger D. Cone
Publikováno v:
Nature Metabolism. 4:44-59
Autor:
Michael J. Litt, Sharlene M. Day
Publikováno v:
Innovations (Philadelphia, Pa.).
Publikováno v:
New England Journal of Medicine. 385:1421-1427
Hard to Swallow A previously healthy 20-year-old college student presented before the Covid-19 pandemic with a 3-day history of throat pain, malaise, cough, and chills. She had no congestion or rhi...
Autor:
Michael J Litt, G Donald Okoye, Daniel Lark, Isin Cakir, Christy Moore, Mary C Barber, James Atkinson, Josh Fessel, Javid Moslehi, Roger D Cone
Publikováno v:
eLife, Vol 6 (2017)
Haploinsufficiency of the melanocortin-4 receptor, the most common monogenetic obesity syndrome in humans, is associated with a reduction in autonomic tone, bradycardia, and incidence of obesity-associated hypertension. Thus, it has been assumed that
Externí odkaz:
https://doaj.org/article/be1fdf60b9af4a499d962141b59a7a77
Autor:
Christa E. Flück, Felix Berger, Egbert Voss, Michael J Litt, Peter Kühnen, Sophie Roth, Esther Schulz, Robert Opitz, Lajos Markó, Marcus Kelm, Titus Kuehne, Susanna Wiegand, Peter Linz, Martin Bald, Lia Puder, Roger D. Cone, Dominik N. Müller, Philipp Krabusch
Publikováno v:
J Clin Endocrinol Metab
Context Pro-opiomelanocortin (POMC) and the melanocortin-4 receptor (MC4R) play a pivotal role in the leptin–melanocortin pathway. Mutations in these genes lead to monogenic types of obesity due to severe hyperphagia. In addition to dietary-induced
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bdf55da45aa3f40de7133c1166e121bc
https://europepmc.org/articles/PMC8372645/
https://europepmc.org/articles/PMC8372645/
Autor:
Işın, Çakır, Colleen K, Hadley, Pauline Lining, Pan, Rushita A, Bagchi, Masoud, Ghamari-Langroudi, Danielle T, Porter, Qiuyu, Wang, Michael J, Litt, Somnath, Jana, Susan, Hagen, Pil, Lee, Andrew, White, Jiandie D, Lin, Timothy A, McKinsey, Roger D, Cone
Publikováno v:
Nature metabolism. 4(1)
The adipose tissue-derived hormone leptin can drive decreases in food intake while increasing energy expenditure. In diet-induced obesity, circulating leptin levels rise proportionally to adiposity. Despite this hyperleptinemia, rodents and humans wi
Autor:
Roger D. Cone, Michael J Litt, Sheridan J. S. Carrington, Isin Cakir, Masoud Ghamari-Langroudi, Taneisha Gillyard, Luis E. Gimenez, Erica J. P. Anderson
Publikováno v:
Journal of Molecular Endocrinology. 56:T157-T174
The melanocortin peptides derived from pro-opiomelanocortin (POMC) were originally understood in terms of the biological actions of α-melanocyte-stimulating hormone (α-MSH) on pigmentation and adrenocorticotrophic hormone on adrenocortical glucocor
Autor:
Michael J Litt, Roger D. Cone, Kate L. J. Ellacott, Patrick Sweeney, Masoud Ghamari-Langroudi, Isin Cakir, Rachel N. Lippert
Publikováno v:
Science Advances
The melanocortin-3 receptor acts as a rheostat on energy homeostasis through presynaptic inhibition of MC4R neuronal activity.
Like most homeostatic systems, adiposity in mammals is defended between upper and lower boundary conditions. While lep
Like most homeostatic systems, adiposity in mammals is defended between upper and lower boundary conditions. While lep
Publikováno v:
Methods in Molecular Biology ISBN: 9781493973613
Methods Mol Biol
Methods Mol Biol
The family of inward rectifying potassium channels (Kir channels) plays crucial roles in the regulation of heart rhythms, renal excretion, insulin release, and neuronal activity. Their dysfunction has been attributed to numerous diseases such as card
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e8f890ee4ac4740be83be09e5d54115f
https://doi.org/10.1007/978-1-4939-7362-0_16
https://doi.org/10.1007/978-1-4939-7362-0_16