Zobrazeno 1 - 10
of 22
pro vyhledávání: '"Richard K. P. Benninger"'
Autor:
Mikaela L. Follmer, Trevor J. Isner, Yunus H. Ozekin, Claire H. Levitt, Carolyn L. Burek, Richard K. P. Benninger, Emily Anne Bates
Publikováno v:
Nature Communications, Vol 15, Iss 1, Pp 1-19 (2024)
Abstract Bone Morphogenetic Protein (BMP) signaling is essential for craniofacial development, though little is known about the mechanisms that govern BMP secretion. We show that depolarization induces calcium-dependent BMP4 release from mouse embryo
Externí odkaz:
https://doaj.org/article/10147660be784b15b35e0a438fc49f2c
Autor:
Nikki L. Farnsworth, Robert A. Piscopio, Wolfgang E. Schleicher, David G. Ramirez, Jose G. Miranda, Richard K. P. Benninger
Publikováno v:
Frontiers in Physiology, Vol 13 (2022)
In type 1 diabetes (T1D), islet dysfunction occurs prior to diabetes onset. Pro-inflammatory cytokines can disrupt insulin secretion and Ca2+ homeostasis. Connexin36 (Cx36) gap junctions electrically couple β-cells to coordinate glucose-stimulated C
Externí odkaz:
https://doaj.org/article/8f6e7598ecc54d338d5d6e9c9e2a84a0
Autor:
Arjun K. Fontaine, David G. Ramirez, Samuel F. Littich, Robert A. Piscopio, Vira Kravets, Wolfgang E. Schleicher, Naoko Mizoguchi, John H. Caldwell, Richard F. ff. Weir, Richard K. P. Benninger
Publikováno v:
Scientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)
Abstract Previous studies have demonstrated stimulation of endocrine pancreas function by vagal nerve electrical stimulation. While this increases insulin secretion, expected concomitant reductions in circulating glucose do not occur. A complicating
Externí odkaz:
https://doaj.org/article/a57569d33df4487d82b410837e3941d0
Autor:
David G. Ramirez, Eric Abenojar, Christopher Hernandez, David S. Lorberbaum, Lucine A. Papazian, Samantha Passman, Vinh Pham, Agata A. Exner, Richard K. P. Benninger
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-13 (2020)
Infiltration of immune cells to the pancreatic islets precedes clinical symptoms of type 1 diabetes, and lack of methods to detect this insulitis impedes early interventions. Here the authors report a contrast enhanced ultrasound method that can dete
Externí odkaz:
https://doaj.org/article/ea834bcc10ac40038a26340fb8b2edc0
Publikováno v:
Nature Communications, Vol 9, Iss 1, Pp 1-12 (2018)
Non-invasive techniques to assess the progression of type 1 diabetes prior to clinical onset are needed. Here the authors apply a contrast-enhanced ultrasound measurement of mouse pancreatic blood flow to detect changes in the islet microvasculature
Externí odkaz:
https://doaj.org/article/e5ffc27a8776409ea3d318e4d002166a
Autor:
Jillian Collins, Robert A. Piscopio, Mary E. Reyland, Richard K. P. Benninger, Nikki L. Farnsworth
SummaryIn type 1 diabetes (T1D), autoreactive immune cells infiltrate the pancreas and secrete pro-inflammatory cytokines that initiate cell death in insulin producing islet β-cells. Protein kinase C δ (PKCδ) plays a role in mediating cytokine-ind
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::67cb2acca26625dcba727639fc6467c0
https://doi.org/10.1101/2022.07.20.500512
https://doi.org/10.1101/2022.07.20.500512
Publikováno v:
PLoS Computational Biology, Vol 12, Iss 9, p e1005116 (2016)
Diabetes is caused by dysfunction to β-cells in the islets of Langerhans, disrupting insulin secretion and glucose homeostasis. Gap junction-mediated electrical coupling between β-cells in the islet plays a major role in coordinating a pulsatile se
Externí odkaz:
https://doaj.org/article/21ac402290314d54a37781d86d24567a
Diabetes is caused by dysfunction of electrically coupled heterogeneous β-cells within the pancreatic islet. Functional networks have been used to represent cellular synchronization and study β-cells subpopulations, which play an important role in
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::6dda14d91b3330e27e169b75d1a52ab1
https://doi.org/10.1101/2022.02.06.479331
https://doi.org/10.1101/2022.02.06.479331
Autor:
Holger A. Russ, Richard K. P. Benninger, Taylor M. Triolo, Clayton E. Mathews, Mark A. Wallet, Katherine E. Santostefano, Lucas H. Armitage, Shane P. M. Williams, Maria S. Hansen, Ali H. Shilleh, JaeAnn M. Dwulet, Roberto Castro-Gutierrez, Kent A. Riemondy, Fiona M. Docherty
Stem cell derived beta-like cells (sBC) carry the promise of providing an abundant source of insulin-producing cells for use in cell replacement therapy for patients with diabetes, potentially allowing widespread implementation of a practical cure. T
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ccc22ee33eb5e88c90298fcf3096fbdf
https://doi.org/10.2337/figshare.15124980.v3
https://doi.org/10.2337/figshare.15124980.v3
Autor:
Jose G, Miranda, Wolfgang E, Schleicher, Kristen L, Wells, David G, Ramirez, Samantha P, Landgrave, Richard K P, Benninger
Publikováno v:
Molecular Metabolism
Objective Diabetes occurs because of insufficient insulin secretion due to β-cell dysfunction within the islet of Langerhans. Elevated glucose levels trigger β-cell membrane depolarization, action potential generation, and slow sustained free-Ca2+