Publication: rupress.org | Publication Date: June 25, 2012
Authors: Shiyu Wang, Randal J. Kaufman
A central function of the endoplasmic reticulum (ER) is to coordinate protein biosynthetic and secretory activities in the cell. Alterations in ER homeostasis cause accumulation of misfolded/unfolded proteins in the ER. Read more
Publication: ncbi.nlm.nih.gov | Publication Date: July 1, 2012
Authors: Lale Ozcan and Ira Tabas
Perturbations in the normal functions of the endoplasmic reticulum (ER) trigger a signaling network that coordinates adaptive and apoptotic responses. There is accumulating evidence implicating prolonged ER stress in the development and progression of many diseases, including neurodegeneration, atherosclerosis, type 2 diabetes, liver disease, and cancer. Read more
Publication: ncbi.nlm.nih.gov | Publication Date: March 31, 2014
Authors: Rammohan V Rao and Dale E Bredesen
The accumulation of misfolded proteins (e.g. mutant or damaged proteins) triggers cellular stress responses that protect cells against the toxic buildup of such proteins. Read more
Publication: ncbi.nlm.nih.gov | Publication Date: January 7, 2016
Authors: Fumihiko Urano
The endoplasmic reticulum (ER) as an intracellular Ca2+ store not only sets up cytosolic Ca2+ signals, but, among other functions, also assembles and folds newly synthesized proteins. Alterations in ER homeostasis, including severe Ca2+ depletion, are an upstream event in the pathophysiology of many diseases. Read more
Publication: pubmed.ncbi.nlm.nih.gov | Publication Date: July 14, 2011
Authors: Damien Abreu, Rie Asada, John M. P. Revilla, Zeno Lavagnino, Kelly Kries, David W. Piston & Fumihiko Urano
Purpose of review: Balancing glucose homeostasis is crucial to maintain appropriate energy and metabolic state. Chronic hyperglycemia with insulin resistance and development of type II diabetes mellitus is a growing health and health-economic threat. Read more
Publication: ncbi.nlm.nih.gov | Publication Date: April 23, 2009
Authors: Manjinder S Sandhu, Michael N Weedon, Katherine A Fawcett, Jon Wasson, Sally L Debenham, Allan Daly, Hana Lango, Timothy M Frayling, Rosalind J Neumann, Richard Sherva, Ilana Blech, Paul D Pharoah, Colin N A Palmer, Charlotte Kimber, Roger Tavendale, Andrew D Morris, Mark I McCarthy, Mark Walker, Graham Hitman, Benjamin Glaser, M Alan Permutt, Andrew T Hattersley, Nicholas J Wareham and Inês Barroso
We studied genes involved in pancreatic β cell function and survival, identifying associations between SNPs in WFS1 and diabetes risk in UK populations that we replicated in an Ashkenazi population and in additional UK studies. Read more
Publication: nature.com | Publication Date: November 23, 2017
Authors: Theodora Panagaki, Maria Michael & Christian Hölscher
Growing evidence suggests that agonists of glucagon-like peptide (GLP-1) receptor exert neuroprotective and neurorestorative effects across a range of experimental models of neuronal degeneration, and, recently, a pilot clinical trial of Liraglutide in Alzheimer’s disease patients showed improvements in cerebral glucose consumption that signifies disease progression. Read more
Publication: Nature.com | Publication Date: May 4, 2020
Authors: Jana Mahadevan, Shuntaro Morikawa, Takuya Yagi, Damien Abreu, Simin Lu, Kohsuke Kanekura, Cris M. Brown & Fumihiko Urano
Endoplasmic reticulum (ER) stress-mediated cell death is an emerging target for human chronic disorders, including neurodegeneration and diabetes. However, there is currently no treatment for preventing ER stress-mediated cell death. Here, we show that mesencephalic astrocyte-derived neurotrophic factor (MANF), a neurotrophic factor secreted from ER stressed cells, prevents ER stress-mediated β cell death and enhances β cell proliferation in cell and mouse models of Wolfram syndrome, a prototype of ER disorders. Read more
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