- ►diabetesjournals.org WC Ladiges, SE Knoblaugh, JF Morton, MJ Korth, BL … - Diabetes, 2005 - Am Diabetes Assoc The endoplasmic reticulum (ER) transmits apoptotic signals in the pancreas during ER
stress, implicating ER stress–mediated apoptosis in the development of diabetes. P58 IPK
(DNAJC3) is induced during ER stress and functions as a negative feedback component ... Cited by 63 - Related articles - All 6 versions
W Yan, CL Frank, MJ Korth, BL Sopher, I … - Proceedings of the …, 2002 - National Acad Sciences P58 IPK is an Hsp40 family member known to inhibit the interferon (IFN)-induced, double-stranded
RNA-activated, eukaryotic initiation factor 2α (eIF2α) protein kinase R (PKR) by binding to its
kinase domain. We find that the stress of unfolded proteins in the endoplasmic reticulum ... Cited by 99 - Related articles - BL Direct - All 15 versions
R van Huizen, JL Martindale, M Gorospe, NJ … - Journal of Biological …, 2003 - ASBMB The unfolded protein response, which is activated in response to the loss of endoplasmic reticulum
(ER) Ca 2+ homeostasis and/or the accumulation of misfolded, unassembled, or aggregated
proteins in the ER lumen, involves both transcriptional and translational regulation. In the ... Cited by 74 - Related articles - BL Direct - All 6 versions
- ►cell.com S Oyadomari, C Yun, EA Fisher, N Kreglinger, G … - Cell, 2006 - Elsevier The ER's capacity to process proteins is limited, and stress caused by accumulation of unfolded
and misfolded proteins (ER stress) contributes to human disease. ER stress elicits the unfolded
protein response (UPR), whose components attenuate protein synthesis, increase folding ... Cited by 74 - Related articles - All 16 versions
- ►molbiolcell.org DT Rutkowski, SW Kang, AG Goodman, JL … - Molecular biology of …, 2007 - Am Soc Cell Biol The preemptive quality control (pQC) pathway protects cells from acute endoplasmic reticulum
(ER) stress by attenuating translocation of nascent proteins despite their targeting to translocons
at the ER membrane. Here, we investigate the hypothesis that the DnaJ protein p58 IPK ... Cited by 32 - Related articles - BL Direct - All 8 versions
AK Cardozo, F Ortis, J Storling, YM Feng, J Rasschaert, … - Diabetes, 2005 - Am Diabetes Assoc Cytokines and free radicals are mediators of β-cell death in type 1 diabetes. Under in vitro
conditions, interleukin-1β (IL-1β) + γ-interferon (IFN-γ) induce nitric oxide (NO) production and
apoptosis in rodent and human pancreatic β-cells. We have previously shown, by ... Cited by 102 - Related articles - All 8 versions
AC Riggs, E Bernal-Mizrachi, M Ohsugi, J Wasson, S … - Diabetologia, 2005 - Springer Page 1. Diabetologia (2005) 48: 2313–2321 DOI 10.1007/s00125-005-1947-4 ARTICLE
AC Riggs . E. Bernal-Mizrachi . M. Ohsugi . J. Wasson . S. Fatrai . C. Welling . J. Murray .
RE Schmidt . PL Herrera . MA Permutt Mice conditionally ... Cited by 42 - Related articles - BL Direct - All 3 versions
- ►ulb.ac.be [PDF] P Pirot, DL Eizirik, AK Cardozo - Diabetologia, 2006 - Springer Abstract Aims/hypothesis: A tight control of endoplas- mic reticulum homeostasis is crucial for
beta cell function and survival. We recently described that IL-1β plus IFN-γ deplete endoplasmic
reticulum Ca 2+ stores in beta cells, leading to endoplasmic reticulum stress and ... Cited by 22 - Related articles - BL Direct - All 5 versions
K Petrova, S Oyadomari, LM Hendershot, D Ron - EMBO J, 2008 - skirball.med.nyu.edu P58/DNAJc3 defends cells against endoplasmic reticulum (ER) stress. Most P58 molecules are
translocated into the ER lumen, and here we report selective and stable binding to misfolded
proteins by P58's TPR-containing N-terminal domain. In vitro, too, P58 binds selectively to ... Cited by 6 - Related articles - View as HTML - All 6 versions
