ArticleCellular and molecular life sciences : CMLS2009
Suppressor of cytokine signaling-1 inhibits caspase activation and protects from cytokine-induced beta cell death.
Article in Cellular and molecular life sciences : CMLS, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- New insight into the role of SOCS family in immune regulation and autoimmune pathogenesis.Journal of advanced research · 2026Review
- RISING STARS: Evidence for established and emerging forms of β-cell death.The Journal of endocrinology · 2024Review
- ATAC-seq reveals alterations in open chromatin in pancreatic islets from subjects with type 2 diabetes.Scientific reports · 2019Article
- Suppressors of Cytokine Signaling in Sickness and in Health of Pancreatic β-Cells.Frontiers in immunology · 2016Review
- Stress and the inflammatory process: a major cause of pancreatic cell death in type 2 diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2014Review
- Suppressors of cytokine signaling (SOCS) and type 2 diabetes.Molecular biology reports · 2014Review
- SOCS5 and SOCS6 have similar expression patterns in normal and cancer tissues.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
- Bilirubin protects grafts against nonspecific inflammation-induced injury in syngeneic intraportal islet transplantation.Experimental & molecular medicine · 2010Article
- Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic beta cell damage caused by proinflammatory cytokines interleukin-1beta (IL-1beta), interferon-gamma (IFNgamma) and tumor necrosis factor-alpha (TNFalpha) is a key event in the pathogenesis of type 1 diabetes. The suppressor of cytokine signaling-1 (SOCS-1) blocks IFNgamma-induced signaling and prevents diabetes in the non-obese diabetic mouse. Here, we investigated if SOCS-1 overexpression in primary beta cells provides protection from cytokine-induced islet cell dysfunction and death. We demonstrate that SOCS-1 does not prevent increase in NO production and decrease in glucose-stimulated insulin secretion in the presence of IL-1beta, IFNgamma, TNFalpha. However, it decreases the activation of caspase-3, -8 and -9, and thereby, promotes a robust protection from cytokine-induced beta cell death. Our data suggest that SOCS-1 overexpression may not be sufficient in preventing all the biological activities of IFNgamma in beta cells. In summary, we show that interference with IFNgamma signal transduction pathways by SOCS-1 inhibits cytokine-stimulated pancreatic beta cell death.
Indexed as
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.