Insulin Receptor Substrate Proteins
"Insulin Receptor Substrate Proteins" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A structurally-related group of signaling proteins that are phosphorylated by the INSULIN RECEPTOR PROTEIN-TYROSINE KINASE. The proteins share in common an N-terminal PHOSPHOLIPID-binding domain, a phosphotyrosine-binding domain that interacts with the phosphorylated INSULIN RECEPTOR, and a C-terminal TYROSINE-rich domain. Upon tyrosine phosphorylation insulin receptor substrate proteins interact with specific SH2 DOMAIN-containing proteins that are involved in insulin receptor signaling.
Descriptor ID |
D055504
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MeSH Number(s) |
D12.644.360.024.301 D12.776.157.057.039 D12.776.476.024.382
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Concept/Terms |
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Below are MeSH descriptors whose meaning is more general than "Insulin Receptor Substrate Proteins".
Below are MeSH descriptors whose meaning is more specific than "Insulin Receptor Substrate Proteins".
This graph shows the total number of publications written about "Insulin Receptor Substrate Proteins" by people in this website by year, and whether "Insulin Receptor Substrate Proteins" was a major or minor topic of these publications.
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Year | Major Topic | Minor Topic | Total |
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1993 | 0 | 1 | 1 | 1995 | 0 | 2 | 2 | 1996 | 0 | 1 | 1 | 1998 | 0 | 2 | 2 | 1999 | 0 | 1 | 1 | 2000 | 0 | 1 | 1 | 2002 | 0 | 3 | 3 | 2003 | 0 | 2 | 2 | 2004 | 0 | 5 | 5 | 2005 | 0 | 3 | 3 | 2006 | 0 | 3 | 3 | 2009 | 2 | 3 | 5 | 2010 | 1 | 1 | 2 | 2011 | 2 | 1 | 3 | 2012 | 2 | 0 | 2 | 2013 | 0 | 2 | 2 | 2014 | 2 | 0 | 2 | 2015 | 0 | 2 | 2 | 2016 | 1 | 1 | 2 | 2019 | 0 | 1 | 1 |
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Below are the most recent publications written about "Insulin Receptor Substrate Proteins" by people in Profiles.
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Minogue PJ, Beyer EC, Berthoud VM. CHOP is dispensable for lens transparency in wild-type and connexin50 mutant mice. Mol Vis. 2019; 25:535-545.
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Chen J, Sun J, Prinz RA, Li Y, Xu X. Gingerenone A Sensitizes the Insulin Receptor and Increases Glucose Uptake by Inhibiting the Activity of p70 S6 Kinase. Mol Nutr Food Res. 2018 12; 62(23):e1800709.
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Takatani T, Shirakawa J, Roe MW, Leech CA, Maier BF, Mirmira RG, Kulkarni RN. IRS1 deficiency protects ß-cells against ER stress-induced apoptosis by modulating sXBP-1 stability and protein translation. Sci Rep. 2016 07 05; 6:28177.
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Berthoud VM, Minogue PJ, Lambert PA, Snabb JI, Beyer EC. The Cataract-linked Mutant Connexin50D47A Causes Endoplasmic Reticulum Stress in Mouse Lenses. J Biol Chem. 2016 08 19; 291(34):17569-78.
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Pereira S, Park E, Moore J, Faubert B, Breen DM, Oprescu AI, Nahle A, Kwan D, Giacca A, Tsiani E. Resveratrol prevents insulin resistance caused by short-term elevation of free fatty acids in vivo. Appl Physiol Nutr Metab. 2015 Nov; 40(11):1129-36.
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Chang E, Choi JM, Park SE, Rhee EJ, Lee WY, Oh KW, Park SW, Park CY. Adiponectin deletion impairs insulin signaling in insulin-sensitive but not insulin-resistant 3T3-L1 adipocytes. Life Sci. 2015 Jul 01; 132:93-100.
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Pekow J, Meckel K, Dougherty U, Butun F, Mustafi R, Lim J, Crofton C, Chen X, Joseph L, Bissonnette M. Tumor suppressors miR-143 and miR-145 and predicted target proteins API5, ERK5, K-RAS, and IRS-1 are differentially expressed in proximal and distal colon. Am J Physiol Gastrointest Liver Physiol. 2015 Feb 01; 308(3):G179-87.
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Ren D, Sun J, Mao L, Ye H, Polonsky KS. BH3-only molecule Bim mediates ß-cell death in IRS2 deficiency. Diabetes. 2014 Oct; 63(10):3378-87.
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Wei Z, Hurtt R, Gu T, Bodzin AS, Koch WJ, Doria C. GRK2 negatively regulates IGF-1R signaling pathway and cyclins' expression in HepG2 cells. J Cell Physiol. 2013 Sep; 228(9):1897-901.
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Wang Y, Yuan JL, Zhang YT, Ma JJ, Xu P, Shi CH, Zhang W, Li YM, Fu Q, Zhu GF, Xue W, Lei YH, Gao JY, Wang JY, Shao C, Yi CG, Wang H. Inhibition of both EGFR and IGF1R sensitized prostate cancer cells to radiation by synergistic suppression of DNA homologous recombination repair. PLoS One. 2013; 8(8):e68784.
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