ArticleMolecular and cellular biology2000
IRS-4 mediates protein kinase B signaling during insulin stimulation without promoting antiapoptosis.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 69 citations in OpenAlex.
- Biochemical characterization of the Drosophila insulin receptor kinase and longevity-associated mutants.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Is Insulin Receptor Substrate4 (IRS4) a Platform Involved in the Activation of Several Oncogenes?Cancers · 2023Review
- Class I PI3K Biology.Current topics in microbiology and immunology · 2022Article
- The Genetics and Mechanisms of T-Cell Acute Lymphoblastic Leukemia.Cold Spring Harbor perspectives in medicine · 2020Review
- IRS4, a novel modulator of BMP/Smad and Akt signalling during early muscle differentiation.Scientific reports · 2017Article
- Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking.Nature genetics · 2017Article
- Insulin receptor substrate-4 binds to Slingshot-1 phosphatase and promotes cofilin dephosphorylation.The Journal of biological chemistry · 2014Article
- Insulin receptor substrate signaling suppresses neonatal autophagy in the heart.The Journal of clinical investigation · 2013Article
- MicroRNAs: a new ray of hope for diabetes mellitus.Protein & cell · 2012Review
- Insulin receptor substrate-1 prevents autophagy-dependent cell death caused by oxidative stress in mouse NIH/3T3 cells.Journal of biomedical science · 2012Article
- Insulin receptor substrate-2 mediated insulin-like growth factor-I receptor overexpression in pancreatic adenocarcinoma through protein kinase Cdelta.Cancer research · 2009Article
- Role of the GH/IGF-1 axis in lifespan and healthspan: lessons from animal models.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2008Review
- Role of microRNAs in diabetes.Biochimica et biophysica acta · 2008Review
- The role of intracellular signaling in insulin-mediated regulation of drug metabolizing enzyme gene and protein expression.Pharmacology & therapeutics · 2007Review
- Article
- Insulin receptor substrate-2 deficiency impairs brain growth and promotes tau phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Pdx1 restores beta cell function in Irs2 knockout mice.The Journal of clinical investigation · 2002Article
- Association of insulin receptor substrate 1 (IRS-1) y895 with Grb-2 mediates the insulin signaling involved in IRS-1-deficient brown adipocyte mitogenesis.Molecular and cellular biology · 2001Article
- Insulin receptor substrate 3 (IRS-3) and IRS-4 impair IRS-1- and IRS-2-mediated signaling.Molecular and cellular biology · 2001Article
- Both src-dependent and -independent mechanisms mediate phosphatidylinositol 3-kinase regulation of colony-stimulating factor 1-activated mitogen-activated protein kinases in myeloid progenitors.Molecular and cellular biology · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Insulin receptor substrate (IRS) proteins are tyrosine phosphorylated and mediate multiple signals during activation of the receptors for insulin, insulin-like growth factor 1 (IGF-1), and various cytokines. In order to distinguish common and unique functions of IRS-1, IRS-2, and IRS-4, we expressed them individually in 32D myeloid progenitor cells containing the human insulin receptor (32D(IR)). Insulin promoted the association of Grb-2 with IRS-1 and IRS-4, whereas IRS-2 weakly bound Grb-2; consequently, IRS-1 and IRS-4 enhanced insulin-stimulated mitogen-activated protein kinase activity. During insulin stimulation, IRS-1 and IRS-2 strongly bound p85alpha/beta, which activated phosphatidylinositol (PI) 3-kinase, protein kinase B (PKB)/Akt, and p70(s6k), and promoted the phosphorylation of BAD. IRS-4 also promoted the activation of PKB/Akt and BAD phosphorylation during insulin stimulation; however, it weakly bound or activated p85-associated PI 3-kinase and failed to mediate the activation of p70(s6k). Insulin strongly inhibited apoptosis of interleukin-3 (IL-3)-deprived 32D(IR) cells expressing IRS-1 or IRS-2 but failed to inhibit apoptosis of cells expressing IRS-4. Consequently, 32D(IR) cells expressing IRS-4 proliferated slowly during insulin stimulation. Thus, the activation of PKB/Akt and BAD phosphorylation might not be sufficient to inhibit the apoptosis of IL-3-deprived 32D(IR) cells unless p85-associated PI 3-kinase or p70(s6k) are strongly activated.
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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 OpenQuestion graph.