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. 1994 Nov 10;372(6502):182-6.
doi: 10.1038/372182a0.

Insulin resistance and growth retardation in mice lacking insulin receptor substrate-1

H Tamemoto  1 , T Kadowaki, K Tobe, T Yagi, H Sakura, T Hayakawa, Y Terauchi, K Ueki, Y Kaburagi, S Satoh, et al.
Affiliations

Insulin resistance and growth retardation in mice lacking insulin receptor substrate-1

H Tamemoto et al. Nature. .

Abstract

Insulin receptor substrate-1 (IRS-1) is the major substrate of insulin receptor and IGF-1 receptor tyrosine kinases; it has an apparent relative molecular mass of 160-190,000 (M(r), 160-190K) on SDS polyacrylamide gel. Tyrosine-phosphorylated IRS-1 binds the 85K subunit of phosphatidylinositol 3-kinase which may be involved in the translocation of glucose transporters and the abundant src homology protein (ASH)/Grb2 which may be involved in activation of p21ras and MAP kinase cascade. IRS-1 also has binding sites for Syp and Nck and other src homology 2 (SH2) signalling molecules. To clarify the physiological roles of IRS-1 in vivo, we made mice with a _targeted disruption of the IRS-1 gene locus. Mice homozygous for _targeted disruption of the IRS-1 gene were born alive but were retarded in embryonal and postnatal growth. They also had resistance to the glucose-lowering effects of insulin, IGF-1 and IGF-2. These data suggest the existence of both IRS-1-dependent and IRS-1-independent pathways for signal transduction of insulin and IGFs.

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Comment in

  • Insulin. Life without the IRS.
    Lienhard GE. Lienhard GE. Nature. 1994 Nov 10;372(6502):128-9. doi: 10.1038/372128a0. Nature. 1994. PMID: 7969441 No abstract available.

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