IRS-1: Essential for Insulin- and IL-4-Stimulated Mitogenesis in Hematopoietic Cells

Although several interleukin-3 (IL-3)-dependent cell lines proliferate in response to IL-4 or insulin, the 32D line does not. Insulin and IL-4 sensitivity was restored to 32D cells by expression of IRS-1, the principal substrate of the insulin receptor. Although 32D cells possessed receptors for bot...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1993-09, Vol.261 (5128), p.1591-1594
Main Authors: Wang, Ling-Mei, Myers, Martin G., Sun, Xiao-Jian, Aaronson, Stuart A., White, Morris, Pierce, Jacalyn H.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cell Division - drug effects
Cell growth
Cell Line
Cell lines
Cell physiology
Cellular immunity
Cellular receptors
Complementary DNA
Fundamental and applied biological sciences. Psychology
Genetic vectors
Hematopoietic Stem Cells - cytology
Hematopoietic Stem Cells - drug effects
Hematopoietic system
Insulin
Insulin - pharmacology
Insulin Receptor Substrate Proteins
Insulin receptors
Interleukin-4 - pharmacology
Mice
Mitogens
Molecular and cellular biology
Phosphoproteins - metabolism
Phosphorylation
Receptor, Insulin - metabolism
Receptors
Receptors, Interleukin-4
Receptors, Mitogen - metabolism
Signal transduction
Transfection
Tyrosine - metabolism
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Summary:Although several interleukin-3 (IL-3)-dependent cell lines proliferate in response to IL-4 or insulin, the 32D line does not. Insulin and IL-4 sensitivity was restored to 32D cells by expression of IRS-1, the principal substrate of the insulin receptor. Although 32D cells possessed receptors for both factors, they lacked the IRS-1-related protein, 4PS, which becomes phosphorylated by tyrosine in insulin- or IL-4-responsive lines after stimulation. These results indicate that factors that bind unrelated receptors can use similar mitogenic signaling pathways in hematopoietic cells and that 4PS and IRS-1 are functionally similar proteins that are essential for insulin- and IL-4-induced proliferation.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.8372354