Abstract
The type 1 insulin-like growth factor receptor (IGF-IR) activates the extracellular signal-regulated kinases (ERK1 and -2). The two major substrates of the IGF-IR, insulin receptor substrate-1 (IRS-1) and the Shc proteins, are known to contribute to this activation. We investigated the domains of the IGF-IR required for the activation of the ERK proteins. To facilitate this study, we used a cell line (32D cells) that lacks IRS-1. In the absence of IRS-1, ERK activation is inhibited if the IGF-IR is mutated at two domains: tyrosine Y950 and a serine quartet at 1280-1283. Expression of IRS-1 in 32D cells expressing the double mutant IGF-IR restores ERK activation. The importance of the C-terminus of the IGF-IR in ERK activation (in the absence of IRS-1) is confirmed by the failure of the insulin receptor to give a sustained activation of ERK. In this model system, there is a good, but not exact, correlation between ERK activation and cell survival after withdrawal of growth factors.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adaptor Proteins, Signal Transducing*
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Adaptor Proteins, Vesicular Transport*
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Cell Line / physiology
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Cell Survival
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Enzyme Activation / physiology
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Enzyme Inhibitors / pharmacology
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Flavonoids / pharmacology
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Insulin Receptor Substrate Proteins
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Mitogen-Activated Protein Kinases / metabolism*
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Phosphoproteins
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Phosphorylation
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Protein Serine-Threonine Kinases / antagonists & inhibitors
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Proteins / metabolism
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Proto-Oncogene Proteins / physiology
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Proto-Oncogene Proteins c-akt
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Receptor, IGF Type 1 / genetics*
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Receptor, IGF Type 1 / physiology*
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Shc Signaling Adaptor Proteins
Substances
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Adaptor Proteins, Signal Transducing
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Adaptor Proteins, Vesicular Transport
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Enzyme Inhibitors
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Flavonoids
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Insulin Receptor Substrate Proteins
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Phosphoproteins
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Proteins
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Proto-Oncogene Proteins
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Shc Signaling Adaptor Proteins
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Receptor, IGF Type 1
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-akt
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Mitogen-Activated Protein Kinases
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2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one