Abstract
R-Ras and insulin-like growth factor-1 (IGF-1) synergistically inhibit apoptosis of BaF3 cells upon interleukin-3 deprivation. To characterize the mechanism of this synergistic inhibition, we examined the effect of R-Ras and IGF-1 on several apoptosis-related proteins. Extracellular signal-regulated kinase (ERK) was activated by IGF-1, but not by R-Ras. In contrast, Akt was activated strongly by R-Ras, but weakly by IGF-1. It was also found that R-Ras and IGF-1 cooperatively induced Bcl-xL expression and inhibited caspase-3 activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis
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Caspase 3
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Caspases / metabolism*
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Cells, Cultured
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Drug Synergism
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GTP Phosphohydrolases / pharmacology*
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Gene Expression Regulation
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Insulin-Like Growth Factor I / pharmacology*
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Interleukin-3 / pharmacology
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Mitogen-Activated Protein Kinases / metabolism*
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Protein Serine-Threonine Kinases*
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins c-akt
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Proto-Oncogene Proteins c-bcl-2 / metabolism*
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bcl-X Protein
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ras Proteins / pharmacology*
Substances
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Interleukin-3
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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bcl-X Protein
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Insulin-Like Growth Factor I
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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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CASP3 protein, human
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Caspase 3
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Caspases
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GTP Phosphohydrolases
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ras Proteins