Title : Posttranslational regulation of Myc function in response to phorbol ester/interferon-gamma-induced differentiation of v-Myc-transformed U-937 monoblasts.

Pub. Date : 1999 Jun 1

PMID : 10339499






8 Functional Relationships(s)
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1 Constitutive expression of v-Myc blocks phorbol ester (TPA)-induced differentiation of human U-937 monoblasts. Tetradecanoylphorbol Acetate MYC proto-oncogene, bHLH transcription factor Homo sapiens
2 However, costimulation with interferon-gamma (IFN-gamma) and TPA restores terminal differentiation and G1 cell-cycle arrest despite continuous expression of v-Myc. Tetradecanoylphorbol Acetate MYC proto-oncogene, bHLH transcription factor Homo sapiens
3 The mechanism by which TPA + IFN-gamma counteract v-Myc activity has not been unravelled. Tetradecanoylphorbol Acetate MYC proto-oncogene, bHLH transcription factor Homo sapiens
4 Our results show that TPA + IFN-gamma treatment led to an inhibition of v-Myc- and c-Myc-dependent transcription, and a specific reduction of v-Myc:Max complexes and associated DNA-binding activity, whereas the steady state level of the v-Myc protein was only marginally affected. Tetradecanoylphorbol Acetate MYC proto-oncogene, bHLH transcription factor Homo sapiens
5 Our results show that TPA + IFN-gamma treatment led to an inhibition of v-Myc- and c-Myc-dependent transcription, and a specific reduction of v-Myc:Max complexes and associated DNA-binding activity, whereas the steady state level of the v-Myc protein was only marginally affected. Tetradecanoylphorbol Acetate MYC proto-oncogene, bHLH transcription factor Homo sapiens
6 Our results show that TPA + IFN-gamma treatment led to an inhibition of v-Myc- and c-Myc-dependent transcription, and a specific reduction of v-Myc:Max complexes and associated DNA-binding activity, whereas the steady state level of the v-Myc protein was only marginally affected. Tetradecanoylphorbol Acetate MYC proto-oncogene, bHLH transcription factor Homo sapiens
7 Our results show that TPA + IFN-gamma treatment led to an inhibition of v-Myc- and c-Myc-dependent transcription, and a specific reduction of v-Myc:Max complexes and associated DNA-binding activity, whereas the steady state level of the v-Myc protein was only marginally affected. Tetradecanoylphorbol Acetate MYC proto-oncogene, bHLH transcription factor Homo sapiens
8 Phosphatase treatment of Myc:Max complexes lead to their dissociation, thus mimicking the effect of TPA + IFN-gamma. Tetradecanoylphorbol Acetate MYC proto-oncogene, bHLH transcription factor Homo sapiens