作者: Arthur S Alberts , Olivier Geneste , Richard Treisman
DOI: 10.1016/S0092-8674(00)80941-1
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摘要: Constitutively active forms of the small GTPases RhoA (RhoA.V14) and Cdc42 (Cdc42.V12) induce expression extrachromosomal SRF reporter genes in microinjection experiments, but only Cdc42.V12 can efficiently activate a chromosomal template. Both SAPK/JNK-dependent or -independent signals cooperate with RhoA.V14 to reporters, it is SAPK/JNK activation by that allows templates. Cooperating be bypassed deacetylase inhibitors. Three findings show histone H4 hyperacetylation one target for cooperating signals, although alone not sufficient: (1) Cdc42.V12, RhoA.V14, induces hyperacetylation; (2) use same pathways (3) growth factor stress stimuli substantial hyperacetylation, detectable gene chromatin. These data establish link between signal-regulated acetylation events transcription.