Transcription profiling of mouse embryonic fibroblasts from embryos with ?CH1 mutation in p300 and/or CBP atreated with hypoxia or dipyridyl (a hypoxia mimetic) and trichostatin A (a histone deacetylase inhibitor) reveals two transactivation mechanisms are responsible for the bulk of HIF-1alpha-responsive gene expression
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Transcription profiling of mouse embryonic fibroblasts from embryos with ?CH1 mutation in p300 and/or CBP atreated with hypoxia or dipyridyl (a hypoxia mimetic) and trichostatin A (a histone deacetylase inhibitor) reveals two transactivation mechanisms are responsible for the bulk of HIF-1alpha-responsive gene expression
创建时间：
2008-06-12
