MED19 and MED26 are synergistic functional targets of the RE1 silencing transcription factor in epigenetic silencing of neuronal gene expression.

ABSTRACT: A key hub for the orchestration of epigenetic modifications necessary to restrict neuronal gene expression to the nervous system is the RE1 silencing transcription factor (REST; also known as neuron restrictive silencer factor, NRSF). REST suppresses the nonspecific and premature expression of neuronal genes in non-neuronal and neural progenitor cells, respectively, via recruitment of enzymatically diverse corepressors, including G9a histone methyltransferase (HMTase) that catalyzes di-methylation of histone 3-lysine 9 (H3K9me2). Recently, we identified the RNA polymerase II transcriptional Mediator to be an essential link between RE1-bound REST and G9a in epigenetic suppression of neuronal genes in non-neuronal cells. However, the means by which REST recruits Mediator to facilitate G9a-de

SUBMITTER: Ding N 

PROVIDER: S-EPMC2631966 | biostudies-literature | 2009 Jan

REPOSITORIES: biostudies-literature