A cis-element within the ARF locus mediates repression of p16^INK4A expression via long-range chromatin interactions.

ABSTRACT: Loss of function of CDKN2A/B, also known as INK4/ARF [encoding p16^INK4A, p15^INK4B, and p14^ARF (mouse p19^Arf)], confers susceptibility to cancers, whereas its up-regulation during organismal aging provokes cellular senescence and tissue degenerative disorders. To better understand the transcriptional regulation of p16^INK4A, a CRISPR screen targeting open, noncoding chromatin regions adjacent to p16^INK4A was performed in a human p16^{INK4A-P2A-mCherry} reporter cell line. We identified a repressive element located in the 3' region adjacent to the ARF promoter that controls p16^INK4A expression via long-distance chromati

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC6936709 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature