Abstract
p16INK4a in cellular senescence
Highlights
A crucial mechanism in the establishment of cellular senescence is the activation of the INK4/ARF locus, which is epigenetically regulated and under tight control of the Polycomb group (PcG) Trithorax group (TrxG) proteins [1]
Editorial knockdown cells that was characterized by hyperacetylation of histones H3 and H4, as well as increased Ets1/2 occupancy, a transcription factor required for activation of the INK4/ARF locus [5]
To better understand how the loss of DPY30 can lead to a senescence-like phenotype, we screened for direct DPY30 target genes using a genome-wide approach that combined ChIP sequencing for DPY30 and H3K4me3 with expression arrays in wild-type and DPY30 knockdown cells
Summary
A crucial mechanism in the establishment of cellular senescence is the activation of the INK4/ARF locus, which is epigenetically regulated and under tight control of the Polycomb group (PcG) Trithorax group (TrxG) proteins [1]. Editorial knockdown cells that was characterized by hyperacetylation of histones H3 and H4, as well as increased Ets1/2 occupancy, a transcription factor required for activation of the INK4/ARF locus [5]. To better understand how the loss of DPY30 can lead to a senescence-like phenotype, we screened for direct DPY30 target genes using a genome-wide approach that combined ChIP sequencing for DPY30 and H3K4me3 with expression arrays in wild-type and DPY30 knockdown cells.
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