Oncogene-induced senescent cells display a robust change in their epigenome and have increased transcription and secretion of numerous pro-inflammatory cytokines and chemokines termed the senescence-associated secretory phenotype (SASP). Therefore, understanding how and if the epigenome is involved in regulating the transcription of the SASP is critical to understanding how to restrain the harmful effects of the SASP. The active histone marks H3K79me2 and H3K79me3 and their methyltransferase DOT1L are increased during oncogene-induced senescence.  Whether H3K79 methylation and DOT1L expression are involved in the transcriptional regulation of the SASP is unknown. SOURCE: Katherine Aird (kaird@psu.edu) -  Penn State College of MEdicine

Pluto Bioinformatics

GSE156648: Gene expression data from IMR90 Control, IMR90 HRAS-G12V, IMR90 HRAS-G12V+shDOT1L, IMR90 DOT1L Overexpression