E2F1-MEDIATED INDUCTION OF NFYB ATTENUATES APOPTOSIS VIA JOINT REGULATION OF A PRO-SURVIVAL TRANSCRIPTIONAL PROGRAM.

E2F1-Mediated Induction of NFYB Attenuates Apoptosis via Joint Regulation of a Pro-Survival Transcriptional Program.

E2F1-Mediated Induction of NFYB Attenuates Apoptosis via Joint Regulation of a Pro-Survival Transcriptional Program.

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The E2F1 transcription factor regulates cell proliferation and apoptosis through the control of a considerable simply southern cat shirt variety of target genes.Previous work has detailed the role of other transcription factors in mediating the specificity of E2F function.Here we identify the NF-YB transcription factor as a novel direct E2F1 target.Genome-wide expression analysis of the effects of NFYB knockdown on E2F1-mediated transcription identified a large group of genes that are co-regulated by E2F1 and NFYB.We read more also provide evidence that knockdown of NFYB enhances E2F1-induced apoptosis, suggesting a pro-survival function of the NFYB/E2F1 joint transcriptional program.

Bioinformatic analysis suggests that deregulation of these NFY-dependent E2F1 target genes might play a role in sarcomagenesis as well as drug resistance.

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