Abstract
NF-Y joins E2Fs, p53 and other stress transcription factors at the apoptosis table
Highlights
Most of the key effectors of apoptosis are constitutively expressed in cells and ready to operate; activation of diverse transcription factors (TFs), specific for noxious conditions, eventually leads to alteration of the transcriptome and expression of proapoptotic proteins
NF-Y is a heterotrimer composed of two histone-fold domain (HFD)-subunits NF-YB/NF-YC and of NF-YA, which provides the capacity to bind avidly to the CCAAT sequence in transcriptional regulatory regions.[1]
The difference might have to do with separate roles of NF-YA and the HFD dimer in DNA metabolism, related to specific groups of genes whose transcription might be differentially sensitive to depletion of the single subunits
Summary
NF-Y joins E2Fs, p53 and other stress transcription factors at the apoptosis table. R Gatta[1], D Dolfini[1] and R Mantovani*,1 Cell Death and Disease (2011) 2, e162; doi:10.1038/cddis.2011.45; published online 26 May 2011. Genes inhibited by NF-YA inactivation, instead, mostly belong to metabolism terms, which is not immediately translatable into a phenotype of S-phase progression impairment, nor activation of the DNA-damage response.[4] In general, it is far from apparent to discern an enrichment of proapoptotic terms among genes controlled by NF-Y. The first came from ChIP-on-chip assays showing that NF-Y is associated to active, and to inactive loci, which are activated after NF-Y removal; interestingly, apoptosis was one of the few terms that popped up in GO analysis of this repressed subset.[7] The second comes from a recent report on transcriptional control of Bim, a strong proapototic gene, essential to mediate cell death of sympathetic neurons upon NGF withdrawal. In essence, such deviant site(s) would go completely unnoticed in a TFBS inspection of promoters, even
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