The B Subunit of the CAAT-binding Factor NFY Binds the Central Segment of the Co-activator p300

Abstract

We report that the heterotrimeric transcription factor NFY or "CAAT-binding factor" binds the ؊60 region of the human H ferritin promoter, the B site. DNA binding analysis with specific antibodies demonstrates that NFY/B/C subunits tightly bind this site and that NFY/C subunit is masked in vivo by binding with other protein(s). NFY binds the co-activator p300. Specifically, the NFY/B subunit interacts with the central segment of p300 in vivo and in vitro. cAMP substantially increases the formation of the NFY⅐p300 complex. Taken together these data provide a general model of cAMP induction of non-CRE-containing promoters and suggest that the NFY-B⅐p300 complex is located at the 5 end of the promoter and the NFY-B⅐C⅐TFIIB on the 3 end toward the transcription start site.

Molecular Mechanisms for Transcriptional Regulation of Human High-Affinity IgE Receptor β-Chain Gene Induced by GM-CSF

“…Among the three subunits constituting NFY, A and B-subunits have been reported to bind HDAC and p300/CBP, respectively (24,35). These reports indicate that NFY can directly interact with both histone acetyl transferase and HDAC, which are known to act as a transcriptional coactivator and corepressor, respectively.…”

Histone deacetylase inhibitors induce FPGS mRNA expression and intracellular accumulation of long-chain methotrexate polyglutamates in childhood acute lymphoblastic leukemia: implications for combination therapy

“…Further, transcription factors other than NFY and Sp1 could also be involved in the binding and recruitment of HAT to the FPGS promoter. For instance, interactions between NFY and HAT proteins such as the coactivator p300 [66][67][68][69][70][71] have been described previously. This dual mechanism of regulation involving both HATs and HDACs has recently been shown for the TbRII promoter in which transforming growth factor-b expression was found to be induced both by trichostatin-A, a HDACI, and by acetylation of Sp1 after recruitment of PCAF/ p300 to an Sp1/NFY complex.…”

JunD activates transcription of the human ferritin H gene through an antioxidant response element during oxidative stress

“…To date, only a proximal 0.15 kb promoter/enhancer region containing the CCAAT box (termed B site) has been elucidated in the transcriptional regulation of the human ferritin H gene (Bevilacqua et al, 1997;Marziali et al, 1997;Faniello et al, 1999). We therefore asked whether the proximal ferritin H enhancer is the sole enhancer element for transcriptional regulation of the human ferritin H gene, in particular, in response to oxidative stress.…”

“…It has been reported by two independent research groups that transcription of the human ferritin H gene is activated by cyclic AMP (Bevilacqua et al, 1997) and hemin (Marziali et al, 1997) via a proximal cis-acting element containing CCAAT motif. This element, termed B site, located within 0.1 kb upstream from transcription initiation site, is regulated by NF-Y transcription factors (Bevilacqua et al, 1997;Marziali et al, 1997) and transcriptional coactivators harboring histone acetyltransferase activity such as p300/CBP (Faniello et al, 1999) and P/CAF (Bevilacqua et al, 1998). The element also serves as a basal transcription apparatus that contributes to the tissue-specific expression of the ferritin H gene (Bevilacqua et al, 1998).…”