SINHCAF/FAM60A and SIN3A specifically repress HIF-2α expression | Zendy

John Biddlestone | Zendy; Michael Batie | Zendy; Daniel Bandarra | Zendy; Iván Muñoz | Zendy; Sónia Rocha | Zendy

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SINHCAF/FAM60A and SIN3A specifically repress HIF-2α expression

Author(s) -

John Biddlestone,

Michael Batie,

Daniel Bandarra,

Iván Muñoz,

Sónia Rocha

Publication year - 2018

Publication title -

biochemical journal

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.706

H-Index - 265

eISSN - 1470-8728

pISSN - 0264-6021

DOI - 10.1042/bcj20170945

Subject(s) - hdac1 , repressor , transcription factor , histone deacetylase , microbiology and biotechnology , biology , histone , histone deacetylase 2 , transcription (linguistics) , epigenetics , transcriptional regulation , regulation of gene expression , hdac11 , genetics , gene , linguistics , philosophy

The SIN3A-HDAC (histone deacetylase) complex is a master transcriptional repressor, required for development but often deregulated in disease. Here, we report that the recently identified new component of this complex, SINHCAF (SIN3A and HDAC-associated factor)/FAM60A (family of homology 60A), links the SIN3A-HDAC co-repressor complex function to the hypoxia response. We show that SINHCAF specifically represses HIF-2α mRNA and protein expression, via its interaction with the transcription factor SP1 (specificity protein 1) and recruitment of HDAC1 to the HIF-2α promoter. SINHCAF control over HIF-2α results in functional cellular changes in in vitro angiogenesis and viability. Our analysis reveals an unexpected link between SINHCAF and the regulation of the hypoxia response.

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