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10.1042/BCJ20170945

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suck abstract from ncbi


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pmid29784889
      Biochem+J 2018 ; 475 (12 ): 2073-2090
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  • SINHCAF/FAM60A and SIN3A specifically repress HIF-2? expression #MMPMID29784889
  • Biddlestone J ; Batie M ; Bandarra D ; Munoz I ; Rocha S
  • Biochem J 2018[Jun]; 475 (12 ): 2073-2090 PMID29784889 show ga
  • 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-2? mRNA and protein expression, via its interaction with the transcription factor SP1 (specificity protein 1) and recruitment of HDAC1 to the HIF-2? promoter. SINHCAF control over HIF-2? 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.
  • |*Gene Expression Regulation [MESH]
  • |A549 Cells [MESH]
  • |Basic Helix-Loop-Helix Transcription Factors/*biosynthesis/genetics [MESH]
  • |DNA-Binding Proteins/genetics/*metabolism [MESH]
  • |HeLa Cells [MESH]
  • |Histone Deacetylase 1/genetics/metabolism [MESH]
  • |Humans [MESH]
  • |Promoter Regions, Genetic [MESH]
  • |RNA, Messenger/*biosynthesis/genetics [MESH]
  • |Repressor Proteins/genetics/*metabolism [MESH]


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