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HDAC1 — STAT1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: STAT1 → HDAC1 (increases, HDAC1 Activity) Klampfer et al., J Biol Chem 2004*
  Evidence: silencing of HDAC1, HDAC2, and HDAC3 through RNA interference markedly decreased IFNgamma-driven gene activation and that overexpression of HDAC1, HDAC2, and HDAC3 enhanced STAT1-dependent transcriptional activity.

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: HDAC1 — STAT1 (physical association, affinity chromatography technology) Krämer et al., Genes Dev 2006*

Text-mined interactions from Literome

Klampfer et al., J Biol Chem 2004 (Inflammation) : In this study we demonstrated that inhibitors of histone deacetylase (HDAC) activity, butyrate, trichostatin A, and suberoylanilide hydroxamic acid, prevented IFNgamma induced JAK1 activation, STAT1 phosphorylation, its nuclear translocation, and STAT1 dependent gene activation
Jamaluddin et al., J Virol 2005 : Nondenaturing co-IP assays indicate that nuclear Bcl-3 associates with STAT-1 and histone deacetylase 1 (HDAC-1), increasing HDAC-1 recruitment to the IL-8 promoter
Maecker et al., Cell 2005 (Hypersensitivity) : TWEAK inhibited stimulation of the transcriptional activator STAT-1 and induced p65 nuclear factor (NF)-kappaB association with histone deacetylase 1 , repressing cytokine production
Ivanov et al., Oncogene 2007 : Involvement of HDAC activity in STAT1 regulation was validated by TSA inhibition and chromatin immunoprecipitation ( ChIP ) assay