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CDKN2A — HDAC1

Pathways - manually collected, often from reviews:

• NCI Pathway Database Regulation of retinoblastoma protein: RB1/E2F1-3/DP/HDAC1 complex (RB1-HDAC1-E2F3_E2F2_E2F1-TFDP1) → CDK4-6/Cyclin D/p16INK4a complex (CDK6_CDK4-CCND3_CCND2_CCND1-CDKN2A) (modification, collaborate)
  Zhang et al., Cell 2000, Rubin et al., Cell 2005, Kato et al., Genes Dev 1993, Fåhraeus et al., Curr Biol 1996
  Evidence: mutant phenotype, assay, physical interaction
• NCI Pathway Database Regulation of retinoblastoma protein: CDK4-6/Cyclin D/p16INK4a complex (CDK6_CDK4-CCND3_CCND2_CCND1-CDKN2A) → HDAC1 (HDAC1) (modification, inhibits) Zhang et al., Cell 2000, Rubin et al., Cell 2005, Kato et al., Genes Dev 1993, Fåhraeus et al., Curr Biol 1996
  Evidence: mutant phenotype, assay, physical interaction

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: HDAC1 — CDKN2A (direct interaction, pull down) Choi et al., Nucleic Acids Res 2011*
• IRef Biogrid Interaction: HDAC1 — CDKN2A (physical association, affinity chromatography technology) Choi et al., Nucleic Acids Res 2011*

Text-mined interactions from Literome

Chung et al., Mol Ther 2003 (Arthritis, Rheumatoid...) : We found that the histone deacetylase (HDAC) inhibitors ( phenylbutyrate and trichostatin A ) causing histone hyperacetylation to modulate multiple gene expression not only induced the expression of p21 ( Cip1 ) and p16(INK4) in synovial cells but also inhibited the expression of tumor necrosis factor-alpha in affected tissues in adjuvant arthritis, an animal model of RA
Wang et al., Biochim Biophys Acta 2008 : Specifically, HDAC3 and HDAC4 inhibited the p16(INK4a) promoter activity
Zhou et al., Nucleic Acids Res 2009 : We also find that Lsh requires histone deacetylase (HDAC) activity to repress p16(INK4a) and treatment with trichostatin A (TSA) is sufficient to block the repressor effect of Lsh
Feng et al., FEBS J 2009 (Lung Neoplasms) : We also show that histone deacetylase (HDAC) 3 and HDAC4 inhibited p16(INK4a) promoter activity in a dose dependent manner
Yamaguchi et al., Cancer Sci 2010 (Gallbladder Neoplasms) : In TGBC2TKB cells, the expression of EZH2 and HDAC1/2 were decreased by SAHA treatment, and p16(INK4a) , E-cadherin, and p21were simultaneously activated ; however, no such findings were obtained in HGECs, suggesting that the effect of SAHA depends on the EZH2 mediated tumor suppressor loss
Skalska et al., PLoS Pathog 2010 (Epstein-Barr Virus Infections) : Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP ... These novel LCLs have revealed that the chromatin remodelling and epigenetic repression of p16(INK4A) requires the interaction of both EBNA3A and EBNA3C with CtBP