◀ Back to HDAC1

HDAC1 — MDM2

Pathways - manually collected, often from reviews:

• NCI Pathway Database Regulation of Androgen receptor activity: HDAC1 (HDAC1) → MDM2 (MDM2) (transcription, inhibits) Brady et al., J Biol Chem 1999*, Gaughan et al., J Biol Chem 2001, Gaughan et al., J Biol Chem 2002*
  Evidence: mutant phenotype, reporter gene, physical interaction
• NCI Pathway Database Regulation of Androgen receptor activity: MDM2 (MDM2) → HDAC1 (HDAC1) (proteasomal ubiquitin-dependent protein catabolic process, activates) Gaughan et al., Nucleic Acids Res 2005*
  Evidence: mutant phenotype, assay

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: HDAC1 — MDM2 (physical association, affinity chromatography technology) Gaughan et al., Nucleic Acids Res 2005*
• IRef Biogrid Interaction: HDAC1 — MDM2 (colocalization, imaging technique) Gaughan et al., Nucleic Acids Res 2005*
• IRef Biogrid Interaction: HDAC1 — MDM2 (physical association, affinity chromatography technology) Ito et al., EMBO J 2002*
• IRef Biogrid Interaction: HDAC1 — MDM2 (direct interaction, pull down) Ito et al., EMBO J 2002*
• IRef Hprd Interaction: HDAC1 — MDM2 (in vivo) Ito et al., EMBO J 2002*
• IRef Ophid Interaction: MDM2 — HDAC1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: MDM2 — HDAC1 (aggregation, confirmational text mining) Ito et al., EMBO J 2002*

Text-mined interactions from Literome

Ito et al., EMBO J 2002 : Ectopic expression of a dominant negative HDAC1 mutant restores p53 acetylation in the presence of MDM2 , whereas wild-type HDAC1 and MDM2 deacetylate p53 synergistically
Gaughan et al., Nucleic Acids Res 2005 : Regulation of androgen receptor and histone deacetylase 1 by Mdm2 mediated ubiquitylation ... Furthermore, we demonstrate that Mdm2 mediated modification of AR and HDAC1 catalyses protein destabilization and attenuates AR sactivity, suggesting that ubiquitylation of the AR and HDAC1 may constitute an additional mechanism for regulating AR function
McCormack et al., Leukemia 2012 (Leukemia, Myeloid, Acute) : Our results suggest the concomitant targeting of MDM2-p53 and HDAC inhibition , may be an effective therapeutic strategy for the treatment of AML