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HDAC1 — JUN

Pathways - manually collected, often from reviews:

• NCI Pathway Database Glucocorticoid receptor regulatory network: HDAC1 (HDAC1) → JUN/FOS/NFAT1-c-4 complex (FOS-JUN) (transcription, inhibits)
  Jee et al., J Biol Chem 2005*
  Evidence: mutant phenotype, reporter gene

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: HDAC1 — JUN (physical association, affinity chromatography technology) Tenbrock et al., J Immunol 2006*

Text-mined interactions from Literome

Rahman et al., Biochem Pharmacol 2002 (Pneumonia) : Pharmacological inhibition of HDAC leads to the increased HAT activity, AP-1 and NF-kappaB activation, and IL-8 release by H2O2 or TNF-alpha treatments
Yamaguchi et al., J Biol Chem 2005 : Chromatin immunoprecipitation assays indicated that HDAC inhibitors suppressed c-Jun binding to the COX-2 promoter and thereby blocked transcription
Wang et al., J Biol Chem 2006 : In this study, we found that c-Jun NH2-terminal kinase 1 activation triggered CtBP phosphorylation on Ser-422 and subsequent degradation, inducing p53 independent apoptosis in human lung cancer cells
Huang et al., J Cell Physiol 2009 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Moreover, c-Jun did not alter growth inhibition and apoptotic induction by histone deacetylase (HDAC) inhibitors ( apicidin, sodium butyrate, and MS275 ) treatment, but inhibited HDAC inhibitors induced erythroid differentiation
Farhana et al., Mol Cancer Ther 2009 : SHP and Sin3A expression are essential for adamantyl substituted retinoid related molecule mediated nuclear factor-kappaB activation, c-Fos/c-Jun expression, and cellular apoptosis ... We examined the effect of loss of SHP and Sin3A expression in a number of cell types on 3-Cl-AHPC mediated growth inhibition and apoptosis induction, 3-Cl-AHPC mediated nuclear factor-kappaB (NF-kappaB) activation, and 3-Cl-AHPC mediated increase in c-Fos and c-Jun expression
Zhou et al., Leukemia 2013 (Leukemia, Myeloid, Acute) : We here report that inhibition of histone deacetylase (HDAC) using the specific class I HDAC inhibitor SNDX-275 restored the expression of Nur77/Nor1 and induced expression of activator protein 1 transcription factors c-Jun and JunB, and of death receptor TRAIL, in AML cells and in CD34 ( + ) /38 ( - ) AML LSCs. Importantly, SNDX-275 induced extensive apoptosis in AML cells, which could be suppressed by silencing nur77 and nor1