Gene interactions and pathways from curated databases and text-mining

◀ Back to NOTCH1

HDAC1 — NOTCH1

Pathways - manually collected, often from reviews:

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Chen et al., Basic Clin Pharmacol Toxicol 2007 (Leukemia) : Curcumin, both histone deacetylase and p300/CBP-specific inhibitor, represses the activity of nuclear factor kappa B and Notch 1 in Raji cells
Xiao et al., Mol Cancer Ther 2009 (Adenocarcinoma, Follicular...) : We have previously shown that Notch1 may function as a tumor suppressor and that histone deacetylase (HDAC) inhibitors can induce Notch1 expression in some endocrine cancers ... These results indicate that HDAC inhibitors activate Notch1 signaling in thyroid cancer cells and lead to the suppression of proliferation by cell cycle arrest
Cayo et al., American journal of translational research 2009 : We hypothesized that the HDAC inhibitor Sodium Butyrate ( NaB ) might activate Notch1 in pheochromocytoma resulting in altered tumor cell proliferation
Hughes et al., Cancer Treat Res 2009 (Bone Neoplasms...) : Further, exposure to valproic acid at therapeutic concentrations induced expression of Notch genes and caused a 250-fold increase in invasiveness for non-invasive cell lines, but had no discernible effect on those lines that expressed high levels of Notch without valproic acid treatment, suggesting a role for HDAC in regulating Notch pathway expression in osteosarcoma
Mulligan et al., Mol Cell 2011 : A SIRT1-LSD1 corepressor complex regulates Notch target gene expression and development
Tseng et al., PloS one 2011 : Inhibition of HDAC function resulted in aberrant expression of Notch1 and BMP2, two genes known to be required for tail regeneration
Tang et al., Journal of the American Heart Association 2012 : However, inhibition of HDAC activity did not suppress Notch activation of the HRT target genes ... Although CBF-1 mediated Notch signaling was increased by HDAC inhibition in human SMCs and in a C3H10T1/2 model, SMC differentiation was inhibited in both cases ... Although CBF-1 mediated Notch signaling is not suppressed by HDAC inhibition, HDAC activity is required for Notch differentiation signals through mitogen activated protein kinase and PI3K pathways in SMCs. ( J Am Heart Assoc. 2012 ; 1 : e000901 doi : 10.1161/JAHA.112.000901 )
Zhao et al., Neoplasia (New York, N.Y.) 2013 : We showed that hD1R could bind to ECs specifically through its RGD motif and effectively triggered Notch signaling in ECs