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NOTCH1 — RBBP4
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
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
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 )