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RBBP4 — TP53

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

Studies that report less than 10 interactions are marked with *

• STRING interaction: TP53 — RBBP4 (interaction, mapped from kegg_pathways)
• STRING interaction: RBBP4 — TP53 (interaction, mapped from grid kegg_pathways)

Text-mined interactions from Literome

Juan et al., J Biol Chem 2000 : Down-regulation of p53 activity by HDACs is HDAC dosage dependent , requires the deacetylase activity of HDACs, and depends on the region of p53 that is acetylated by p300/CREB binding protein (CBP)
Luo et al., Nature 2000 : PID specifically interacts with p53 both in vitro and in vivo, and its expression reduces significantly the steady-state levels of acetylated p53
Koumenis et al., Mol Cell Biol 2001 (Cell Transformation, Neoplastic) : At the molecular level, DNA damage induces the interaction of p53 with the transcriptional activator p300 as well as with the transcriptional corepressor mSin3A ... In contrast, hypoxia primarily induces an interaction of p53 with mSin3A , but not with p300
Peltonen et al., Pigment Cell Res 2005 (Melanoma) : Inhibiting p53 function by a dominant negative p53 ( p53 ( 175His ) ) confirmed that the HDAC inhibitor induced apoptosis was independent of wild-type p53 , even though TSA slightly activated p53 in a reporter assay
Shetty et al., Mol Cell Biol 2005 (Breast Neoplasms) : Indeed, HDAC inhibitors activate NF-kappaB and p53 and upregulate DR5 expression
Tsuyama et al., Biochem Biophys Res Commun 2005 (Multiple Myeloma) : Expression of p53 , a direct target gene of Bcl6, was downregulated in the IL-6 stimulated cells, and this process was impaired by an HDAC inhibitor
Zhang et al., Cancer Lett 2008 (Carcinoma, Hepatocellular...) : Researches have shown that ING2 can activate p53 and p53 mediated apoptotic pathway involved in the hepatocarcinogenesis
LeBoeuf et al., Dev Cell 2010 : Mutant embryos display increased levels of acetylated p53 , which opposes p63 functions, and p53 is required for HDAC inhibitor mediated p21 expression in keratinocytes
Zeng et al., Cancer Res 2011 : We show that p53 is required for both HDAC and PcG to repress Arf expression
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
Li et al., Cancer Lett 2012 (Bone Neoplasms...) : Pharmacologic inhibitor of HDAC , trichostatin A (TSA) promoted p53-p300 interaction and recruitment of p53 Lys-382 to promoter regions of its target genes p21 and Puma, consequently inducing apoptosis and stabilizing the acetylation of p53 at Lys-382 together with the upregulation of p21 and Puma, which were impaired in EFTs cells after the knockdown of p53 expression
Yan et al., Oncogene 2013 : Here we found that histone deacetylase (HDAC) inhibitors suppress both wild-type and mutant p53 transcription in time- and dose dependent manners
Madapura et al., Cell cycle (Georgetown, Tex.) 2012 : Modifying p53 levels using Nutlin-3, which specifically dissociates the MDM2-p53 interaction, was sufficient to upregulate SAP expression, indicating that SAP is a target of p53 in T cells