Gene interactions and pathways from curated databases and text-mining

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HSP90AA1 — TP53

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Walerych et al., J Biol Chem 2004 : A minor decrease in p53 protein level following the treatment of human fibroblasts with the inhibitors suggests the potential involvement of Hsp90 in the stabilization of wild-type p53 ... To support our in vivo findings, we used a reconstituted system with highly purified recombinant proteins to examine the effects of Hsp90 on wild-type p53 binding to the p21 promoter sequence
Müller et al., J Biol Chem 2004 : Hsp90 regulates the activity of wild type p53 under physiological and elevated temperatures
Naoe et al., Cancer Sci 2006 (Hematologic Neoplasms...) : Nucleophosmin (NPM) is a nucleolar phosphoprotein that plays multiple roles in ribosome assembly and transport, cytoplasmic-nuclear trafficking, centrosome duplication and regulation of p53
Bergstralh et al., Exp Cell Res 2007 (Lung Neoplasms) : Mass spectroscopy identified the protein as nucleophosmin/B23 (NPM), a multifunctional protein with diverse roles : ribosome biosynthesis, p53 regulation , nuclear-cytoplasmic shuttling, and centrosome duplication
Habib et al., Arch Biochem Biophys 2009 (MAP Kinase Signaling System) : p53 regulates Hsp90beta during arsenite induced cytotoxicity in glutathione-deficient cells ... In addition, p53 transcriptionally repressed Hsp90beta gene expression
Walerych et al., Oncogene 2009 : Hsp90 stabilizes the binding of p53 to the promoter sequence at 37 degrees C, whereas under heat-shock conditions the requirement for the Hsp70-Hsp40 system and its cooperation with Hsp90 increases
Regan et al., Int J Oncol 2011 (Neuroblastoma) : Hsp90 inhibition increases p53 expression and destabilizes MYCN and MYC in neuroblastoma ... It was found that Hsp90 inhibition in neuroblastoma cell lines resulted in significant growth suppression, a decrease in MYCN and MYC expression, and an increase in the expression of p53
Banu et al., Toxicol Appl Pharmacol 2011 : Our data indicated that CrVI : ( i ) induced DNA fragmentation and increased apoptosis, ( ii ) increased cytochrome c release from the mitochondria to cytosol, ( iii ) downregulated anti-apoptotic Bcl-2, Bcl-XL, HSP70 and HSP90 ; upregulated pro-apoptotic BAX and BAD, ( iv ) altered translocation of Bcl-2, Bcl-XL, BAX, BAD, HSP70 and HSP90 to the mitochondria, ( v ) upregulated p-ERK and p-JNK, and selectively translocated p-ERK to the mitochondria and nucleus, ( vi ) activated caspase-3 and PARP, and ( vii ) increased phosphorylation of p53 at ser-6, ser-9, ser-15, ser-20, ser-37, ser-46 and ser-392, increased p53 transcriptional activation, and downregulated MDM-2
Mantel et al., Blood 1999 (Polyploidy) : p53 has already been implicated in centrosome regulation