Gene interactions and pathways from curated databases and text-mining

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TP53 — XIAP

Text-mined interactions from Literome

Sasaki et al., Cancer Res 2000 (Adenocarcinoma...) : Xiap down-regulation resulted in caspase-3 activation, caspase mediated MDM2 processing, and p53 accumulation
Li et al., Proc Natl Acad Sci U S A 2002 : These results indicate that p53 status is an important modulator of NO ( * ) -induced mutagenesis and apoptosis, and suggest that levels of the Apaf-1 and XIAP proteins, but not mitochondrial depolarization and cytochrome c release, are regulated by p53 in these human lymphoblastoid cells
Tun et al., J Neurochem 2007 : Activation of the extrinsic caspase pathway in cultured cortical neurons requires p53 mediated down-regulation of the X-linked inhibitor of apoptosis protein to induce apoptosis ... These findings suggest that p53 regulates neuronal apoptosis, in part, by suppressing the anti-apoptotic protein XIAP via transcriptional activation of Omi/HtrA2
Chang et al., Eur J Pharmacol 2008 (Adenocarcinoma...) : Incubation of human lung adenocarcinoma A549 cells with 25 microM Gefitinib resulted in phosphorylation and activation of p53 such as enhanced DNA binding activity, which was accompanied by the upregulation of PUMA ( p53 upregulated modulator of apoptosis ) and Fas, and downregulation of survivin and XIAP ( X-linked inhibitor of apoptosis protein ) ... p53 may induce apoptosis through the regulation of apoptotic ( Fas and PUMA ) and anti-apoptotic ( XIAP and survivin ) genes
Carter et al., Blood 2010 (Blast Crisis...) : Activation of p53 by murine double minute ( MDM2 ) antagonist nutlin-3a or inhibition of X-linked inhibitor of apoptosis (XIAP) induces apoptosis in acute myeloid leukemia ( AML ) cells ... Knockdown of p53 by shRNA blunted the synergy, and down-regulation of XIAP by antisense oligonucleotide ( ASO ) enhanced nutlin-3a induced apoptosis, suggesting that the synergy was mediated by p53 activation and XIAP inhibition ... Importantly, p53 activation and XIAP inhibition enhanced apoptosis in blasts from patients with primary AML, even when the cells were protected by stromal cells