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PLK1 — TP53

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: PLK1 — TP53 (direct interaction, enzymatic study) Dias et al., FEBS Lett 2009*
• IRef Hprd Interaction: TP53 — PLK1 (two hybrid) Chen et al., FEBS Lett 2006*
• IRef Hprd Interaction: TP53 — PLK1 (in vivo) Chen et al., FEBS Lett 2006*
• IRef Intact Interaction: Complex of 29 proteins (association, anti tag coimmunoprecipitation) Coffill et al., EMBO Rep 2012
• IRef Intact Interaction: PLK1 — TP53 (physical association, two hybrid) Chen et al., FEBS Lett 2006*
• IRef Intact Interaction: PLK1 — TP53 (physical association, anti bait coimmunoprecipitation) Chen et al., FEBS Lett 2006*
• IRef Intact Interaction: PLK1 — TP53 (phosphorylation reaction, protein kinase assay) Dias et al., FEBS Lett 2009*

Text-mined interactions from Literome

Ando et al., J Biol Chem 2004 : Intriguingly, Plk1 mediated repression of p53 was attenuated with ATM
Incassati et al., Oncogene 2006 : Using the p53 binding-defective mutant of E6 and p53 RNAi, we show that p53 represses Plk1 , suggesting that loss of p53 results in tetraploidy through upregulation of Plk1
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
Martin et al., Cell cycle (Georgetown, Tex.) 2006 : The activity of p53 is in turn controlled by Plk1 itself indicating the existence of an auto-regulatory mechanism involved in the cell cycle dependent regulation of the Plk1 gene
Salvatore et al., Cancer Res 2007 (Carcinoma...) : Adoptive overexpression of p53 , p21 ( CIP1/WAF1 ), and E2F4 down-regulated transcription from the PLK1 and TTK promoters in ATC cells, suggesting that these genes might be under the negative control of tumor suppressors of the p53 and pRB families
Komatsu et al., Oncogene 2009 (Liver Neoplasms) : We previously found that Plk1 inhibited the p53/p73 activity through its direct phosphorylation
McKenzie et al., Cell cycle (Georgetown, Tex.) 2010 : p53 dependent repression of polo-like kinase-1 (PLK1) ... Repression of PLK1 by p53 occurs independently of p21 and of arrest at G1/S where PLK1 levels are normally repressed in a cell cycle dependent manner through a CDE/CHR element ... Additionally, wild type, but not mutant, p53 represses expression of the PLK1 promoter when fused upstream of a reporter gene
King et al., Breast Cancer Res 2012 (Breast Neoplasms) : The significant association between elevated PLK1 and TP53 mutation in women with breast cancer is consistent with escape from repression of PLK1 expression by mutant p53
Louwen et al., Oncotarget 2013 (Neoplasms) : p53 represses the promoter of Polo-like kinase 1, whereas Polo-like kinase 1 inhibits p53 and its family members p63 and p73 in cancer cells lacking functional p53
Mantel et al., Blood 1999 (Polyploidy) : p53 has already been implicated in centrosome regulation