◀ Back to TP53
TP53 — VRK1
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
TP53
→
VRK1
(increases, TP53 Activity)
Vega et al., Mol Cell Biol 2004*
Evidence: VRK1 is located in the nucleus outside the nucleolus. Overexpression of VRK1 increases the stability of p53 by a posttranslational mechanism leading to its accumulation Catalytically inactive VRK1 protein (a K179E mutant) does not induce p53 accumulation.
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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IRef Biogrid Interaction:
TP53
—
VRK1
(direct interaction, enzymatic study)
Lopez-Borges et al., Oncogene 2000*
-
IRef Biogrid Interaction:
TP53
—
VRK1
(physical association, affinity chromatography technology)
Vega et al., Mol Cell Biol 2004*
-
IRef Biogrid Interaction:
TP53
—
VRK1
(direct interaction, enzymatic study)
Vega et al., Mol Cell Biol 2004*
-
IRef Biogrid Interaction:
TP53
—
VRK1
(direct interaction, enzymatic study)
Barcia et al., Arch Biochem Biophys 2002*
-
IRef Hprd Interaction:
TP53
—
VRK1
(in vitro)
Sayed et al., J Biol Chem 2000, Lopez-Borges et al., Oncogene 2000*, Latonen et al., Oncogene 2001*, Barcia et al., Arch Biochem Biophys 2002*
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IRef Hprd Interaction:
TP53
—
VRK1
(in vivo)
Sayed et al., J Biol Chem 2000, Lopez-Borges et al., Oncogene 2000*, Latonen et al., Oncogene 2001*, Barcia et al., Arch Biochem Biophys 2002*
-
IRef Intact Interaction:
TP53
—
VRK1
(colocalization, confocal microscopy)
Vega et al., Mol Cell Biol 2004*
Text-mined interactions from Literome
Vega et al., Mol Cell Biol 2004
:
Overexpression of
VRK1 increases the stability of
p53 by a posttranslational mechanism leading to its accumulation by a mechanism independent of the Chk2 kinase
Valbuena et al., PloS one 2008
:
Downregulation of
VRK1 induced by
p53 is prevented in a dose dependent manner by either p300 or CBP, but not by PCAF, used as transcriptional co-activators, suggesting that p53 has a different specificity depending on the relative level of these transcriptional cofactors ... Specifically, the downregulation of
VRK1/VRK2 protein levels, as a
consequence of
p53 accumulation, is thus dependent on the levels of the p300/CBP protein available for transcriptional complexes, since in this context this cofactor functions as a repressor of the effect
Valbuena et al., PloS one 2011
:
Human
VRK1 induces a stabilization and accumulation of
p53 by specific phosphorylation in Thr18