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PTK2 — TP53
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
PTK2
—
TP53
(physical association, affinity chromatography technology)
Lim et al., Mol Cell 2008*
-
IRef Biogrid Interaction:
PTK2
—
TP53
(direct interaction, pull down)
Lim et al., Mol Cell 2008*
-
IRef Hprd Interaction:
TP53
—
PTK2
(in vitro)
Golubovskaya et al., J Biol Chem 2005*
-
IRef Hprd Interaction:
TP53
—
PTK2
(in vivo)
Golubovskaya et al., J Biol Chem 2005*
-
IRef Intact Interaction:
PTK2
—
TP53
(direct interaction, pull down)
Golubovskaya et al., J Biol Chem 2005*
-
IRef Intact Interaction:
PTK2
—
TP53
(physical association, anti bait coimmunoprecipitation)
Golubovskaya et al., J Biol Chem 2005*
-
IRef Intact Interaction:
PTK2
—
TP53
(colocalization, confocal microscopy)
Golubovskaya et al., J Biol Chem 2005*
-
IRef Intact Interaction:
PTK2
—
TP53
(physical association, anti bait coimmunoprecipitation)
Fanucchi et al., FEBS Lett 2009*
Text-mined interactions from Literome
Pierce et al., Oncogene 2000
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
We conclude that prolonged Bcr-Abl
PTK activity within multipotent cells
results in a reduction of
p53 that drives a delayed and abnormal differentiation
Zhang et al., Pharmacology 2002
(Stomach Neoplasms) :
Further studies showed that As ( 2 ) O ( 3 ) could
regulate protein tyrosine kinase activity, protein tyrosine phosphorylation, and Bcl-2 protein and upregulate
p53 protein
Corey et al., EMBO J 1993
:
Here we show that in human myeloid derived cells GM-CSF can stimulate ; ( i ) the accumulation of PtdIns ( 3,4,5 ) P3 ; ( ii ) increases in
p53/p56lyn and p62c-yes
directed protein tyrosine kinase activities in anti-lyn and anti-c-yes antibody directed immunoprecipitates, respectively and ; ( iii ) increases in phosphoinositide 3OH-kinase activity in antiphosphotyrosine, anti-p53/p56lyn and anti-p62c-yes antibody directed immunoprecipitates