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EIF2AK2 — TP53
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
EIF2AK2
—
TP53
(direct interaction, pull down)
Cuddihy et al., Oncogene 1999*
-
IRef Biogrid Interaction:
EIF2AK2
—
TP53
(physical association, affinity chromatography technology)
Cuddihy et al., Oncogene 1999*
-
IRef Biogrid Interaction:
EIF2AK2
—
TP53
(direct interaction, enzymatic study)
Cuddihy et al., Oncogene 1999*
-
IRef Hprd Interaction:
TP53
—
EIF2AK2
(in vivo)
Cuddihy et al., Oncogene 1999*, Sayed et al., J Biol Chem 2000, Luciani et al., J Mol Biol 2000*
-
IRef Hprd Interaction:
TP53
—
EIF2AK2
(in vitro)
Cuddihy et al., Oncogene 1999*, Sayed et al., J Biol Chem 2000, Luciani et al., J Mol Biol 2000*
-
IRef Ophid Interaction:
EIF2AK2
—
TP53
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Cuddihy et al., Mol Cell Biol 1999
:
Double-stranded-RNA activated protein kinase
PKR enhances transcriptional activation by
tumor suppressor p53
Cuddihy et al., Oncogene 1999
:
In addition, p53 may function as a substrate of PKR since phosphorylation of human
p53 on serine392 is
induced by activated
PKR in vitro
Baltzis et al., J Biol Chem 2007
(Fibrosarcoma) :
This role is not specific for PERK, because the eIF2alpha kinase
PKR also
promotes p53 degradation in response to double stranded RNA
Raven et al., Cell cycle (Georgetown, Tex.) 2008
:
Specifically, we demonstrated that degradation of the cell cycle regulator cyclin D1, and the tumour suppressor
p53 was
promoted by PERK and
PKR during periods of ER stress
Yoon et al., Proc Natl Acad Sci U S A 2009
(Colonic Neoplasms...) :
Activation of
p53 by genotoxic stress
induces a significant level of
PKR expression by acting on the newly identified cis acting element ( ISRE ), which is separated from the IFN stimulated responsive element on the PKR promoter, resulting in translational inhibition and cell apoptosis ... These data indicate that p53 mediated tumor suppression can be attributed at least in part to the biological functions of
PKR induced by
p53 in genotoxic conditions