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EGR1 — TP53
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
EGR1
—
TP53
(physical association, affinity chromatography technology)
Kim et al., Cell Physiol Biochem 2011*
-
IRef Biogrid Interaction:
EGR1
—
TP53
(direct interaction, pull down)
Liu et al., Int J Oncol 2001*
-
IRef Biogrid Interaction:
EGR1
—
TP53
(physical association, affinity chromatography technology)
Liu et al., Int J Oncol 2001*
-
IRef Biogrid Interaction:
EGR1
—
TP53
(physical association, affinity chromatography technology)
Yu et al., Mol Cell 2004*
-
IRef Hprd Interaction:
TP53
—
EGR1
(in vitro)
Liu et al., Int J Oncol 2001*
-
IRef Hprd Interaction:
TP53
—
EGR1
(in vivo)
Liu et al., Int J Oncol 2001*
-
IRef Intact Interaction:
EGR1
—
TP53
(colocalization, cosedimentation)
Qu et al., Genes Dev 2004*
-
IRef Ophid Interaction:
EGR1
—
TP53
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
-
IRef Ophid Interaction:
EGR1
—
TP53
(aggregation, confirmational text mining)
Liu et al., Int J Oncol 2001*
Text-mined interactions from Literome
Zhang et al., Exp Cell Res 2001
(Neoplasms) :
The presence of wild-type
p53 suppressed the induction of
EGR-1 after UV treatment
Nair et al., J Biol Chem 2004
(MAP Kinase Signaling System) :
Whereas the proportion of cells activating ERK versus p53 at 1 h depended on H ( 2 ) O ( 2 ) concentration, individual cells showed exclusively either
phospho-p53 formation or
activation of ERK and
egr1 induction
Weisz et al., Cancer Res 2004
:
Functional assays indicate that
induction of
EGR1 by mutant
p53 contributes to enhanced transformed properties and resistance to apoptosis
Sabourin et al., J Cell Physiol 1990
:
Upon readdition of IL-6 to G1-arrested B9 cells, viability is maintained and entry into S phase occurs after a lag period of 10 to 12 hr. Northern blot analysis showed that the immediate-early mRNAs normally induced shortly after growth factor stimulation in quiescent fibroblasts ( c-fos, c-jun,
Egr-1 , c-myc, JE, and KC ), and other growth related genes ( 2F1, c-Ha-ras, and
p53 ), are either not
induced or remain unchanged during G1 to S phase progression
Park et al., Cancer Lett 2008
(Carcinoma, Hepatocellular...) :
Furthermore, HS-1200 treatment markedly induced the
Egr-1 expression at an early time point, and the increased expression levels of
p53 , p21 WAF1/CIP1, p27 KIP1, and COX-2 after treatment with HS-1200 were completely
inhibited in HepG2 cells and partially inhibited in Hep3B cells by silencing of Egr-1, respectively
Sauer et al., Oncogene 2010
(MAP Kinase Signaling System...) :
Although forced expression of wild-type
p53 was not
sufficient to trigger
Egr-1 transcription, four different mutants of p53 were shown to induce Egr-1