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EGR1 — MAPK3
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Park et al., J Neurochem 1999
:
PD098059, an inhibitor of the Erk 1/2 upstream kinase mitogen activated protein kinase kinase 1 ( MEK1 ), blocked
Erk 1/2 activation,
Egr-1 induction , and neuronal death by zinc
Bernal-Mizrachi et al., J Biol Chem 2000
:
Pharmacological inhibition of the
Egr-1 induction by H89 ( 48 % ) and calmidazolium ( 35 % ), but not by
mitogen activated protein kinase/extracellular signal regulated kinase kinase 1 and 2 or phosphatidylinositol 3-kinase inhibitors, implied that protein kinase A and Ca ( 2+ ) /calmodulin pathways are involved
Bea et al., Circ Res 2003
(MAP Kinase Signaling System) :
Furthermore, C pneumoniae stimulated phosphorylation of ERK1/2 and Elk-1 and pharmacological inhibition of
mitogen activated protein kinase activity
reduced the expression of TF and
Egr-1
Giri et al., J Immunol 2003
:
Our results indicate that A beta induced expression of cytokines ( TNF-alpha and IL-1 beta ) and chemokines ( MCP-1, IL-8, and MIP-1 beta ) in THP-1 monocytes involves activation of
ERK-1/ERK-2 and downstream
activation of
Egr-1
Jones et al., J Cell Physiol 2003
(Hyperoxia) :
MEK inhibitor PD98059, but not inhibitors of p38
MAPK or PI3-kinase pathway,
prevented Egr-1 induction by hyperoxia
Choi et al., J Neurochem 2004
:
In addition,
Egr-1 was induced in an Src- and
Erk-1/2 dependent manner
Fujita et al., J Clin Invest 2004
(Ischemia...) :
In vitro, hypoxia/reoxygenation mediated induction of
Egr-1 in MPs was
suppressed by inhibition of PKCbeta, ERK1/2, and JNK, but not by inhibition of p38
MAPK
Chen et al., J Cell Biochem 2004
:
Egr-1 is
activated by 17beta-estradiol in MCF-7 cells by
mitogen activated protein kinase dependent phosphorylation of ELK-1
Buchwalter et al., Mol Cell Biol 2005
:
They form ternary complexes with serum response factor (SRF) on serum response elements of immediate early genes such as c-fos and
egr-1 and mediate
responses to growth factors and
mitogen activated protein kinase signaling
Simó et al., Cereb Cortex 2007
(MAP Kinase Signaling System) :
Reelin
induces the detachment of postnatal subventricular zone cells and the expression of the
Egr-1 through
Erk1/2 activation
Mishra et al., Proc Natl Acad Sci U S A 2006
(Anoxia...) :
In this study we tested the hypothesis that inhibition of
mitogen activated protein kinase dependent
Egr-1 expression may be pivotal in CO-mediated ischemic protection
Ke et al., J Biol Chem 2006
(Lymphoma, B-Cell...) :
Promoter truncation experiments suggested that several serum response elements are required for
MAPK mediated
egr-1 expression ... Unlike ERK and JNK, p38
MAPK reduces constitutive expression of
egr-1
Beidelschies et al., J Cell Physiol 2008
:
Moreover,
ERK1/2 activation by wear particles is also
required for increased expression of the transcription factor
Egr-1 as well as Egr-1 's ability to bind to and activate the TNFalpha promoter
Yasuoka et al., Am J Pathol 2009
(Pulmonary Fibrosis) :
Egr-1 was up-regulated by IGFBP-5 in a
MAPK dependent manner and bound to nuclear IGFBP-5
Allen et al., Toxicol Appl Pharmacol 2010
(MAP Kinase Signaling System) :
Results from these studies demonstrate that activation of
MAPK signaling is
required for upregulation of
Egr-1 by bile acids in hepatocytes and for upregulation of Egr-1 in the liver during cholestasis
Zeng et al., Toxicol Mech Methods 2005
:
The results suggest that silica could induce
Egr-1 activation in macrophages in vivo and in vitro and that phosphorylated
ERK 1/2 may be
involved in this action
Horita et al., J Comp Neurol 2010
:
Dusp1 is an inactivator of mitogen activated protein kinase ( MAPK ), and
MAPK activates expression of
egr1 , one of the most commonly studied IEGs, as determined in cultured cells
Shen et al., Am J Pathol 2011
(Pulmonary Disease, Chronic Obstructive) :
The accumulation of
EGR-1 and GGPPS was
induced by
MAPK/ERK pathway activation when Beas-2B human bronchial epithelial cells were exposed to cigarette smoke extract (CSE) ... Further examination showed that
EGR-1 in turn
regulated Erk1/2 activity because inhibition of EGR-1 transcription activity decreased CSE induced Erk1/2 phosphorylation
Shen et al., J Biol Chem 2011
(Diabetes Mellitus, Type 2...) :
In this report, we found that chronic exposure to hyperinsulinism caused persistent
Erk/MAPK activity in adipocytes and enhanced insulin resistance in an
Egr-1 dependent manner ... The loss of
Egr-1 function, knockdown of GGPPS, or
inhibition of
Erk1/2 activity in insulin-resistant adipocytes restored insulin receptor substrate-1 tyrosine phosphorylation and increased insulin sensitivity
Shen et al., Am J Pathol 2011
(MAP Kinase Signaling System...) :
EGR-1 overexpression enhances Ras prenylation and membrane association in a GGPPS dependent manner, and it
augments ERK 1/2 activation
Haschemi et al., PloS one 2011
(Inflammation) :
In addition to PPAR? SUMOylation, CO-activated p38
MAPK was
responsible for
Egr-1 repression
Iyoda et al., J Biol Chem 2012
(MAP Kinase Signaling System) :
Our data demonstrate that activation of ERK1/2 and JNK, but not p38
MAPK , is
required for LPA induced
Egr-1 expression in smooth muscle cells
Tao et al., Biomed Pharmacother 2013
:
These findings suggest that
Erk1/2 induced
Egr-1 accumulation activates MDR1 transcription and thereby induces the drug resistance observed in paclitaxel-resistant MCF-7 cells ... Further mechanistic studies indicate that
Egr-1 most likely does not
induce the constitutive activation of
Erk1/2 through its target gene geranylgeranyl diphosphate synthase ( GGPPS ), which regulates Ras prenylation
Ha et al., The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 2013
:
Finally,
ERK1/2 signaling
regulated Egr-1 protein expression and treatment with recombinant CTGF reversed the Egr-1 expression in high glucose induced VSMCs
Beno et al., J Biol Chem 1995
:
Protein kinase C and
mitogen activated protein kinase are
required for 1,25-dihydroxyvitamin D3-stimulated
Egr induction ... These results suggest that 1 ) D3 stimulates MAPK via a protein kinase C-dependent pathway, 2 ) D3-induced Egr expression can occur via a pathway independent of Ras induced Raf, and 3 ) D3 absolutely
requires MAPK activity for
Egr expression