We have a suspicion that you are an automated web bot software, not a real user. To keep our site fast for other users, we have slowed down this page. The slowdown will gradually disappear. If you think this is a mistake, please contact us at genome-www@soe.ucsc.edu. Also note that all data for hgGeneGraph can be obtained through our public MySQL server and all our software source code is available and can be installed locally onto your own computer. If you are unsure how to use these resources, do not hesitate to contact us.
UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to MAPK8

EGR1 — MAPK8

Text-mined interactions from Literome

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
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
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
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
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
Burger et al., Biol Reprod 2009 : Additionally, GNRH induced Egr1 gene expression is mediated by MAPK8/9 and MAPK1/3, and both are critical for Lhb gene transcription
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
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)
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
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
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