Gene interactions and pathways from curated databases and text-mining

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CXCR4 — MAPK3

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: MAPK3 → CXCR4 (increases, CXCR4 Activity, MAPK3 Activity) Pan et al., J Biol Chem 2008*
    Evidence: Moreover, CXCR4-evoked activation of extracellular signal-regulated kinase 1/2 (ERK1/2) was attenuated by CyPA RNAi, by overexpression of a PPIase-deficient mutant of CyPA (CyPA-R55A), and by pretreatment of the immunosuppressive drugs, cyclosporine A and sanglifehrin A.

Text-mined interactions from Literome

Molino et al., Biochim Biophys Acta 2000 (Calcium Signaling...) : It also caused CXCR4 mediated activation of MAPK , release of PGI ( 2 ), endothelial migration, and the formation of capillary-like structures by endothelial cells in culture
Majka et al., Eur J Haematol 2000 (Leukemia-Lymphoma, Adult T-Cell) : First, we found that activation of CXCR4 in human T cell lines ( Jurkat and ATL-2 ) rapidly induced phosphorylation of mitogen activated protein kinases ( MAPK ) ( p44 ERK-1 and p42 ERK-2 )
van den Blink et al., J Clin Immunol 2004 (Endotoxemia) : To investigate the role of p38 mitogen activated protein kinase ( MAPK ) in the regulation of CXCR expression during an inflammatory response in vivo, 24 healthy volunteers received an intravenous injection with lipopolysaccharide (LPS) preceded ( -3 hr ) by a specific p38 MAPK inhibitor ( BIRB 796 BS ) at a high dose ( 600 mg ) or a low dose ( 50 mg ) or a placebo
Fukuda et al., Blood 2005 (Acute Disease...) : In contrast, prolonged exposure of CD34+ or Ba/F3-Flt3 cells to FL down-regulated CXCR4 expression, inhibited CXCL12 mediated phosphorylation of MAPK ( p42/p44 ), CREB, and Akt, and impaired migration toward CXCL12
Hu et al., Circulation 2007 (Anoxia...) : In isolated myocytes, CXCR4 activation by SDF-1alpha resulted in increased phosphorylation of both ERK 1/2 and AKT and decreased phosphorylation of JNK and p38 ... In isolated myocytes, CXCR4 activation by SDF-1alpha resulted in increased phosphorylation of both ERK 1/2 and AKT and decreased phosphorylation of JNK and p38
Thomas et al., Gut 2008 (Carcinoma in Situ...) : Finally, we show that expression of CXCR4 in murine PanIN cells is partially dependent on mitogen activated protein kinase ( MAPK ) signalling and that the effect of CXCL12 on PanIN proliferation can be abrogated by an MAPK inhibitor
Hong et al., Hepatology 2009 (Liver Cirrhosis) : Inhibitor studies suggest that SDF-1alpha/CXCR4 dependent extracellular signal regulated kinase 1/2 and Akt phosphorylation mediate effects on collagen I expression and stellate cell proliferation
Rahimi et al., Int J Cancer 2010 (Breast Neoplasms...) : More interestingly, inhibition of p38 MAPK activity significantly reduced CXCR4 expression and inhibited the invasive potential of EGFRvIII expressing breast cancer cells, suggesting an essential role for p38 MAPK in EGFRvIII/CXCR4 induced invasion
Malik et al., J Biol Chem 2012 : Depletion of AIP4 and STAM-1 by siRNA caused significant inhibition of CXCR4 induced ERK-1/2 activation , whereas overexpression of these proteins enhanced CXCR4 signaling ... Overexpression of an AIP4 catalytically inactive mutant and a mutant that shows poor binding to STAM-1 fails to enhance CXCR4 induced ERK-1/2 signaling, as compared with wild-type AIP4, suggesting that the interaction between AIP4 and STAM-1 and the ligase activity of AIP4 are essential for ERK-1/2 activation
Du et al., Hum Reprod 2012 : CsA up-regulated CXCL12 and CXCR4 expression in human first-trimester cytotrophoblast cells, but not in DSCs. Blocking the mitogen activated proteinkinase/extracellular signal regulated kinase ( MAPK/ERK1/2 ) signaling by U0126 abrogated the CsA induced increase in CXCL12 and CXCR4 expression and neutralizing antibodies to CXCL12 or CXCR4 completely inhibited the CsA induced increase in cell number, invasion and MMP-9 and MMP-2 activity of cytotrophoblast
Adams et al., Int J Cardiol 2013 : Adiponectin induced CAC migration and CXCR4-upregulation were mediated through adipo-receptor 1 (AdipoR1) and blocked by an inhibitor of PI3-kinase, p38MAP kinase and NF?b. Adipo stimulated migration of CACs, CXCR4 expression and p38MAPK-activation is impaired in patients with coronary artery disease ( CAD )