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CXCL5 — MAPK9

Text-mined interactions from Literome

Ottonello et al., Cell Signal 2005 : When the activation of ERK-1/2 and p38 MAPK by CCL3 and the classical neutrophilic chemokine CXCL8 ( IL-8 ) were compared, both the chemokines were capable of activating p38 MAPK
Méndez-Samperio et al., Cell Immunol 2005 (MAP Kinase Signaling System) : Our data also demonstrate that M. bovis BCG induced CXC chemokine ligand ( CXCL ) 8 release in epithelial cells was reduced by a mitogen activated protein/ERK kinase ( MEK ) inhibitor ( PD98059 ), but not by a p38 MAPK ( SB203580 ) inhibitor
Lane et al., Int Immunol 2006 : However, wild-type Cbl or its mutants had no effect on the CXCL8 induced activation of MAPK , indicating that Cbl specifically modulated CXCL8 induced chemotaxis
Petrai et al., Int J Biochem Cell Biol 2008 : In human microvascular endothelial cells, which selectively express CXCR3-B, in a cell cycle dependent fashion, CXCL10 and CXCL4 increased the enzymatic activity of p38 ( MAPK )
Cao et al., Microbes Infect 2010 (Pneumococcal Infections) : Both PspA and PspC could activate p38 MAPK and NF-?B pathways in neutrophils, while inhibition of NF-?B and p38 MAPK could suppress the release of CXCL8 from neutrophils induced by PspA and PspC. Together, our results demonstrated that the induction of CXCL8 in human neutrophils activated by PspA and PspC was regulated by p38 MAPK and NF-?B pathways
Dogan et al., Microbes Infect 2011 : Pneumolysin induced CXCL8 production by nasopharyngeal epithelial cells is dependent on calcium flux and MAPK activation via Toll-like receptor 4
Chen et al., Molecular vision 2011 : Inhibition of p38MAPK , phosphoinositide 3-kinase (PI3K)-Akt and nuclear factor-kappaB ( NF-?B ), with the inhibitors SB203580, LY294002 and pyrrolydine dithiocarbamate ( PDTC ) respectively, reduced IL-17 ( 100 ng/ml ) mediated production of CXCL8 , CCL2, and IL-6 in a concentration dependent manner
Dumitru et al., J Leukoc Biol 2012 (Head and Neck Neoplasms...) : Most importantly, HNC induced p38-MAPK activation strongly stimulates the release of CCL4, CXCL8 , and MMP9 by neutrophils