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CCR5 — MAPK3
Text-mined interactions from Literome
Majka et al., Stem Cells 2000
:
In contrast, the
CCR5 ligands ( macrophage inflammatory protein-1alpha [ MIP-1alpha ], MIP-1beta, and RANTES ) did not
activate calcium flux,
MAPK and AKT phosphorylation or chemotaxis of CD34 ( + ) KIT ( + ) cells or cells isolated from the BFU-E colonies
Makuta et al., Biol Pharm Bull 2003
:
These results first indicate that
Erk1/2 and STAT-3
regulate CCR5 expression, and that Erk mediated phosphorylation of Ser is required for full stimulation of STAT-3 in CCR5 expression
Ottonello et al., Cell Signal 2005
:
CCL3 ( MIP-1alpha ) induces in vitro migration of GM-CSF primed human neutrophils via
CCR5 dependent
activation of
ERK 1/2
Tomkowicz et al., Blood 2006
(Acquired Immunodeficiency Syndrome...) :
Stimulation of human monocyte derived macrophages with either HIV-1 gp120 or MIP-1beta results in the
CCR5 mediated activation of Lyn and the concomitant Lyn dependent
activation of the mitogen activated protein ( MAP ) kinase
ERK-1/2
Christmann et al., Am J Pathol 2011
:
Antibody neutralization and gene knockout strategies were used to show that the presence of
Ccr5 is
required for EMCV stimulated
mitogen activated protein ( MAP ) kinase and nuclear factor-kappa B ( NF-?B ) activation, and the subsequent expression of the inflammatory gene-inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2)