◀ Back to CXCL12
CXCL12 — CXCR1
Pathways - manually collected, often from reviews:
-
KEGG Chemokine signaling pathway:
CCL1/CCL11/CCL13/CCL14/CCL15/CCL16/CCL17/CCL18/CCL19/CCL2/CCL20/CCL21/CCL22/CCL23/CCL24/CCL25/CCL26/CCL27/CCL28/CCL3/CCL3L1/CCL3L3/CCL4/CCL4L1/CCL4L2/CCL5/CCL7/CCL8/CX3CL1/CXCL1/CXCL10/CXCL11/CXCL12/CXCL13/CXCL14/CXCL16/CXCL2/CXCL3/CXCL5/CXCL6/CXCL9/IL8/PF4/PF4V1/PPBP/XCL1/XCL2
→
CCR1/CCR10/CCR2/CCR3/CCR4/CCR5/CCR6/CCR7/CCR8/CCR9/CX3CR1/CXCR1/CXCR2/CXCR3/CXCR4/CXCR5/CXCR6/XCR1
(protein-protein, activation)
-
Reactome Reaction:
CXCR1
→
CXCL12
(reaction)
Lambert et al., Science signaling 2008, Lerea et al., Neuron 1989, Van Dop et al., Nucleic Acids Res 1989, Itoh et al., J Biol Chem 1988, Takami et al., Brain Res Mol Brain Res 1994
Text-mined interactions from Literome
Amara et al., J Biol Chem 1999
:
Importantly, the amino-terminal domain of
SDF-1alpha which is required for binding to, and
activation of,
CXCR4 remains exposed after binding to HS and is recognized by a neutralizing monoclonal antibody directed against the first residues of the chemokine
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
Sierro et al., Proc Natl Acad Sci U S A 2007
:
CXCL12 did not
induce signaling through CXCR7 ; however,
CXCR7 formed functional heterodimers with CXCR4 and enhanced CXCL12 induced signaling
Gouwy et al., J Leukoc Biol 2009
:
In turn, the induced
CXCL8 synergized with CCL2 for mononuclear cell chemotaxis, and the chemotactic effect was
mediated by
CXCR1/CXCR2 , because CXCL8 receptor antagonists or antibodies were capable of blocking the synergy, while keeping the responsiveness to CCL2 intact
Nasser et al., J Immunol 2009
:
CXCL8 ( also known as IL-8 )
activates CXCR1 and CXCR2 to mediate neutrophil recruitment and trigger cytotoxic effect at sites of infection
Duda et al., Clin Cancer Res 2011
(Neoplasms) :
CXCL12 ( SDF1alpha )
-CXCR4/CXCR7 pathway
inhibition : an emerging sensitizer for anticancer therapies ?
Singh et al., Microvasc Res 2011
:
Additionally, we examined the mechanism of
CXCL8 dependent
CXCR1 and/or CXCR2 mediated phenotypic changes by evaluating ERK phosphorylation and cytoskeletal rearrangement and observed inhibition of ERK phosphorylation and cytoskeletal rearrangement in HMEC-1-shCXCR1, HMEC-1-shCXCR2 and HMEC-1-shCXCR1/2 cells
Sundaram et al., Lab Invest 2013
(Osteitis Deformans) :
Moreover,
CXCL5 increased ( 5.2-fold )
CXCR1 receptor expression in these cells
Mueller et al., PloS one 2013
(Immunologic Deficiency Syndromes...) :
Upon
stimulation by the endogenous ligand
CXCL12 ,
CXCR4 becomes phosphorylated at multiple sites in its C-terminal domain