Gene interactions and pathways from curated databases and text-mining

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CXCL12 — CXCR1

Pathways - manually collected, often from reviews:

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