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CXCL2 — CXCR3
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)
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Reactome Reaction:
CXCL2
→
CXCR3
(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
Jopling et al., Br J Pharmacol 2007
:
Surface
CXCR3 expression was specifically decreased in
response to CXCL9,
CXCL10 and CXCL11
Mukherjee et al., Cell Mol Immunol 2008
:
The oligomer
induced the expression of
CXCR3 , associated with B cell activation, while the monomer induced the expression of
CXCL4 , a powerful angiostatic chemokine
Groom et al., Immunol Cell Biol 2011
:
CXCR3 is
activated by three interferon ( IFN ) -?-inducible ligands CXCL9 ( monokine induced by gamma-interferon ),
CXCL10 ( interferon induced protein-10 ) and CXCL11 ( interferon-inducible T-cell alpha chemoattractant )
Korniejewska et al., Immunology 2011
:
Surprisingly, and in contrast with the other CXCR3 agonists, stimulation of T lymphocytes with
CXCL4 failed to elicit migratory responses and did not
lead to loss of surface
CXCR3 expression
Groom et al., Exp Cell Res 2011
:
CXCR3 is
activated by three interferon-inducible ligands CXCL9 ( MIG ),
CXCL10 ( IP-10 ) and CXCL11 ( I-TAC )
Romagnani et al., Clin Chim Acta 2012
:
By binding to its specific cognate receptor
CXCR3 ,
CXCL10 critically
regulates chemotaxis during several immune-inflammatory processes
Wang et al., Cancer Lett 2013
(Neoplasms) :
This report reviews the mechanisms of CXCL4/PF-4 angiostatic activity, including interference with angiogenic growth factors bFGF-2 and VEGF165,
activation of
CXCR3B , interactions with integrins, interference with cell cycle, interactions with factors such as VEGF121 and CXCL8/IL-8, and derived molecules of
CXCL4/PF-4 with angiostatic and anti-tumoral activities in different models in vivo or in vitro