Gene interactions and pathways from curated databases and text-mining

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CXCL2 — CXCR3

Pathways - manually collected, often from reviews:

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