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CCL13 — CCR2

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CCR2 → CCL13 (increases, CCL13 Activity)
  Evidence: Table 1. Lymphoid chemokine receptors
• KEGG Cytokine-cytokine receptor interaction: CCL13 → CCR2 (protein-protein, activation)
• 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)
  

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Dip Interaction: CCR2 — CCL13 (physical association, biochemical) Berkhout et al., J Biol Chem 1997*
• IRef Hprd Interaction: CCR2 — CCL13 (in vivo) McQuibban et al., Blood 2002, Berkhout et al., J Biol Chem 1997*
• IRef Ophid Interaction: CCR2 — CCL13 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Breland et al., Cardiovasc Res 2010 (Carotid Stenosis...) : Our main findings were : ( i ) patients with symptomatic carotid stenosis ( n = 29 ), but not those with asymptomatic plaques ( n = 31 ), had significantly raised plasma levels of MCP-4 compared with healthy controls ( n = 20 ) ; ( ii ) in vitro, releasate from activated platelets markedly increased the expression of MCP-4 and CCR2 in THP-1 monocytes, and enhanced the MCP-4 mediated effect on interleukin-8 secretion in these cells, involving the platelet derived chemokine RANTES ; ( iii ) while MCP-1 had no effect on the release of RANTES and interferon-inducible protein of 10 kDa in tumour necrosis factor alpha-pre activated THP-1 monocytes, MCP-4 profoundly enhanced the release of these pro-atherogenic chemokines ; and ( iv ) the data indicate an inflammatory interaction between RANTES and MCP-4, involving CCR2, and mRNA levels of these mediators were markedly up-regulated within symptomatic atherosclerotic carotid plaque ( n = 81 ) ... Our findings suggest that the pro-atherogenic effects of CCR2 may not be restricted to interaction with MCP-1, but could also involve activation by MCP-4 , being an inflammatory link between platelet and monocyte activation
Stellato et al., J Clin Invest 1997 : MCP-4 inhibited binding of 125I-eotaxin to eosinophils and CCR3 transfected cells and inhibited 125I-MCP-1 binding to CCR2b-transfectants