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CCL2 — S100B

Text-mined interactions from Literome

Reddy et al., J Biol Chem 2006 (Diabetes Mellitus, Type 2) : An inhibitor of Src kinase, PP2, significantly blocked S100B induced activation of Src kinase, mitogen activated protein kinases, transcription factors NF-kappaB and STAT3, superoxide production, tyrosine phosphorylation of Cav-1, VSMC migration, and expression of the pro-inflammatory genes monocyte chemotactic protein-1 and interleukin-6
Hayakawa et al., J Atheroscler Thromb 2012 : S100B induced NF-?B activation and the expression of several proinflammatory genes ( MCP-1 , IL-6, ICAM-1 ) at mRNA and protein levels in RAGE-A10, among which MCP-1 expression was the most robust ... S100B induced MCP-1 expression was dose-dependently blocked by inhibitors of JNK ( SP600125 ), p38 ( SB203580 ), MEK-1 ( U0126 ) as well as NF-?B ( Bay117085 ) ... S100B induced MCP-1 promoter activity via NF-?B binding sites and nuclear translocation of NF-?B p65 subunit were blocked by SP600125, U0126, and SB203580 in RAGE-A10 ... Our study demonstrates that S100B increased MCP-1 expression via NF-?B and mitogen activated protein kinase ( JNK, ERK1/2, and p38 ) pathways in RAGE overexpressed A10 cell lines