Gene interactions and pathways from curated databases and text-mining

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CCL2 — TLR2

Text-mined interactions from Literome

Kurt-Jones et al., J Endotoxin Res 2004 : MEFs were highly responsive to TLR-ligand activation and secreted high levels of both IL-6 and MCP-1 in response to TLR ligands
Hung et al., Nephrol Dial Transplant 2006 : The LMPS enhanced the secretion of CCL2/MCP-1 and CXCL8/interleukin-8 (CXCL8/IL-8) in TLR-defective human embryonic kidney (HEK) 293 cells only when transfected with a TLR2 expressing plasmid
Yang et al., Kidney Int 2006 (Leptospirosis) : In conclusion, these findings indicate that the stimulation of iNOS and CCL2/MCP-1 caused by pathogenic leptospiral OMPs, in particular LipL32, in proximal tubule cells requires TLR2 for the early inflammatory response
Riccioli et al., J Immunol 2006 : Moreover, we studied the role of NF-kappaB and of MAPKs in regulating TLR mediated MCP-1 secretion by using inhibitors specific for each transduction pathway and we demonstrated a pivotal role of the IkappaB/NF-kappaB and JNK systems
Moon et al., Infect Immun 2007 (Acute Disease...) : Toll-like receptor 2-dependent NF-kappaB activation is involved in nontypeable Haemophilus influenzae induced monocyte chemotactic protein 1 up-regulation in the spiral ligament fibrocytes of the inner ear ... TLR2 ( -/- ) - and MyD88 ( -/- ) -derived SLFs revealed involvement of TLR2 and MyD88 in NTHI induced MCP-1 up-regulation
Yoshimura et al., J Immunol 2007 : IFN-gamma mediated survival enables human neutrophils to produce MCP-1/CCL2 in response to activation by TLR ligands
Lee et al., Cell Signal 2008 : This study highlights the importance of cytosolic phospholipase A2 (cPLA2) mediated reactive oxygen species ( ROS ) signaling processes in the regulation of MCP-1 release as a result of toll-like receptor ( TLR ) activation
Masamune et al., J Gastroenterol 2008 : TLR ligands induced expression of monocyte chemoattractant protein 1 , cytokine induced neutrophil chemoattractant 1 ( a rat homolog of interleukin-8 ), and inducible nitric oxide synthase, but not proliferation or type I collagen production
Lee et al., J Clin Immunol 2009 : These results indicate that TLR2-ROS signaling plays a crucial role in the 30-kDa Ag-mediated expression of CXCL8 and CCL2 in human monocytes
Lee et al., Cell Microbiol 2009 : In addition, TLR2 , Dectin-1 and, to an extent, TLR4 are essential for the MU-mediated expression of CXCL8, CCL2 and LL-37 in keratinocytes
Jia et al., J Immunol 2009 (Listeriosis) : The first phase is rapid, induces low-level production of MCP-1 , and is dependent on TLR/MyD88 signaling
Dasu et al., Am J Physiol Endocrinol Metab 2011 (Diabetes Mellitus, Type 2...) : Silencing TLR2, TLR4 , and p47phox with small inhibitory RNAs ( siRNAs ) significantly reduced superoxide release, NF-?B activity, IL-1ß, and MCP-1 secretion in HG and palmitate treated THP-1 cells ... Silencing TLR2 , TLR4, and p47phox with small inhibitory RNAs ( siRNAs ) significantly reduced superoxide release, NF-?B activity, IL-1ß, and MCP-1 secretion in HG and palmitate treated THP-1 cells
Agarwal et al., Arthritis Res Ther 2011 (Fibrosis...) : The ability of IFNa2 to regulate TLR induced interleukin (IL)-6 and CC chemokine ligand 2 production was also assessed
Tang et al., Contrib Nephrol 2011 (Diabetic Nephropathies...) : In human DN biopsies and PTEC, TLR4is upregulated and plays a permissive role in HG-induced IL-6 and CCL-2 overexpression and monocyte transmigration
Miura et al., Am J Physiol Gastrointest Liver Physiol 2012 (Fatty Liver...) : Toll-like receptor (TLR)4 ( -/- ), TLR9 ( -/- ), and MyD88 ( -/- ) mice had reduced hepatic macrophage infiltration with decreased MCP-1 and CCR2 expression because TLR signaling is a potent inducer of MCP-1
Salagianni et al., Circulation 2012 (Carotid Artery Diseases...) : Mechanistically, TLR7 interfered with macrophage proinflammatory responses to TLR2 and TLR4 ligands, reduced monocyte chemoattractant protein-1 production, and prevented expansion of Ly6C ( hi ) inflammatory monocytes and accumulation of inflammatory M1 macrophages into developing atherosclerotic lesions