Gene interactions and pathways from curated databases and text-mining

◀ Back to EPHB2

CCL2 — EPHB2

Text-mined interactions from Literome

Rovin et al., Cytokine 1999 : In contrast, ERK2 does not mediate IL-1beta induced MCP-1 gene expression
Cambien et al., Blood 2001 : Pertussis toxin, a blocker of Go/Gi proteins, abrogated MCP-1 induced ERK activation, but was without any effect on SAPK1/JNK1 and SAPK2/p38 activation
Chen et al., Diabetologia 2001 (Diabetes Mellitus, Type 1...) : Both ERK1/2 and p38 MAPK, but not nitric oxide, contribute to MCP-1 expression
Panenka et al., J Neurosci 2001 : Blocking either the ERK1/ERK2 or the p38 pathway ( with PD98059 or SB203580, respectively ) significantly inhibited Bz-ATP induced MCP-1 expression
Nanki et al., J Immunol 2001 (Arthritis, Rheumatoid) : Moreover, activation of ERK1/2 was inhibited by pertussis toxin, a G ( i ) -coupled protein inhibitor, and RS-504393, CCR2 antagonist, suggesting that ERK1/2 was activated by CCL2 via CCR2 and G ( i ) -coupled protein
Werle et al., Cardiovasc Res 2002 : MCP-1 induces activation of MAP-kinases ERK , JNK and p38 MAPK in human endothelial cells
Takaya et al., American journal of physiology. Renal physiology 2003 (Cell Transformation, Viral) : In conclusion, these findings indicate that ERK signaling is involved in BSA induced MCP-1 expression in mProx cells
Sengul et al., American journal of physiology. Renal physiology 2003 : Inhibitors of ERK , JNK, and p38 reduced LC-induced IL-6 and MCP-1 production
Bian et al., Exp Eye Res 2003 (Translocation, Genetic) : In addition, anti-inflammatory drugs dexamethasone ( DEX ) and cyclosporin A ( CSA ) both blocked activation of JNKS/SAPK and the cell-cell contact induced production of hRPE IL-8 and MCP-1 , while activation of p38 and ERK was only inhibited by DEX, but not by CSA
Ni et al., J Cell Physiol 2003 : The use of an inhibitor ( calphostin C ) to PKC-alpha and PKC-epsilon decreased ERK1/2 activation and MCP-1 induction by shear, whereas an inhibitor ( Go6976 ) to PKC-alpha did not affect ERK1/2 activation or MCP-1 induction ... Inhibition of ERK1/2 activation by PD98059 blocked MCP-1 induction ... Consistently, overexpression of endothelial nitric oxide synthase (eNOS) to enhance the endogenous generation of NO in ECs decreased the activation of PKC-epsilon and ERK1/2 , and also inhibited MCP-1 expression
Wuyts et al., Respir Med 2003 (Asthma...) : We conclude that p38 MAPK, JNK kinase, ERK and NF-kappaB are involved in the IL-1beta induced eotaxin, MCP-1 , and MCP-3 expression and release in HASMC
Jiménez-Sainz et al., Mol Pharmacol 2003 : We show that ERK activation by MCP-1 involves heterotrimeric Gi protein subunits, protein kinase C, phosphoinositide-3-kinase, and Ras ... In addition, we find that internalization of CCR2B itself is not necessary for efficient MCP-1 induced activation of ERK , although a dynamin mutant partially inhibits ERK stimulation
Marra et al., Am J Physiol Gastrointest Liver Physiol 2004 : In contrast, inhibition of ERK did not affect the upregulation of CCL2 induced by the two cytokines
Kato et al., J Am Soc Nephrol 2004 (Peritonitis) : mRNA expression of MCP-1 was abolished by NF-kappaB inhibition, but were not affected by the inhibition of ERK , JNK, or p38
Hiraoka et al., Life Sci 2004 : Western blotting analysis using an anti-ERK1/2 Ab and an antibody against phosphorylated-ERK1/2 ( p-ERK ) revealed that pitavastatin treatment significantly inhibited the MCP-1 induced phosphorylation of ERK1/2
Huang et al., Arterioscler Thromb Vasc Biol 2004 : Selective inhibitors of ERK1/2 or JNK MAPK effectively blocked the LTB4 induced MCP-1 production
Lo et al., J Biomed Sci 2005 : These results demonstrate that MCP-1 is a chemoattractant for SMCs and that MCP-1 stimulated migration requires both ROS production and ERK 1/2 activation in a positive activation loop, which may contribute to the atherogenic effects of MCP-1
Hagiwara et al., Nephrol Dial Transplant 2006 (Diabetes Mellitus, Type 2...) : EPA and specific inhibitors of ERK1/2, JNK and PI3K decreased levels of MCP-1 in MMCs. EPA suppressed phosphorylation of ERK1/2 and p38 in MMCs, and decreased p-ERK positive cells in glomeruli of KKAy/Ta mice
Wong et al., Allergy 2006 : Using various selective inhibitors for signaling molecules, we found that the inductions of IL-8, MCP-1 , and I-309 were mediated by either SCF activated ERK or TNF-alpha activated p38 MAPK, while the induction of IP-10 by TNF-alpha was mediated by both activated p38 MAPK and NF-kappaB
Ip et al., Clin Exp Immunol 2006 (MAP Kinase Signaling System) : Inhibition of p38 MAPK, ERK and JAK-2 activities by pretreating the cells with their corresponding inhibitors SB203580, PD98059 and AG490, respectively, significantly suppressed IL-4- and IL-13 induced MCP-1 production in BEAS-2B cells
Guest et al., Antioxid Redox Signal 2006 (Mechanotransduction, Cellular) : In conclusion, redox-sensitive activation of ERK1/2 ( MAPK ) and redox-insensitive activation of p38 ( MAPK ) regulate straininduced MCP-1 expression in RASM cells
Chipitsyna et al., Endocrinology 2007 (Diabetes Mellitus, Type 1...) : Inhibition of ERK1/2 activation reduced the AngII induced MCP-1 synthesis
Chou et al., Invest Ophthalmol Vis Sci 2007 : The MMC related IL-8 and MCP-1 expression was inhibited by both a p38 inhibitor ( SB203580 ) and an ERK inhibitor ( PD98059 )
Nakazawa et al., Invest Ophthalmol Vis Sci 2007 (Disease Models, Animal...) : RD-induced reactive gliosis, characterized by GFAP and vimentin upregulation, Erk and c-fos activation, MCP-1 induction , and increased monocyte recruitment in WT mice
Ip et al., Immunology 2007 (Asthma...) : Selective inhibitors of p38 MAPK ( SB203580 ), ERK ( PD98059 ), and JNK ( SP600125 ) could differentially inhibit the production of EGF, VEGF and CCL2 , thereby suggesting a role for MAPKs in IL-31 functions
Kleibeuker et al., J Neurochem 2008 : Culturing astrocytes with IL-1beta for 24 h induced a 2-3-fold increase in GRK2 and decreased C-C chemokine ligand 2 (CCL2) induced ERK1/2 activation ... Conversely, the 45 % decrease in GRK2 expression in astrocytes from GRK2+/- animals resulted in a more pronounced CCL2 induced ERK1/2 phosphorylation
Ho et al., Immunobiology 2008 (Inflammation...) : Selective inhibitors of p38 MAPK ( SB203580 ), JNK ( SP600125 ) and ERK ( PD98059 ) could suppress TNF-alpha induced CCL2 and ICAM-1 expression, while only p38 MAPK and ERK inhibitors could suppress TNF-alpha induced VCAM-1 expression
Lee et al., J Clin Immunol 2009 : Using highly specific signaling pathway inhibitors, we found that both p38 and ERK1/2 activation are essential for 30-kDa Ag-induced CCL2 but not CXCL8 production in human monocytes ... In addition, both p38 and ERK1/2 activation are essential for 30-kDa Ag-stimulated CCL2 production by monocytes
Yao et al., J Neurosci 2009 : Blocking TRPC channels and specific downregulation of TRPC channels 1 and 5 resulted in suppression of CCL2 induced ERK/CREB activation but not Akt/NF-kappaB activation
Struyf et al., Eur J Immunol 2009 (Neoplasms) : MCP-2/CCL8 ( 6-75 ) induced internalization of CCR2, inhibited MCP-1/CCL2 and MCP-2/CCL8 ERK signaling and antagonized the chemotactic activity of several CCR2 ligands ( MCP-1/CCL2 , MCP-2/CCL8, MCP-3/CCL7 )
Majkova et al., Toxicol Appl Pharmacol 2009 (Atherosclerosis...) : Also, MCP-1 up-regulation by PCB77 was prevented by inhibiting p38 and c-Jun N-terminal kinase (JNK), but not ERK1/2 , suggesting regulatory functions via p38 and JNK MAPK pathways
Lim et al., Food Chem Toxicol 2010 : Curcumin inhibits phorbol myristate acetate ( PMA ) -induced MCP-1 expression by inhibiting ERK and NF-kappaB transcriptional activity
Chehl et al., J Gastrointest Surg 2009 (Adenocarcinoma...) : Inhibition of ERK1/2 activation reduced the AngII induced MCP-1 synthesis
Iyoda et al., American journal of physiology. Renal physiology 2010 : Additionally, we observed that IL-17A and IL-17F induced MAPK ( p38 MAPK, ERK1/2, and JNK ) activation and that pharmacological inhibitors of p38 MAPK ( SB203580 ) and ERK1/2 ( U0126 ), but not JNK ( SP600125 ), blocked the IL-17A/IL-17F mediated MCP-1 and MIP-2 release
Katayama et al., Eur J Neurosci 2010 (Brain Injuries...) : Sustained activation of ERK signaling in astrocytes is critical for neuronal injury induced monocyte chemoattractant protein-1 production in rat corticostriatal slice cultures ... In this case, MCP-1 production was not suppressed, suggesting that activation of neuronal ERK is not necessary for MCP-1 production
Shi et al., J Neurosci Res 2011 : Inhibiting ERK/MAP kinase activation blocked expression of MCP-1
Cai et al., PloS one 2011 : MCP-1 rapidly induced ERK1/2 and JNK phosphorylation
Cicha et al., J Atheroscler Thromb 2011 : In resveratrol treated monocytic cells, MCP-1 induced Erk phosphorylation downstream of CCR2 receptor was dose-dependently inhibited, as observed by Western blot analysis
Paik et al., Molecular vision 2012 (Graves Ophthalmopathy...) : IL-6 expression was mediated by the p38, ERK, JNK pathways, whereas MCP-1 expression was mediated by ERK and JNK, but not by p38, in palmitate treated orbital fibroblasts
Bethel-Brown et al., Journal of neuroinflammation 2012 (HIV Infections) : MCP-1 induction was regulated by activation of extracellular-signal regulated kinase ( ERK ) 1/2, c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein ( MAP ) kinases and phosphatidylinositol 3-kinase (PI3K)/Akt pathways and the downstream transcription factor, nuclear factor ?B ( NF?B )
Nawaz et al., Exp Eye Res 2013 (Diabetic Retinopathy...) : On the other hand, phosphorylation of ERK induced by VEGF and MCP-1 was inhibited by PF-4, Mig and IP-10
Kempuraj et al., J Neuroimmune Pharmacol 2013 : IL-33 induces CCL2 , TNF-a and nitric oxide release through phosphorylation of ERK in mouse astrocytes