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CCL2 — EPHB2
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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