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CXCR4 — EPHB2
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Bonacchi et al., J Biol Chem 2001
:
In MC, which respond to CXCR3 ligands with increased DNA synthesis,
CXCR3 activation
resulted in a biphasic stimulation of
ERK activation, a pattern similar to the one observed in HSC exposed to platelet derived growth factor, indicating that this type of response is related to the stimulation of cell proliferation
Peng et al., Mol Cancer Res 2005
:
The SDF-1alpha induced Akt and
ERK1/2 activations are
CXCR4 dependent as confirmed by their total inhibition by T134, a CXCR4-specific peptide antagonist
Redondo-Muñoz et al., Blood 2006
(Leukemia, B-Cell...) :
Accordingly, alpha4beta1 engagement activated the PI3-K/Akt/NF-kappaB pathway, while
CXCL12/CXCR4 interaction
activated ERK1/2/c-Fos signaling
Li et al., Blood 2007
(MAP Kinase Signaling System) :
Specific inhibition of
ERK during CB DC maturation
enhanced LPS induced up-regulation of CCR7 and
CXCR4 on CB DCs and their chemotaxis toward CCL19 and CXCL12, to a level similar to that of mature AB DCs
Schutyser et al., Eur Cytokine Netw 2007
(Anoxia...) :
Furthermore, hypoxia and serum starvation were required for cell surface display of
CXCR4 and CXCL12
induction of
ERK activation in HMEC-1 cells
Pan et al., J Biol Chem 2008
:
Cyclophilin A is required for
CXCR4 mediated nuclear export of heterogeneous nuclear ribonucleoprotein A2, activation and nuclear translocation of
ERK1/2 , and chemotactic cell migration
Billadeau et al., Int J Gastrointest Cancer 2006
(MAP Kinase Signaling System...) :
We show that after CXCR4 activation, EGFR becomes tyrosine phosphorylated, and the kinase activity of this receptor, together with the activation of MMPs, Src, and PI3-Kinase, is required for
CXCR4 mediated
ERK activation
Lee et al., Journal of cell communication and signaling 2007
:
The differential requirement for ROS in the
activation of
ERK , JNK, p38, and Akt by the BCR, CD40, and
CXCR4 likely reflects the multiplicity of upstream activators for each of these kinases, only some of which may be regulated in a redox dependent manner
Ryser et al., Mol Immunol 2008
:
S1P(1) overexpression resulted in reduced
CXCR4 surface expression levels and strong
inhibition of SDF-1 dependent
ERK1/2 phosphorylation and Ca ( 2+ ) flux
Mines et al., J Biol Chem 2009
:
Finally, the indistinguishable
activation of
ERK by wild typeor
3K/R-CXCR4 suggests that chemotaxis in response to CXCL12 may be independent of the ERK cascade
Sun et al., Molecular cancer 2010
(Chondrosarcoma...) :
CXCR4/SDF1 mediate hypoxia induced chondrosarcoma cell invasion through
ERK signaling and increased MMP1 expression ... Chondrosarcoma cell invasion is increased by hypoxia induced expression of
CXCR4 and MMP1 and is
mediated by HIF-1a and
ERK
Oh et al., Biochem Biophys Res Commun 2010
(Myocardial Ischemia) :
In addition, SDF-1alpha induced migration and
ERK1/2 , Akt, and eNOS activation were
reduced by AMD3100, a CXCR4-specific peptide antagonist, or by
siRNA-CXCR4
Badr et al., PloS one 2011
(Multiple Myeloma) :
Activation of
CXCR4 by CXCL12
resulted in the association of CXCR4 with CD45 and activation of PLCß3, AKT, RhoA, I?Ba and
ERK1/2
Heinrich et al., Journal of translational medicine 2012
(Pancreatic Neoplasms) :
We observed that ß-arrestin-2 knockdown also inhibited increases in
ERK1/2 phosphorylation
mediated by both
CXCR4 and CXCR7
Du et al., Hum Reprod 2012
:
CsA
up-regulated CXCL12 and
CXCR4 expression in human first-trimester cytotrophoblast cells, but not in DSCs. Blocking the mitogen activated proteinkinase/extracellular signal regulated kinase (
MAPK/ERK1/2 ) signaling by U0126 abrogated the CsA induced increase in CXCL12 and CXCR4 expression and neutralizing antibodies to CXCL12 or CXCR4 completely inhibited the CsA induced increase in cell number, invasion and MMP-9 and MMP-2 activity of cytotrophoblast
Badr et al., PloS one 2012
(Multiple Myeloma) :
We found that WEV and WEV+NP clearly decreased the
CXCL12/CXCR4 mediated
activation of AKT,
ERK , NF?B and Rho-A using western blot analysis ; abrogated the CXCL12 mediated proliferation of MM cells using the CFSE assay ; and induced apoptosis in MM cell as determined by PI/annexin V double staining followed by flow cytometry analysis
Golec et al., PloS one 2013
(MAP Kinase Signaling System) :
RasGRP1, but Not RasGRP3, Is Required for Efficient Thymic ß-Selection and
ERK Activation Downstream of
CXCR4 ... Also, we report that RasGRP1 is required for
ERK activation downstream of
CXCR4 signaling, which we hypothesize represents a potential mechanism of RasGRP1 regulation of ß-selection
Esencay et al., BMC cancer 2013
(Glioma...) :
Inhibiting
CXCR4 in LN229 and LN308 glioma cells that were knocked down for CXCR7 did not further reduce migration towards SDF-1a in hypoxic conditions and did not
affect the levels of phosphorylated
ERK1/2 and Akt