◀ Back to EPHB2
CD40 — EPHB2
Text-mined interactions from Literome
Suttles et al., J Biol Chem 1999
:
Pretreatment of monocytes with IL-4 and IL-10 inhibited
CD40 mediated activation of
ERK1/2 kinase activity when used individually, and are enhanced in effectiveness when used in combination
Eliopoulos et al., EMBO J 2003
:
The selective signaling defect resulting from the inactivation of Tpl2 allowed us to demonstrate that
CD40 mediated
ERK activation contributes to immunoglobulin production but is not essential for B-cell proliferation
Inoue et al., J Immunol 2004
(MAP Kinase Signaling System) :
IL-10 significantly inhibited
CD40 induced activation of the
ERK , p38 MAPK, and NF-kappaB pathways ; however, inhibition by IL-4 was limited to the ERK pathway in monocytes
Qian et al., Immunity 2004
(Hypergammaglobulinemia) :
CD40- and BAFF mediated survival is significantly
increased in Act1-deficent B cells, with stronger IkappaB phosphorylation, processing of NF-kappaB2 ( p100/p52 ), and activation of JNK,
ERK , and p38 pathways, indicating that Act1 negatively regulates CD40- and BAFF mediated signaling events
Mukundan et al., J Immunol 2005
:
However, ligation of a CD40 mutant lacking a functional TRAF6 binding site did not initiate inflammatory cytokine production, and this mutant was found to be defective in
CD40 mediated activation of
ERK1/2 , as well as IkappaB kinase (IKK) and NF-kappaB ... Finally, treatment of monocytes with a cell-permeable peptide corresponding to the TRAF6 binding motif of CD40 inhibited
CD40 activation of
ERK1/2 , IKK, and inflammatory cytokine production
Hollmann et al., Cancer Res 2006
(Lymphoma, B-Cell...) :
In contrast, CD40-resistant lines showed no constitutive activation of ERK and no increase in
ERK activity in
response to
CD40 stimulation
Papoutsopoulou et al., Nat Immunol 2006
:
Here, using antigen presenting cells from ABIN-2-deficient mice, we show that ABIN-2 was required for optimal activation of
Erk induced by receptors that signal via TPL-2, including Toll-like receptor 4 and tumor necrosis factor receptor 1 in macrophages, and
CD40 in B cells
Chai et al., Surgery 2006
:
The CD40L induced upregulation of
CD40 may be
mediated by oxidative stress and
ERK1/2 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
Ha et al., J Leukoc Biol 2008
:
We found that in CB B cells
activation of extracellular signal regulated kinase (
ERK ) and p38 following ligation of
CD40 but not of the B-cell antigen receptor (BCR) was inefficient ...
CD40 mediated
activation of
ERK and p38 was also minimal in these B cells of CB
Blix et al., BMC cancer 2012
(Leukemia, Lymphocytic, Chronic, B-Cell...) :
Similarly,
CD40L induced
p-ERK and p-p38 were also significantly reduced in lymphoma B cells, whereas p-p65 ( NF-?B ) was equal to that of normal B cells
Li et al., J Immunol 1996
:
CD40 ligation
results in protein kinase C-independent activation of
ERK and JNK in resting murine splenic B cells ... Overnight treatment of cells with phorbol ester as well as pharmacologic inhibitors of protein kinase C abrogated these signaling events after BCR treatment ; however, no effect was seen on
CD40 mediated activation of
ERK or c-Jun NH2-terminal kinase, suggesting that the BCR and CD40 differentially utilize protein kinase C to couple with these signaling pathways
Hara et al., Hokkaido Igaku Zasshi 1997
:
In addition, the same segment was also important for
CD40 mediated activation of extracellular signal regulated protein kinase 2 (
ERK2 )
Kashiwada et al., J Exp Med 1998
:
The deletion mutant of TRAF6 lacking the NH2-terminal domain acted as a dominant negative mutant to suppress
ERK activation by full-length
CD40 and suppress prominently ERK activation by a deletion mutant of CD40 only containing the binding site for TRAF6 in the cytoplasmic tail ( CD40 delta 246 ) ... Transient expression of the dominant negative H-Ras significantly suppressed
ERK activation by full-length
CD40 , but marginally suppressed ERK activation by CD40 delta 246, compatible with the possibility that TRAF6 is a major transducer of ERK activation by CD40 delta 246, whose activity is mediated by a Ras independent pathway
Purkerson et al., J Immunol 1998
(Lymphoma, B-Cell) :
However, several lines of evidence suggest that
CD40 and the B cell Ag
regulate ERK through distinct pathways that converge at the level of MEK-1, mitogen activated protein kinase kinase ... Finally, agents that elevate cAMP, causing protein kinase A-mediated inhibition of Raf-1, inhibited activation of ERK in response to mIg cross linking, but had no affect on
ERK activation in
response to
anti-CD40 or Jun N-terminal kinase activation by signals through either receptor
Lee et al., J Immunol 1998
(Lymphoma, B-Cell) :
N-acetyl-L-cysteine pretreatment, which blocks CD40 mediated JNK activation, does not affect the ability of
CD40 to
inhibit anti-IgM mediated
ERK2 activation and apoptosis