◀ Back to CD40

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