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CD79B — EPHB2

Text-mined interactions from Literome

Adachi et al., J Immunol 2000 (Calcium Signaling...) : In this paper we demonstrate that expression of CD72 down-modulates both extracellular signal related kinase ( ERK ) activation and Ca2+ mobilization induced by BCR ligation in the mouse B lymphoma line K46micromlambda, whereas BCR mediated ERK activation was not reduced by the ITIM mutated form of CD72
Richards et al., J Immunol 2001 (MAP Kinase Signaling System) : PD98059 or U0126 treatment substantially inhibited the BCR induced activation of the extracellular signal regulated kinase ( ERK ) forms of mitogen activated protein kinase in the immature B cell line WEHI-231, in immature splenic B cells, and in mature splenic B cells
Wu et al., J Immunol 2001 (Severe Combined Immunodeficiency) : Although both CD72 and BCR induced Btk dependent ERK activation, CD72 mediated proliferation is more resistant to blocking of ERK activity than that of BCR, as shown by the proliferation response of B cells treated with PD98059 and dibutyryl cAMP, agents that inhibit ERK activity
Niiro et al., J Exp Med 2002 (Calcium Signaling) : Moreover, BCR induced activation of extracellular signal regulated kinase ( ERK ), c-jun NH2-terminal kinase ( JNK ), and p38 mitogen activated protein kinase ( MAPK ) pathways was impaired in Bam32 ( -/- ) cells but not the activation of Akt related pathways
Jacob et al., J Biol Chem 2002 : Here we demonstrate through the use of PI 3-kinase inhibitors and a dominant negative PI 3-kinase construct that the BCR induced phosphorylation and activation of ERK is dependent on PI 3-kinase
Wilson et al., Oncogene 2002 (Cell Transformation, Neoplastic...) : These data implicate the Src kinase family in Stat5 and Erk activation downstream of Bcr-Abl , and identify myeloid-specific Src kinases as potential drug targets in CML
Guo et al., J Immunol 2005 : B cell receptor (BCR) cross-talk : IL-4 creates an alternate pathway for BCR induced ERK activation that is phosphatidylinositol 3-kinase independent
de la Fuente et al., Mol Cell Biol 2006 : B-cell proliferation, cell cycle progression, PLC-gamma2 phosphorylation, calcium mobilization, NF-ATp dephosphorylation, and Erk and Jnk activation in response to B-cell receptor (BCR) ligation were all impaired
Angyal et al., Ann N Y Acad Sci 2006 : RNA silencing experiments showed that knocking down Gab1 adaptor protein in BL41 human Burkitt lymphoma cells significantly reduced B cell receptor (BCR) induced Erk phosphorylation, indicating that Gab1 plays a pivotal role in regulating Erk activity in B cells
Lee et al., Journal of cell communication and signaling 2007 : In contrast, BCR induced activation of ERK , JNK, p38, and Akt was not affected by ROS depletion
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
Gross et al., J Immunol 2009 : Wild-type mature follicular B cells were less sensitive to BCR stimulation than were immature transitional stage 1 B cells with regard to BCR induced calcium elevation and ERK MAPK activation
Taniguchi et al., PloS one 2013 : Here, we present data indicating that the increase in intracellular zinc level induced by ZIP9/SLC39A9 ( a ZIP Zrt-/Irt-like protein ) plays an important role in the activation of Akt and Erk in response to BCR activation
Uhde et al., Int Immunol 2013 : BCR engagement led to reduced activation of LYN, SYK and ERK1/2 resulting in reduced numbers of proliferating cells in all CD83tg B cell subsets
Sutherland et al., J Immunol 1996 : We found that BCR engagement in WEHI-231 cells caused a 15- to 20-fold activation of ERK2 and a 2- to 3-fold stimulation of ERK1 ... In summary, the BCR strongly activates ERK2 and weakly activates ERK1 , JNK, and p38, while CD40 markedly stimulates the JNK and p38 kinases
Chan et al., Curr Biol 1998 : Although the initiation of BCR signaling in lyn-/- B cells is delayed, BCR induced ERK2 activation and proliferation are enhanced
Hashimoto et al., J Exp Med 1998 : Here we demonstrate that the BCR induced ERK activation is reduced by loss of Grb2 or expression of a dominant negative form of Ras, RasN17, whereas this response is not affected by loss of Shc
Jiang et al., J Exp Med 1998 : BCR mediated activation of ERK2, although maintained in Lyn-deficient cells, was abolished in Syk-deficient cells and partially inhibited in Btk-deficient cells, indicating that BCR mediated ERK2 activation requires Syk and that sustained ERK2 activation requires Btk