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BCR — GRAP2

Text-mined interactions from Literome

Swart et al., Biochem Biophys Res Commun 2000 : We have recently demonstrated that BCR cross linking leads to a transient activation of p38 mitogen activated protein kinase ( MAPK ) in CH31 B cells
Ogimoto et al., FEBS Lett 2001 (MAP Kinase Signaling System) : We found that CD45 negatively regulated BCR induced c-Jun NH ( 2 ) -terminal kinase ( JNK ) and p38 activation in immature WEHI-231 cells, whereas in mature BAL-17 cells, CD45 positively regulated JNK and p38 activation and negatively regulated extracellular signal regulated kinase activity
Bandyopadhyay et al., Blood 2004 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive...) : NaChl did not increase phosphorylation of p38 in Bcr-Abl negative cells including HSC-2 and HSG that are responsive to this compound, indicating that p38 activation by NaChl is dependent on Bcr-Abl kinase inhibition
Togni et al., Mol Cell Biol 2005 : Similarly, B-cell receptor (BCR) mediated total tyrosine phosphorylation and phosphorylation of Erk, p38 , and JNK, as well as immunoreceptor mediated Ca ( 2+ ) responses, are normal in SKAP-HOM ( -/- ) animals
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