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BCR — CRK
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Herrin et al., J Biol Chem 2005
(Lymphoma, B-Cell) :
With respect to MAPK activation, HSH2 was not observed to alter the activation of ERK or
p38 in
response to
BCR ligation, but it does significantly potentiate JNK activation
Pérez-Chacón et al., J Immunol 2012
(Genetic Predisposition to Disease...) :
In contrast, TRAF2 deficiency had no effect on CD40 mediated p38 MAPK activation but significantly reduced
BCR mediated
p38 activation
Liu et al., Science signaling 2012
:
Knocking down SAP97 in IgG? B cells or mutating the putative PDZ binding motif in the BCR tail impaired formation of the immunological synapse, initiation of IgG
BCR signaling, and downstream
activation of the mitogen activated protein kinase
p38
Smit et al., Oncogene 1996
(Burkitt Lymphoma) :
In summary, we observe that the
BCR activates Shc/Grb2-, Grb2- and
Crk adaptor complexes of distinct composition, which may allow selective coupling to different signal transduction cascades
Ingham et al., J Biol Chem 1996
:
We show that engaging the
B cell antigen receptor (BCR) on the RAMOS B cell line
caused both Crk-L and
Crk II to associate with several tyrosine phosphorylated proteins
Hashimoto et al., J Exp Med 1998
:
Similar to cooperation of Ras with PKC activation in ERK response, both PLC-gamma2 dependent signal and GTPase are required for
BCR induced JNK and
p38 responses
McLeod et al., J Biol Chem 1998
:
We had previously shown that C3G, an activator of Rap1, associates with the Crk adaptor proteins in B cells and that
BCR engagement
causes Crk to bind to the Cas and Cbl docking proteins