Gene interactions and pathways from curated databases and text-mining

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BCR — RAC1

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

Bassermann et al., J Biol Chem 2002 : The oncogenic tyrosine kinase Bcr-Abl has been shown to activate Rac-1 , which is important for Bcr-Abl induced leukemogenesis ... Activation of Rac-1 by Bcr-Abl was abrogated by co-expression of the Vav C terminus encoding the SH3-SH2-SH3 domains as a dominant negative construct
Inabe et al., FEBS Lett 2002 (Agammaglobulinemia) : Here we show that the BCR mediated Rac1 activation is significantly inhibited by loss of Btk, while this Rac1 activation is not affected by loss of phospholipase C-gamma2 ( PLC-gamma2 )
Grill et al., Blood 2002 (MAP Kinase Signaling System) : Rac-1 was also activated by colony stimulating factor-1 (CSF-1), Steel locus factor ( SLF ), granulocyte-macrophage colony stimulating factor ( GM-CSF ), and IL-5 or by cross linking the B-lymphocyte receptor for antigen (BCR) ... The activation of Rac-1 induced by cross linking the BCR or by IL-3 stimulation was blocked only partially by Ly294002, with about 25 % to 30 % of Rac-1 activation still occurring in the absence of detectable increases in phosphatidyl-inositol-3 kinase (PI-3K) activity
Johmura et al., Immunity 2003 : We demonstrate here that adaptor molecules Grb2 and BLNK, in addition to Vav, are required for efficient Rac1 activation in response to BCR stimulation
Brezski et al., J Immunol 2007 : In contrast, BCR induced Vav phosphorylation and Rac1 activation is impaired in transitional immature B cells, resulting in defects in actin polymerization dependent spreading and membrane ruffling while Rac1 independent BCR capping remains intact ... Because transitional immature murine B cells maintain lower steady-state levels of plasma membrane cholesterol, we augmented their levels to that of mature B cells and found that BCR induced Rac1 activation and Rac1 dependent membrane ruffling and cell spreading were restored
Diekmann et al., Nature 1991 : This result suggest that Bcr could be a target for regulation by Rac and has important new implications for the role of bcr translocations in leukaemia
Oh et al., J Neurosci 2010 (Synaptic Transmission) : Regulation of synaptic Rac1 activity, long-term potentiation maintenance, and learning and memory by BCR and ABR Rac GTPase activating proteins ... These results suggest that BCR and ABR have novel roles in the regulation of synaptic Rac1 signaling, synaptic plasticity, and learning and memory, and that excessive Rac1 activity negatively affects synaptic and cognitive functions
Skorski et al., Proc Natl Acad Sci U S A 1998 (Leukemia, Experimental...) : We show here that the small GTP binding protein Rac is activated by BCR/ABL in a tyrosine kinase dependent manner