Gene interactions and pathways from curated databases and text-mining

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BCR — CBL

Pathways - manually collected, often from reviews:

  • KEGG Pathways in cancer: ABL1/BCR → Complex of CBL-CBLB-CBLC-CRK-CRKL (protein-protein, activation)
  • KEGG Chronic myeloid leukemia: ABL1/BCR → Complex of CBL-CBLB-CBLC-CRK-CRKL (protein-protein, activation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Beitz et al., J Biol Chem 1999 : Whereas CD19 does not appear to be involved in this SYK dependent pathway, the SYK substrate CBL is likely involved as the dominant negative SYK markedly attenuates CBL tyrosine phosphorylation and completely blocks the BCR dependent association of CBL with p85 PI3K
Yankee et al., J Immunol 1999 : These studies indicate that c-Cbl may contribute to the regulation of BCR signaling by modulating the ability of Syk to associate with the BCR and couple the receptor to intracellular signaling pathways
Sohn et al., J Exp Med 2003 (Calcium Signaling) : Significantly, prolonged phosphorylation of Syk correlated with reduced ubiquitination of Syk indicating that Cbl-b negatively regulates BCR signaling by targeting Syk for ubiquitination
Dragone et al., Proc Natl Acad Sci U S A 2006 : Coexpression of SLAP and c-Cbl in Bal-17 led to decreased surface and total BCR levels
Mao et al., Proc Natl Acad Sci U S A 2010 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : As4S4 targets RING-type E3 ligase c-CBL to induce degradation of BCR-ABL in chronic myelogenous leukemia
Salgia et al., Exp Hematol 1996 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : p210BCR/ABL induces formation of complexes containing focal adhesion proteins and the protooncogene product p120c-Cbl