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CBL — KIT
Pathways - manually collected, often from reviews:
-
KEGG Endocytosis:
CBL/CBLB/CBLC/ITCH/MDM2/NEDD4/NEDD4L/RNF41/SMURF1/SMURF2/TRAF6/WWP1
→
CSF1R/EGFR/ERBB3/ERBB4/FGFR2/FGFR3/FGFR4/FLT1/IGF1R/KDR/KIT/MET/NTRK1/PDGFRA/RET
(protein-protein, ubiquination)
-
NCI Pathway Database Signaling events mediated by Stem cell factor receptor (c-Kit):
CBL/CRKL/GRB2 complex (CBL-CRKL-GRB2)
→
SCF/KIT complex (KITLG-KIT)
(protein ubiquitination, collaborate)
Zeng et al., Blood 2005
Evidence: assay
-
Reactome Reaction:
CBL
→
KIT
(reaction)
Rao et al., J Leukoc Biol 2002*, Wollberg et al., Biochem J 2003, Masson et al., Biochem J 2006*, Sun et al., Exp Cell Res 2007
-
Reactome Reaction:
CBL
→
KIT
(indirect_complex)
Rao et al., J Leukoc Biol 2002*, Wollberg et al., Biochem J 2003, Masson et al., Biochem J 2006*, Sun et al., Exp Cell Res 2007
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Zeng et al., Blood 2005
:
Upon SCF stimulation,
KIT binds to and
induces the phosphorylation of
Cbl proteins, which in turn act as E3 ligases, mediating the ubiquitination and degradation of KIT and themselves ... The activated
KIT in turn
induces phosphorylation and activation of
Cbl proteins ... The
Cbl proteins then bind and direct the degradation of activated KIT,
leading to down-regulation of
KIT signaling
Zhu et al., Oncogene 2007
(Gastrointestinal Stromal Tumors) :
Activated signaling intermediates were identified by immunoaffinity purification of tyrosine phosphorylated proteins in GIST cells before and after treatment with KIT inhibitors, and these analyses show that GRB2, SHC,
CBL and MAPK activation are largely
KIT dependent in GISTs, whereas PI3-K, STAT1 and STAT3 activation are partially KIT dependent