Associated Papers
CBL mutations in chronic myelomonocytic leukemia often occur in the RING domain with multiple subclones per patient: Implications for targeting.
Lim K et al.
Plos One, 2024
E3 ligase-inactivation rewires CBL interactome to elicit oncogenesis by hijacking RTK-CBL-CIN85 axis.
Ahmed SF et al.
Oncogene, 2021
Src-family kinase-Cbl axis negatively regulates NLRP3 inflammasome activation.
Chung IC et al.
Cell Death & Disease, 2018
Casitas B-lineage lymphoma linker helix mutations found in myeloproliferative neoplasms affect conformation.
Buetow L et al.
Bmc Biology, 2016
Structural basis for autoinhibition and phosphorylation-dependent activation of c-Cbl.
Dou H et al.
Nature Structural & Molecular Biology, 2012
Germline mutations of the CBL gene define a new genetic syndrome with predisposition to juvenile myelomonocytic leukaemia.
Pérez B et al.
Journal of Medical Genetics, 2010
Cbl controls EGFR fate by regulating early endosome fusion.
Visser Smit GD et al.
Science Signaling, 2009
Mutations in CBL occur frequently in juvenile myelomonocytic leukemia.
Loh ML et al.
Blood, 2009
Requirements for pYXXM motifs in Cbl for binding to the p85 subunit of phosphatidylinositol 3-kinase and Crk, and activation of atypical protein kinase C and glucose transport during insulin action in 3T3/L1 adipocytes.
Standaert ML et al.
Biochemistry, 2004
Regulation of ubiquitin protein ligase activity in c-Cbl by phosphorylation-induced conformational change and constitutive activation by tyrosine to glutamate point mutations.
Kassenbrock CK et al.
The Journal of Biological Chemistry, 2004
Src-catalyzed phosphorylation of c-Cbl leads to the interdependent ubiquitination of both proteins.
Yokouchi M et al.
The Journal of Biological Chemistry, 2001
RING finger mutations that abolish c-Cbl-directed polyubiquitination and downregulation of the EGF receptor are insufficient for cell transformation.
Thien CB et al.
Molecular Cell, 2001
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