ArticleBiochemistry and analytical biochemistry : current research2012
Oncogenic Signaling by Leukemia-Associated Mutant Cbl Proteins.
Article in Biochemistry and analytical biochemistry : current research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Locking CBL TKBD in its native conformation presents a novel therapeutic opportunity in mutant CBL-dependent leukemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The ubiquitin ligases Cbl and Cbl-b regulate macrophage growth by controlling CSF-1R import into macropinosomes.Molecular biology of the cell · 2024Article
- Methylation of the epigenetic JMJD2D protein by SET7/9 promotes prostate tumorigenesis.Frontiers in oncology · 2023Article
- Ubiquitin proteasome system in immune regulation and therapeutics.Current opinion in pharmacology · 2022Review
- The spectrum of genetic mutations in myelodysplastic syndrome: Should we update prognostication?EJHaem · 2022Review
- E3 ligase-inactivation rewires CBL interactome to elicit oncogenesis by hijacking RTK-CBL-CIN85 axis.Oncogene · 2021Article
- Acquired expression ofBlood · 2017Article
- Structural Determinants of the Gain-of-Function Phenotype of Human Leukemia-associated Mutant CBL Oncogene.The Journal of biological chemistry · 2017Article
- VAV1-Cre mediated hematopoietic deletion of CBL and CBL-B leads to JMML-like aggressive early-neonatal myeloproliferative disease.Oncotarget · 2016Article
- Article
- Loss of Cbl and Cbl-b ubiquitin ligases abrogates hematopoietic stem cell quiescence and sensitizes leukemic disease to chemotherapy.Oncotarget · 2015Article
- Modulation of Immune Cell Functions by the E3 Ligase Cbl-b.Frontiers in oncology · 2015Review
- Structure-energy-based predictions and network modelling of RASopathy and cancer missense mutations.Molecular systems biology · 2014Article
- Cholesterol efflux in megakaryocyte progenitors suppresses platelet production and thrombocytosis.Nature medicine · 2013Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Members of the Cbl protein family (Cbl, Cbl-b, and Cbl-c) are E3 ubiquitin ligases that have emerged as critical negative regulators of protein tyrosine kinase (PTK) signaling. This function reflects their ability to directly interact with activated PTKs and to target them as well as their associated signaling components for ubiquitination. Given the critical roles of PTK signaling in driving oncogenesis, recent studies in animal models and genetic analyses in human cancer have firmly established that Cbl proteins function as tumor suppressors. Missense mutations or small in-frame deletions within the regions of Cbl protein that are essential for its E3 activity have been identified in nearly 5% of leukemia patients with myelodysplastic/myeloproliferative disorders. Based on evidence from cell culture studies, in vivo models and clinical data, we discuss the potential signaling mechanisms of mutant Cbl-driven oncogenesis. Mechanistic insights into oncogenic Cbl mutants and associated animal models are likely to enhance our understanding of normal hematopoietic stem cell homeostasis and provide avenues for targeted therapy of mutant Cbl-driven cancers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.