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Non canonical c-CBL mutations define a specific phenotype of myeloid neoplasia.
Leukemia
January 2025
Department of Translational Hematology & Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, 44114, USA.
Morphologic and Immunophenotypic Differences in Juvenile Myelomonocytic Leukemias With CBL and Other Canonical RAS-pathway Gene Mutations: A Single Institutional Experience.
J Pediatr Hematol Oncol
August 2021
Department of Pathology and Laboratory Medicine.
The diagnostic criteria for juvenile myelomonocytic leukemia have recently been revised to include clinical findings and RAS-pathway gene mutations per the 2016 World Health Organization Classification of Tumors of Hematopoietic and Lymphoid Tissues. Differing clinical behaviors have been observed in cases with CBL versus other RAS-pathway gene (RAS-p) mutations, notably the patients with CBL mutations can be self-limiting with spontaneous resolution. Additional clinical characteristics and histopathologic findings between these subsets are less well-described.
View Article and Find Full Text PDFSLAP2 Adaptor Binding Disrupts c-CBL Autoinhibition to Activate Ubiquitin Ligase Function.
J Mol Biol
April 2021
The Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada; Program in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada; Department of Medical Biophysics, University of Toronto, 610 University Avenue, Toronto, ON M5G 2M9, Canada. Electronic address:
CBL is a RING type E3 ubiquitin ligase that functions as a negative regulator of tyrosine kinase signaling and loss of CBL E3 function is implicated in several forms of leukemia. The Src-like adaptor proteins (SLAP/SLAP2) bind to CBL and are required for CBL-dependent downregulation of antigen receptor, cytokine receptor, and receptor tyrosine kinase signaling. Despite the established role of SLAP/SLAP2 in regulating CBL activity, the nature of the interaction and the mechanisms involved are not known.
View Article and Find Full Text PDFHaploinsufficiency of Casitas B-Lineage Lymphoma Augments the Progression of Colon Cancer in the Background of Adenomatous Polyposis Coli Inactivation.
Am J Pathol
March 2020
Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Veterans Affairs Boston Healthcare System, Boston, Massachusetts; Global Co-Creation Labs, Institute of Medical Engineering and Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts. Electronic address:
Casitas B-lineage lymphoma (c-Cbl) is a recently identified ubiquitin ligase of nuclear β-catenin and a suppressor of colorectal cancer (CRC) growth in cell culture and mouse tumor xenografts. We hypothesized that reduction in c-Cbl in colonic epithelium is likely to increase the levels of nuclear β-catenin in the intestinal crypt, augmenting CRC tumorigenesis in an adenomatous polyposis coli (APC) mouse model. Haploinsufficient c-Cbl mice (APC c-Cbl) displayed a significant (threefold) increase in atypical hyperplasia and adenocarcinomas in the small and large intestines; however, no differences were noted in the adenoma frequency.
View Article and Find Full Text PDFDNA Damage Activates TGF-β Signaling via ATM-c-Cbl-Mediated Stabilization of the Type II Receptor TβRII.
Cell Rep
July 2019
The State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China. Electronic address:
Activation of both the DNA damage response (DDR) and transforming growth factor β (TGF-β) signaling induces growth arrest of most cell types. However, it is unclear whether the DDR activates TGF-β signaling that in turn contributes to cell growth arrest. Here, we show that in response to DNA damage, ataxia telangiectasia mutated (ATM) stabilizes the TGF-β type II receptor (TβRII) and thus enhancement of TGF-β signaling.
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