LYMPHOID NEOPLASIA E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis
نویسندگان
چکیده
1Research Division, The Peter MacCallum Cancer Centre, East Melbourne, Australia; 2Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Australia; 3Department of Clinical Haematology, Monash Medical Centre, Clayton, Australia; 4Memorial Sloan-Kettering Cancer Center, New York, NY; 5The Hebrew University Hadassah Medical School, Jerusalem, Israel; 6Department of Anatomical Pathology, Southern Health, Victoria, Australia; 7The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia; 8Department of Medical Biology, The University of Melbourne, Melbourne, Australia; 9Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Departments of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; 10Division of Medical Genetics, Department of Pediatrics and Neurobiology, Duke University School of Medicine, Durham, NC; 11Department of Pathology, The University of Melbourne, Parkville, Australia; and 12Department of Biochemistry and Molecular Biology, Monash University, Clayton, Australia
منابع مشابه
E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis.
Neoplastic transformation requires the elimination of key tumor suppressors, which may result from E3 ligase-mediated proteasomal degradation. We previously demonstrated a key role for the E3 ubiquitin ligase E6AP in the regulation of promyelocytic leukemia protein (PML) stability and formation of PML nuclear bodies. Here, we report the involvement of the E6AP-PML axis in B-cell lymphoma develo...
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تاریخ انتشار 2012