alexa Oncogenic Signaling by Leukemia-Associated Mutant Cbl Proteins | OMICS International
ISSN: 2161-1009

Biochemistry & Analytical Biochemistry
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Review Article

Oncogenic Signaling by Leukemia-Associated Mutant Cbl Proteins

Scott Nadeau1,2, Wei An1,2, Nick Palermo1, Dan Feng1, Gulzar Ahmad1, Lin Dong, Gloria E. O. Borgstahl1,3,6,7, Amarnath Natarajan1,2,7, Mayumi Naramura1,2,7, Vimla Band1,2,3,7 and Hamid Band1-5,7*

1Eppley Institute for Research in Cancer and Allied Diseases

2Departments of Genetics, Cell Biology & Anatomy, University of Nebraska Medical Center, 985950 Nebraska Medical Center Omaha, NE 68198-5950, USA

3Departments of Biochemistry & Molecular Biology, University of Nebraska Medical Center, 985950 Nebraska Medical Center Omaha, NE 68198-5950, USA

4Departments of Pathology & Microbiology, University of Nebraska Medical Center, 985950 Nebraska Medical Center Omaha, NE 68198-5950, USA

5Departments of Pharmacology & Experimental Neuroscience, College of Medicine, University of Nebraska Medical Center, 985950 Nebraska Medical Center Omaha, NE 68198-5950, USA

6Departments of Pharmaceutical Sciences, College of Pharmacy, University of Nebraska Medical Center, 985950 Nebraska Medical Center Omaha, NE 68198-5950, USA

7UNMC-Eppley Cancer Center, University of Nebraska Medical Center, 985950 Nebraska Medical Center Omaha, NE 68198-5950, USA

*Corresponding Author:
Dr. Hamid Band
Eppley Institute for Research in Cancer and Allied Diseases
UNMC-Eppley Cancer Center, University of Nebraska Medical Center
985950 Nebraska Medical Center Omaha, NE 68198-5950, USA
Tel: 402-559-8572
Email: [email protected]

Received Date: July 06, 2012; Accepted Date: July 26, 2012; Published Date: July 30, 2012

Citation: Nadeau S, An W, Palermo N, Feng D, Ahmad G, et al. (2012) Oncogenic Signaling by Leukemia-Associated Mutant Cbl Proteins. Biochem Anal Biochem S6:001. doi: 10.4172/2161-1009.S6-001

Copyright: © 2012 Nadeau S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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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