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Transforming pathways activated by the v-Abl tyrosine kinase
Scott K Shore1, Ramana V Tantravahi, E Premkumar Reddy
1Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, 3307 N Broad Street, Philadelphia, Pennsylvania, PA 19140, USA.
Oncogene
|December 12, 2002
Summary
Abelson Murine Leukemia Virus (A-MuLV) causes leukemia by activating the v-Abl oncogene. This review covers A-MuLV transformation, v-Abl protein activity, and oncogenic signaling pathways.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Abelson Murine Leukemia Virus (A-MuLV) is an acute transforming retrovirus encoding the v-abl oncogene.
- Two viral isolates produce p120 and p160 v-Abl proteins, transforming hematopoietic and fibroblastic cells.
- These proteins are non-receptor tyrosine kinases essential for transforming activity.
Purpose of the Study:
- To review early transformation studies of A-MuLV.
- To discuss the structure and biochemical activity of the v-Abl protein.
- To examine v-Abl-mediated transformation mechanisms and activated signal transduction pathways.
Main Methods:
- Review of existing literature on A-MuLV transformation studies.
- Analysis of v-Abl protein structure and biochemical properties.
- Examination of signal transduction pathways activated by v-Abl.
Main Results:
- A-MuLV transforms hematopoietic and fibroblastic cells in vitro, inducing pre-B cell leukemias in vivo.
- v-Abl proteins are plasma membrane-associated tyrosine kinases crucial for transformation.
- A-MuLV infection abrogates cytokine-dependence and impairs differentiation of hematopoietic cells.
Conclusions:
- v-Abl oncogene induces cellular transformation and leukemia through its tyrosine kinase activity.
- Dysregulation of cytokine signaling and differentiation is a key mechanism of v-Abl oncogenesis.
- Understanding v-Abl's role in signal transduction provides insights into retroviral oncogenesis.