Abstract |
c-Abl is activated by oxidative stress but its precise function in cell response to this stress is elusive. Studies of c-Abl(-/-) osteoblasts revealed that c-Abl played a negative role in the induction of peroxiredoxin I (Prx I, Prdx I), an anti-oxidant protein with tumor suppression activity. In contrast, Atm, a signaling molecule that interacts with c-Abl and is required for c-Abl activation, served a totally different function. The significance of these findings is discussed here in the context of aging and tumorigenesis and their links to reactive oxygen species. c-Abl and its derivatives BCR-ABL and v-Abl were discovered more than twenty years ago. BCR-ABL and v-Abl acquire elevated tyrosine kinase activities by fusing to BCR and gag respectively and are capable of transforming myeloid and fibroblast cells. BCR-ABL is also the underlying cause in the development of most cases of chronic myeloid leukemia (CML) in humans. In contrast, c-Abl takes on an auto-inhibiting conformation and its activation requires post-translational modifications such as phosphorylation and myristoylation. The physiological functions of c-Abl remain elusive.
|
Authors | Baojie Li |
Journal | Cell cycle (Georgetown, Tex.)
(Cell Cycle)
Vol. 4
Issue 2
Pg. 246-8
(Feb 2005)
ISSN: 1551-4005 [Electronic] United States |
PMID | 15655364
(Publication Type: Journal Article)
|
Chemical References |
- Cell Cycle Proteins
- DNA-Binding Proteins
- Oncogene Proteins v-abl
- Tumor Suppressor Proteins
- Peroxidases
- Peroxiredoxins
- Fusion Proteins, bcr-abl
- Proto-Oncogene Proteins c-abl
- ATM protein, human
- Ataxia Telangiectasia Mutated Proteins
- Atm protein, mouse
- Protein Serine-Threonine Kinases
- Protein Kinase C-delta
|
Topics |
- Aging
(physiology)
- Animals
- Ataxia Telangiectasia Mutated Proteins
- Cell Cycle Proteins
(genetics, physiology)
- DNA-Binding Proteins
(genetics, physiology)
- Fusion Proteins, bcr-abl
(genetics, physiology)
- Gene Expression Regulation
(physiology)
- Gene Expression Regulation, Neoplastic
- Genes, abl
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive
(etiology, physiopathology)
- Mice
- Neoplasms
(genetics, physiopathology)
- Oncogene Proteins v-abl
(genetics, physiology)
- Oxidative Stress
(physiology)
- Peroxidases
(genetics, physiology)
- Peroxiredoxins
- Protein Kinase C-delta
(physiology)
- Protein Processing, Post-Translational
- Protein Serine-Threonine Kinases
(genetics, physiology)
- Proto-Oncogene Proteins c-abl
(genetics, physiology)
- Tumor Suppressor Proteins
(genetics, physiology)
|