HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

c-Abl in oxidative stress, aging and cancer.

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.
AuthorsBaojie Li
JournalCell cycle (Georgetown, Tex.) (Cell Cycle) Vol. 4 Issue 2 Pg. 246-8 (Feb 2005) ISSN: 1551-4005 [Electronic] United States
PMID15655364 (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)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: