Abstract
Although the carcinogenicity of arsenic has been well established, the underlying molecular mechanisms have not yet been fully identified. Accumulating evidence indicates that the alteration of cellular signal transduction is directly related to the carcinogenesis of arsenic. This review focuses on recent advances in arsenic-induced signal transduction, including reactive oxygen species (ROS) production, tyrosine phosphorylation, MAPK signaling, NF-κB activation, cell cycle arrest, and apoptosis.
| Original language | English |
|---|---|
| Pages (from-to) | 271-278 |
| Number of pages | 8 |
| Journal | Journal of Inorganic Biochemistry |
| Volume | 96 |
| Issue number | 2-3 |
| DOIs | |
| State | Published - Aug 1 2003 |
Keywords
- Apoptosis
- Arsenic
- Cell cycle
- MAPK
- Metal
- NF-κB
- Reactive oxygen species
- Tyrosine phosphorylation
ASJC Scopus subject areas
- Biochemistry
- Inorganic Chemistry
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