Ataxia-telangiectasia mutated kinase (ATM) as a central regulator of radiation-induced DNA damage response
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
- MeSH
- Ataxia Telangiectasia Mutated Proteins MeSH
- Cell Cycle physiology MeSH
- DNA-Binding Proteins genetics physiology MeSH
- Humans MeSH
- Mutation * MeSH
- Tumor Suppressor Proteins genetics physiology MeSH
- DNA Repair physiology MeSH
- DNA Damage radiation effects MeSH
- Protein Serine-Threonine Kinases genetics physiology MeSH
- Cell Cycle Proteins genetics physiology MeSH
- Ataxia Telangiectasia genetics MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- ATM protein, human MeSH Browser
- Ataxia Telangiectasia Mutated Proteins MeSH
- DNA-Binding Proteins MeSH
- Tumor Suppressor Proteins MeSH
- Protein Serine-Threonine Kinases MeSH
- Cell Cycle Proteins MeSH
Ataxia-telangiectasia mutated kinase (ATM) is a DNA damage-inducible protein kinase, which phosphorylates plethora of substrates participating in DNA damage response. ATM significance for the cell faith is undeniable, since it regulates DNA repair, cell-cycle progress, and apoptosis. Here we describe its main signalling targets and discuss its importance in DNA repair as well as novel findings linked to this key regulatory enzyme in the terms of ionizing radiation-induced DNA damage.
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