Abstract
The inability to repair DNA damage properly in mammals leads to various disorders and enhanced rates of tumour development. Organisms respond to chromosomal insults by activating a complex damage response pathway. This pathway regulates known responses such as cell-cycle arrest and apoptosis (programmed cell death), and has recently been shown to control additional processes including direct activation of DNA repair networks.
MeSH terms
-
Animals
-
Ataxia Telangiectasia Mutated Proteins
-
Cell Cycle / genetics
-
Cell Cycle Proteins*
-
Checkpoint Kinase 1
-
Checkpoint Kinase 2
-
DNA Damage*
-
DNA Repair
-
DNA-Binding Proteins
-
Forecasting
-
Humans
-
Protein Kinases / physiology
-
Protein Serine-Threonine Kinases / physiology
-
Signal Transduction*
-
Tumor Suppressor Proteins
Substances
-
Cell Cycle Proteins
-
DNA-Binding Proteins
-
Tumor Suppressor Proteins
-
Protein Kinases
-
Checkpoint Kinase 2
-
ATM protein, human
-
ATR protein, human
-
Ataxia Telangiectasia Mutated Proteins
-
CHEK2 protein, human
-
Checkpoint Kinase 1
-
Protein Serine-Threonine Kinases