[The role of ATM kinase in neurodegeneration].
Neurodegenerative diseases represent a major challenge for modern medicine. Despite many years of research, no effective neuroprotective therapy has been proposed. Ataxia telangiectasia (A-T) is rare disease, which is caused by a mutation of the ATM protein. Cerebellar degeneration is the main symptom of the A-T. The kinase ATM, inter alia is involved in the repair of DNA damage, cell cycle regulation and the control of apoptosis. In recent years the presence of that kinase in the cytoplasm has been demonstrated. This led to the discovery of its participation in the regulation of metabolic processes, homeostasis mitochondrial oxidative stress response or modulation of synaptic function. The pleiotropic effect of ATM kinase requires effective control exercised by, inter alia, proteins having specific binding motifs this kinase, such as ATMIN and NBS1. The regulation of prosurvival processes which are controlled by ATM kinase, may prove an attractive therapeutic strategy in treatment of neurodegenerative diseases.
Jakub
J
Chwastek
Danuta
D
Jantas
Władysław
W
Lasoń
D001260:Ataxia Telangiectasia / Q000201:enzymology; D064007:Ataxia Telangiectasia Mutated Proteins / Q000378:metabolism*; D001665:Binding Sites; D018797:Cell Cycle Proteins / Q000378:metabolism; D002471:Cell Transformation, Neoplastic / Q000378:metabolism; D002526:Cerebellar Diseases / Q000201:enzymology; D058685:Genetic Pleiotropy; D006801:Humans; D009154:Mutation; D009410:Nerve Degeneration / Q000201:enzymology*; D009687:Nuclear Proteins / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology; D014157:Transcription Factors / Q000378:metabolism
C522841:ATMIN protein, human; D018797:Cell Cycle Proteins; C112156:NBN protein, human; D009687:Nuclear Proteins; D014157:Transcription Factors; D064007:Ataxia Telangiectasia Mutated Proteins