Atm Protein is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| ATM Protein |
| Protein Name | Ataxia-Telangiectasia Mutated |
| Gene | ATM |
| UniProt ID | Q13315 |
| PDB IDs | 5NP0, 6K9L |
| Molecular Weight | 350 kDa |
| Subcellular Localization | Nucleus, mitochondria |
| Protein Family | PI3/PI4-related protein kinases |
ATM PROTEIN is a gene/protein encoding a key neuronal protein involved in synaptic function, signal transduction, and cellular homeostasis. Dysfunction of ATM PROTEIN is associated with neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and related disorders.
ATM is a large serine/threonine kinase:
- FAT domain: Protein-protein interactions
- PI3K-like kinase domain: Catalytic activity
- FATC domain: Required for kinase activity
- N-terminal regulatory region: Autoinhibition
- DNA damage response: Primary sensor for DSBs
- Cell cycle checkpoint: Halts cell cycle
- DNA repair coordination: Coordinates repair
- Mitochondrial function: Regulates mitochondrial dynamics
- Neuronal survival: Protects neurons
- Homozygous ATM mutations cause AT
- Progressive neurodegeneration
- Immunodeficiency, cancer risk
- ATM deficiency increases PD risk
- Impaired DNA repair in neurons
- DNA damage accumulates in AD
- ATM signaling dysregulated
- 9050862: ATM in DNA damage response. Cell, 1997.
- 28714940: ATM in neurodegeneration. Nat Rev Neurol, 2017.
The study of Atm Protein has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- Iyaswamy A et al.. "Fe65-engineered neuronal exosomes encapsulating corynoxine-B ameliorate cognition and pathology of Alzheimer's disease." Signal transduction and targeted therapy (2023). DOI: 10.1038/s41392-023-01657-4 PubMed: 37867176
- Litwin T, Dzieżyc K, Członkowska A. "Wilson disease-treatment perspectives." Annals of translational medicine (2019). DOI: 10.21037/atm.2018.12.09 PubMed: 31179305
- Kanungo S et al.. "Glycogen metabolism and glycogen storage disorders." Annals of translational medicine (2018). DOI: 10.21037/atm.2018.10.59 PubMed: 30740405
- Dusek P, Litwin T, Członkowska A. "Neurologic impairment in Wilson disease." Annals of translational medicine (2019). DOI: 10.21037/atm.2019.02.43 PubMed: 31179301
- Post MA, Lefeber DJ. "Clinical glycomics in the diagnostic laboratory." Annals of translational medicine (2019). DOI: 10.21037/atm.2019.08.74 PubMed: 31656799
- Li J, Wang Q, Wang H. "Autoantibodies detection in anti-N-methyl-D-aspartate receptor encephalitis." Annals of translational medicine (2023). DOI: 10.21037/atm-20-2279 PubMed: 37090042
- Gao YL et al.. "Tau in neurodegenerative disease." Annals of translational medicine (2018). DOI: 10.21037/atm.2018.04.23 PubMed: 29951497
- Jaffe RJ, Dave RS, Byrareddy SN. "Meningeal lymphatics in aging and Alzheimer's disease." Annals of translational medicine (2019). DOI: 10.21037/atm.2019.01.06 PubMed: 31032283