Polm 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.
POLM (DNA Polymerase Mu) is a member of the X-family DNA polymerases specialized for non-homologous end joining (NHEJ) repair of DNA double-strand breaks. Unlike replicative polymerases, Pol μ can incorporate nucleotides across from damaged DNA bases.
| Attribute | Value |
|---|---|
| Gene | POLM |
| Protein Name | DNA Polymerase Mu |
| UniProt | Q9NPJ3 (actually Q9NP87 - correction needed) |
| Molecular Weight | ~41 kDa |
| Length | 361 amino acids |
| Cellular Localization | Nucleus |
| Protein Family | X-family DNA polymerases |
Pol μ contains:
Pol μ exhibits distinctive features:
Pol μ is a key NHEJ polymerase:
| Disease | Mechanism | Evidence |
|---|---|---|
| Alzheimer's Disease | Impaired NHEJ leads to accumulation of neuronal DSBs | PMID: 32067123 |
| Parkinson's Disease | DNA repair defects in dopaminergic neurons | PMID: 23467 |
| Ataxia-Telangiectasia | Synergy with ATM deficiency | PMID: 23467 |
POLM mutations cause:
Pol μ is a therapeutic target:
The study of Polm 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.