Ku70 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.
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title: Ku70 Protein [2]
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| Protein Name | Ku70 Protein |
| Gene | XRCC6 |
| UniProt ID | P13010 |
| PDB IDs | 1JJR, 1Q2Z, 2ZKA |
| Molecular Weight | 70 kDa |
| Subcellular Localization | Nucleus |
| Protein Family | Ku Protein Family |
XRCC6 (Ku70) is a subunit of the Ku heterodimer (Ku70/Ku80) that binds to DNA double-strand breaks and initiates non-homologous end joining (NHEJ). Ku70 forms a ring-shaped structure that encircles DNA. The Ku heterodimer recruits DNA-PKcs and other NHEJ factors to process and ligate DNA ends.
The Ku70 Protein (XRCC6) has the following structural features:
Available PDB structures: 1JJR, 1Q2Z, 2ZKA
XRCC6 plays critical roles in:
XRCC6 dysfunction contributes to:
| Disease | Mechanism |
|---|---|
| Alzheimer's Disease | XRCC6 mutations/dysfunction |
| Parkinson's Disease | XRCC6 mutations/dysfunction |
| Ataxia Telangiectasia | XRCC6 mutations/dysfunction |
| SCID | XRCC6 mutations/dysfunction |
XRCC6 is being explored as a therapeutic target:
| Strategy | Agent | Development Stage |
|---|---|---|
| Gene therapy | AAV-based delivery | Preclinical |
| Small molecules | DNA repair enhancers | Research |
| Combination therapy | PARP inhibitors | Clinical (cancer) |
The study of Ku70 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.
Current research on Ku70 in neurodegeneration:
Mimitou EP, Symington LS. DNA end resection: many nucleases make light work. DNA Repair. 2009. ↩︎
Lord CJ, Ashworth A. The DNA damage response and cancer therapy. Nature. 2012. ↩︎
McKinnon PJ. DNA repair deficiency and neurological disease. Nat Rev Neurosci. 2009. ↩︎