Artemis 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: Artemis Protein [2]
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| Protein Name | Artemis Protein |
| Gene | DCLRE1C |
| UniProt ID | Q9Y5T5 |
| PDB IDs | 3O0A, 3O0B, 3O0C |
| Molecular Weight | 82 kDa |
| Subcellular Localization | Nucleus |
| Protein Family | Artemis Family |
Artemis is a DNA endonuclease with specificity for hairpin coding ends formed during V(D)J recombination. The protein forms a complex with DNA-PKcs and becomes activated upon DNA binding. Artemis has additional 5' and 3' exonuclease activity and processes various DNA ends during NHEJ.
The Artemis Protein (DCLRE1C) has the following structural features:
Available PDB structures: 3O0A, 3O0B, 3O0C
DCLRE1C plays critical roles in:
DCLRE1C dysfunction contributes to:
| Disease | Mechanism |
|---|---|
| Alzheimer's Disease | DCLRE1C mutations/dysfunction |
| Parkinson's Disease | DCLRE1C mutations/dysfunction |
| SCID | DCLRE1C mutations/dysfunction |
| Radiosensitivity | DCLRE1C mutations/dysfunction |
DCLRE1C 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 Artemis 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 Artemis:
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. ↩︎