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Literature summary for 3.6.1.70 extracted from
- Genetic interactions between HNT3/aprataxin and RAD27/FEN1 suggest parallel pathways for 5' end processing during base excision repair (2010), DNA Repair, 9, 690-699.
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Saccharomyces cerevisiae | - |
- |
- |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| HNT3 | - |
Saccharomyces cerevisiae |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | deletion of the Saccharomyces cerevisiae Hnt3 gene, which encodes the aprataxin homolog, in combination with known DNA repair genes. While Hnt3 single mutants are not sensitive to DNA damaging agents, loss of Hnt3 causes synergistic sensitivity to H2O2 in backgrounds that accumulate strand breaks with blocked termini, including lack of Apn1, Apn2, Tpp1 and Ntg1, Ntg2, Ogg1. Loss of HNT3 in Rad27 mutant cells, which are deficient in long-patch base excision repair, results in synergistic sensitivity to H2O2 and methylmethane sulfonate. Loss of Hnt3 also increases the sister chromatid exchange frequency. Hnt3 deletion partially rescues H2O2 sensitivity in recombination-deficient mutant Rad51 and mutant Rad52 cells | Saccharomyces cerevisiae |
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