YLR376C
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| Systematic name | YLR376C |
| Gene name | PSY3 |
| Aliases | |
| Feature type | ORF, Verified |
| Coordinates | Chr XII:873554..872826 |
| Primary SGDID | S000004368 |
Description of YLR376C: Component of the Shu complex, which promotes error-free DNA repair; Shu complex mediates inhibition of Srs2p function; structural analysis reveals a similar DNA-binding region in both Psy3p and Csm2p and that both regions work together to form a single DNA binding site; deletion of PSY3 results in a mutator phenotype; deletion increases sensitivity to anticancer drugs oxaliplatin and cisplatin but not mitomycin C[1][2][3][4][5][6]
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References
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- ↑ Ball LG, et al. (2009) The yeast Shu complex couples error-free post-replication repair to homologous recombination. Mol Microbiol 73(1):89-102 SGD PMID 19496932
- ↑ Bernstein KA, et al. (2011) The Shu complex, which contains Rad51 paralogues, promotes DNA repair through inhibition of the Srs2 anti-recombinase. Mol Biol Cell 22(9):1599-607 SGD PMID 21372173
- ↑ Huang ME, et al. (2003) A genomewide screen in Saccharomyces cerevisiae for genes that suppress the accumulation of mutations. Proc Natl Acad Sci U S A 100(20):11529-34 SGD PMID 12972632
- ↑ Mankouri HW, et al. (2007) Shu proteins promote the formation of homologous recombination intermediates that are processed by sgs1-rmi1-top3. Mol Biol Cell 18(10):4062-73 SGD PMID 17671161
- ↑ Tao Y, et al. (2012) Structural analysis of Shu proteins reveals a DNA-binding role essential for resisting damage. J Biol Chem () SGD PMID 22465956
- ↑ Wu HI, et al. (2004) Genome-wide identification of genes conferring resistance to the anticancer agents cisplatin, oxaliplatin, and mitomycin C. Cancer Res 64(11):3940-8 SGD PMID 15173006
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