Difference between revisions of "YLR376C"

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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Systematic name''' || [http://db.yeastgenome.org/cgi-bin/locus.pl?dbid=S000004368 YLR376C]  
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Systematic name''' || [http://www.yeastgenome.org/cgi-bin/locus.pl?dbid=S000004368 YLR376C]  
 
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Gene name'''        ||''PSY3 ''
 
|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Gene name'''        ||''PSY3 ''
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Aliases'''          ||'' ''
 
|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Aliases'''          ||'' ''
 
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Feature type'''          || ORF, Uncharacterized[[Category:ORF]][[Category:ORF, Uncharacterized]]
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Feature type'''          || ORF, Verified[[Category:ORF]][[Category:ORF, Verified]]
 
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Coordinates'''
 
|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Coordinates'''
|nowrap| Chr XII:873553..872825
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|nowrap| Chr XII:873554..872826
 
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Primary SGDID'''          || S000004368
 
|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Primary SGDID'''          || S000004368
 
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'''Description of YLR376C:''' Protein of unknown function; deletion results in a mutator phenotype suggesting a role for this protein as a mutational suppressor; deletion increases sensitivity to anticancer drugs oxaliplatin and cisplatin but not mitomycin C<ref name='S000076460'>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 {{SGDpaper|S000076460}} PMID 15173006</ref><ref name='S000074096'>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
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'''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<ref name='S000130520'>Ball LG, et al. (2009) The yeast Shu complex couples error-free post-replication repair to homologous recombination. Mol Microbiol 73(1):89-102 {{SGDpaper|S000130520}} PMID 19496932</ref><ref name='S000147390'>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 {{SGDpaper|S000147390}} PMID 21372173</ref><ref name='S000074096'>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 {{SGDpaper|S000074096}} PMID 12972632</ref><ref name='S000123652'>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 {{SGDpaper|S000123652}} PMID 17671161</ref><ref name='S000149016'>Tao Y, et al. (2012) Structural analysis of Shu proteins reveals a DNA-binding role essential for resisting damage. J Biol Chem () {{SGDpaper|S000149016}} PMID 22465956</ref><ref name='S000076460'>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
  {{SGDpaper|S000074096}} PMID 12972632</ref>
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  {{SGDpaper|S000076460}} PMID 15173006</ref>
 
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Latest revision as of 14:05, 26 April 2012

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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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  1. 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
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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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