Difference between revisions of "YDR050C"

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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Systematic name''' || [http://db.yeastgenome.org/cgi-bin/locus.pl?locus=YDR050C YDR050C]  
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Systematic name''' || [http://www.yeastgenome.org/cgi-bin/locus.pl?dbid=S000002457 YDR050C]  
 
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Gene name'''        ||''TPI1 ''
 
|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Gene name'''        ||''TPI1 ''
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Coordinates'''
 
|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Coordinates'''
|nowrap| Chr IV:556470..555724
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|nowrap| Chr IV:556472..555726
 
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Primary SGDID'''          || S000002457
 
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'''Description of {{PAGENAME}}:''' Triose phosphate isomerase, abundant glycolytic enzyme; mRNA half-life is regulated by iron availability; transcription is controlled by activators Reb1p, Gcr1p, and Rap1p through binding sites in the 5' non-coding region<ref name='S000049276'>Alber T and Kawasaki G (1982) Nucleotide sequence of the triose phosphate isomerase gene of Saccharomyces cerevisiae. J Mol Appl Genet 1(5):419-34 {{SGDpaper|S000049276}} PMID 6759603</ref><ref name='S000048283'>Scott EW and Baker HV (1993) Concerted action of the transcriptional activators REB1, RAP1, and GCR1 in the high-level expression of the glycolytic gene TPI. Mol Cell Biol 13(1):543-50 {{SGDpaper|S000048283}} PMID 8417350</ref><ref name='S000045272'>Krieger K and Ernst JF (1994) Iron regulation of triosephosphate isomerase transcript stability in the yeast Saccharomyces cerevisiae. Microbiology 140 ( Pt 5)():1079-84
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'''Description of YDR050C:''' Triose phosphate isomerase, abundant glycolytic enzyme; mRNA half-life is regulated by iron availability; transcription is controlled by activators Reb1p, Gcr1p, and Rap1p through binding sites in the 5' non-coding region; inhibition of Tpi1p activity by PEP (phosphoenolpyruvate) stimulates redox metabolism in respiring cells; E104D mutation in human TPI causes a rare autosomal disease<ref name='S000049276'>Alber T and Kawasaki G (1982) Nucleotide sequence of the triose phosphate isomerase gene of Saccharomyces cerevisiae. J Mol Appl Genet 1(5):419-34 {{SGDpaper|S000049276}} PMID 6759603</ref><ref name='S000146781'>Gruning NM, et al. (2011) Pyruvate Kinase Triggers a Metabolic Feedback Loop that Controls Redox Metabolism in Respiring Cells. Cell Metab 14(3):415-27 {{SGDpaper|S000146781}} PMID 21907146</ref><ref name='S000045272'>Krieger K and Ernst JF (1994) Iron regulation of triosephosphate isomerase transcript stability in the yeast Saccharomyces cerevisiae. Microbiology 140 ( Pt 5):1079-84 {{SGDpaper|S000045272}} PMID 8025673</ref><ref name='S000146855'>Rodriguez-Almazan C, et al. (2008) Structural basis of human triosephosphate isomerase deficiency: mutation E104D is related to alterations of a conserved water network at the dimer interface. J Biol Chem 283(34):23254-63 {{SGDpaper|S000146855}} PMID 18562316</ref><ref name='S000048283'>Scott EW and Baker HV (1993) Concerted action of the transcriptional activators REB1, RAP1, and GCR1 in the high-level expression of the glycolytic gene TPI. Mol Cell Biol 13(1):543-50
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  {{SGDpaper|S000048283}} PMID 8417350</ref>
 
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==Community Commentary==
 
==Community Commentary==
 
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Specifically higher expression in carbon limited chemostat cultures versus carbon excess.
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<ref>Boer VM, et al. (2003) The genome-wide transcriptional responses of Saccharomyces cerevisiae grown on glucose in aerobic chemostat cultures limited for carbon, nitrogen, phosphorus, or sulfur.
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J Biol Chem 278(5):3265-74</ref>
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==References==
 
==References==
 
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Latest revision as of 07:45, 23 January 2012

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Systematic name YDR050C
Gene name TPI1
Aliases
Feature type ORF, Verified
Coordinates Chr IV:556472..555726
Primary SGDID S000002457


Description of YDR050C: Triose phosphate isomerase, abundant glycolytic enzyme; mRNA half-life is regulated by iron availability; transcription is controlled by activators Reb1p, Gcr1p, and Rap1p through binding sites in the 5' non-coding region; inhibition of Tpi1p activity by PEP (phosphoenolpyruvate) stimulates redox metabolism in respiring cells; E104D mutation in human TPI causes a rare autosomal disease[1][2][3][4][5]




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References

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  1. Alber T and Kawasaki G (1982) Nucleotide sequence of the triose phosphate isomerase gene of Saccharomyces cerevisiae. J Mol Appl Genet 1(5):419-34 SGD PMID 6759603
  2. Gruning NM, et al. (2011) Pyruvate Kinase Triggers a Metabolic Feedback Loop that Controls Redox Metabolism in Respiring Cells. Cell Metab 14(3):415-27 SGD PMID 21907146
  3. Krieger K and Ernst JF (1994) Iron regulation of triosephosphate isomerase transcript stability in the yeast Saccharomyces cerevisiae. Microbiology 140 ( Pt 5):1079-84 SGD PMID 8025673
  4. Rodriguez-Almazan C, et al. (2008) Structural basis of human triosephosphate isomerase deficiency: mutation E104D is related to alterations of a conserved water network at the dimer interface. J Biol Chem 283(34):23254-63 SGD PMID 18562316
  5. Scott EW and Baker HV (1993) Concerted action of the transcriptional activators REB1, RAP1, and GCR1 in the high-level expression of the glycolytic gene TPI. Mol Cell Biol 13(1):543-50 SGD PMID 8417350

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