1.11.1.27: glutathione-dependent peroxiredoxin
This is an abbreviated version!
For detailed information about glutathione-dependent peroxiredoxin, go to the full flat file.
Word Map on EC 1.11.1.27
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1.11.1.27
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peroxiredoxins
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plasmodium
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falciparum
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malaria
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prxvi
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intraerythrocytic
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medicine
- 1.11.1.27
- peroxiredoxins
- plasmodium
- falciparum
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malaria
- prxvi
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intraerythrocytic
- medicine
Reaction
2 glutathione
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Synonyms
1-Cys peroxiredoxin, 1-Cys Prdx, 1-Cys Prx, 1-CysPrx, 2-Cys peroxiredoxin, 2-Cys peroxiredoxin TPx-1, EC 1.11.1.15, glutathione peroxidase, GPX, HI0572, peroxiredoxin 6, peroxiredoxin II, peroxiredoxin VI, Pf1-Cys-Prx, PGdx, Prdx6, Prx1, Prx3, Prx6, TPx-1
ECTree
1.11.1.27 glutathione-dependent peroxiredoxinAdvanced search results
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results (Expression
Expression on EC 1.11.1.27 - glutathione-dependent peroxiredoxin
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EXPRESSION 
ORGANISM
UNIPROT
LITERATURE
oxidant stress is, e.g. by H2O2, paraquat, a potent inducer of Prdx6 expression and stimulates Prdx6 gene expression by a transcriptional mechanism involving its antioxidant response element, ARE
PRDX6 levels are decreased during osteogenic differentiation in human dental pulp stem cells
the Fe-S cluster regulator IscR activates prx3 expression by sensing reactive oxygen species and iron starvation. IscR controls the prx3 expression by directly binding to the type 2 IscR-binding site centered at positionx0244 from the transcription start site. Biochemical and molecular genetic evidence demonstrates that IscR senses iron starvation as well as ROS and shifts to the clusterless apo-form, which leads to the increase in its own levels in cells and accordingly, the activation of prx3
the Fe-S cluster regulator IscR senses iron starvation as well as reactive oxygen species and shifts to the Fe-S clusterless apo-form, which leads to the increase of cellular IscR and in turn prx3 expression, contributing to the survival and virulence of Vibrio vulnificus during pathogenesis
transcription of Prdx6 message in dermal epithelium is induced by treatment with keratinocyte growth factor, a response of presumed importance related to wound healing, requiring ARE and Nrf2. Dexamethasone induces Prdx6 expression in adult lung cells and regulates transcription through its interaction with a glucocorticoid response element in the promoter region of the Prdx6 gene. Oxidant stress is, e.g. by H2O2, paraquat, a potent inducer of Prdx6 expression and stimulates Prdx6 gene expression by a transcriptional mechanism involving its antioxidant response element, ARE
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oxidant stress is, e.g. by H2O2, paraquat, a potent inducer of Prdx6 expression and stimulates Prdx6 gene expression by a transcriptional mechanism involving its antioxidant response element, ARE
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oxidant stress is, e.g. by H2O2, paraquat, a potent inducer of Prdx6 expression and stimulates Prdx6 gene expression by a transcriptional mechanism involving its antioxidant response element, ARE
-
oxidant stress is, e.g. by H2O2, paraquat, a potent inducer of Prdx6 expression and stimulates Prdx6 gene expression by a transcriptional mechanism involving its antioxidant response element, ARE
-
the Fe-S cluster regulator IscR activates prx3 expression by sensing reactive oxygen species and iron starvation. IscR controls the prx3 expression by directly binding to the type 2 IscR-binding site centered at positionx0244 from the transcription start site. Biochemical and molecular genetic evidence demonstrates that IscR senses iron starvation as well as ROS and shifts to the clusterless apo-form, which leads to the increase in its own levels in cells and accordingly, the activation of prx3
ADV89163
the Fe-S cluster regulator IscR activates prx3 expression by sensing reactive oxygen species and iron starvation. IscR controls the prx3 expression by directly binding to the type 2 IscR-binding site centered at positionx0244 from the transcription start site. Biochemical and molecular genetic evidence demonstrates that IscR senses iron starvation as well as ROS and shifts to the clusterless apo-form, which leads to the increase in its own levels in cells and accordingly, the activation of prx3
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the Fe-S cluster regulator IscR senses iron starvation as well as reactive oxygen species and shifts to the Fe-S clusterless apo-form, which leads to the increase of cellular IscR and in turn prx3 expression, contributing to the survival and virulence of Vibrio vulnificus during pathogenesis
ADV89163
the Fe-S cluster regulator IscR senses iron starvation as well as reactive oxygen species and shifts to the Fe-S clusterless apo-form, which leads to the increase of cellular IscR and in turn prx3 expression, contributing to the survival and virulence of Vibrio vulnificus during pathogenesis
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