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a(CHEBI:"reactive oxygen species") -> r(HGNC:SEC61G)
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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Among the systems that defend against OS in the lens are a high level of reduced glutathione (GSH),5 abundant antioxidant enzymes,6 and the chaperone-like functions of crystallins.7 Aging of the lens is characterized by a diminishing level of GSH and reduced activities of detoxifying enzymes.5 6 Numerous altered levels and activities of antioxidant enzymes and protective proteins have been detected after oxidative damage of lens epithelial cells.5 6 8 The lens also expresses a set of common transcription factors (e.g., AP-1, NF-B, p53, and upstream stimulatory factor [USF]), with activities that are regulated by the redox state of the cell,1 9 and these factors are known to activate batteries of genes that participate in protection and repair. Previous work has provided evidence that the human lens epithelium (HLE) is capable of responding to the presence of OS and cataract through the altered expression of numerous genes, including the regulatory subunit of protein phosphatase 2A,8 metallothionein IIa,10 thioltransferase,11 catalase,12 glutathione peroxidase,13 multiple glutathione S-transferases,6 Na,K-ATPase,14 AP-1,15 and proline isomerase.16 Several members of this subcategory (calnexin, SEC61B, SEC63L) that were present on the chip were not affected by 50 uM H2O2-induced OS. Transcripts encoding SEC61G were induced by a factor of 1.7 only at 8 hours
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Selventa
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2014-07-03T14:30:12.017+02:00
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