NCBI . NLM . NIH . GOV {
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We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC2903358/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC2903358/. The analysis below is for the second page.
Title[redir]:
System xc− and Thioredoxin Reductase 1 Cooperatively Rescue Glutathione Deficiency - PMC
Description:
GSH is the major antioxidant and detoxifier of xenobiotics in mammalian cells. A strong decrease of intracellular GSH has been frequently linked to pathological conditions like ischemia/reperfusion injury and degenerative diseases including ...
Title[redir]:
System xc− and Thioredoxin Reductase 1 Cooperatively Rescue Glutathione Deficiency - PMC
Description:
GSH is the major antioxidant and detoxifier of xenobiotics in mammalian cells. A strong decrease of intracellular GSH has been frequently linked to pathological conditions like ischemia/reperfusion injury and degenerative diseases including ...
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Keywords {🔍}
cells, txnrd, cell, gsh, xct, cys, pubmed, google, scholar, doi, bso, fig, death, expression, control, system, γgcs, uptake, xctoverexpressing, levels, increase, data, biol, knockout, free, panel, overexpression, fold, redox, reduction, pmc, intracellular, extracellular, lines, bsoinduced, reductase, nac, compared, xcttxnrd, thioredoxin, rescue, cellular, deficiency, article, shown, medium, experiments, confirmed, treatment, mock,
Topics {✒️}
antioxidant n-acetylcysteine annexin v-propidium iodide reverse transcription system mitochondrial thioredoxin reductase propidium iodide staining cytosolic thioredoxin reductase egfp-expressing vector pcag-3sip-egfp thioredoxin/thioredoxin reductase system fluorescence microscopy ischemia/reperfusion-induced tissue injury thioredoxin/thioredoxin reductase 1 thioredoxin/thioredoxin reductase 2 γ-gcs−/− embryonic stem mef cell lines xct-expressing γ-gcs−/− cells γ-gcs-specific inhibitor bso cystine/min/mg protein cystine/min/mg protein] nac-supplemented egfp-transfected l-buthionine sulfoximine reverse-transcribed hplc analysis revealed embryonic stem cell γ-glutamylcysteine synthetase knock tat-cre fusion protein quantitative rt-pcr rescue egfp-expressing txnrd2−/− c-terminal peptide sequence egfp-expressing control cells xct-overexpressing cells showed sf-txnrd1-expressing lentivirus egfp-expressing txnrd1+/− cells egfp-expressing txnrd1−/− cells bso-induced cell death xct-expressing cells continued pmc beta search bso-mediated cell death cold phosphate-buffered saline xct-overexpressing cells fails egfp-transfected control cells mock lentivirus [442l1-puro] egfp-transfected txnrd2−/− cells experimental procedures materials xct-expressing txnrd2−/− cells xct-overexpressing cells proliferated monoclonal txnrd2-specific antibody egfp-txnrd1−/− control cells steady-state redox potential γ-glutamylcysteine synthetase xct-overexpressing txnrd2−/− cells
Questions {❓}
- This presented an open question: what is the reducing force behind (Cys)2 reduction in the cells under GSH-deprived conditions?
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