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- W2052473301 abstract "Carbon monoxide (CO) is a gaseous product generated by heme oxygenase (HO), which oxidatively degrades heme. While the stress-inducible HO-1 has well been recognized as an anti-oxidative defense mechanism under stress conditions, recent studies suggest that cancer cells utilize the reaction for their survival. HO-2, the constitutive isozyme, also plays protective roles as a tonic regulator for neurovascular function. Although protective roles of the enzyme reaction and CO have extensively been studied, little information is available on the molecular mechanisms by which the gas exerts its biological actions. Recent studies using metabolomics revealed that CO inhibits cystathionine β-synthase (CBS), which generates H2S, another gaseous mediator. The CO-dependent CBS inhibition may impact on the remethylation cycle and related metabolic pathways including the methionine salvage pathway and polyamine synthesis. This review focuses on the gas-responsive regulation of metabolic systems, particularly the remethylation and transsulfuration pathways, and their putative implications for cancer and ischemic diseases." @default.
- W2052473301 created "2016-06-24" @default.
- W2052473301 creator A5037745876 @default.
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- W2052473301 creator A5073658591 @default.
- W2052473301 creator A5087891304 @default.
- W2052473301 creator A5089970737 @default.
- W2052473301 date "2012-02-14" @default.
- W2052473301 modified "2023-09-25" @default.
- W2052473301 title "Carbon monoxide: impact on remethylation/transsulfuration metabolism and its pathophysiologic implications" @default.
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- W2052473301 doi "https://doi.org/10.1007/s00109-012-0875-2" @default.
- W2052473301 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3296020" @default.
- W2052473301 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22331189" @default.
- W2052473301 hasPublicationYear "2012" @default.
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