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Feedback Control of Adrenal Steroidogenesis via H2O2-Dependent, Reversible Inactivation of Peroxiredoxin III in Mitochondria

DC FieldValueLanguage
dc.contributor.author길인섭-
dc.contributor.author배수한-
dc.contributor.author이서구-
dc.date.accessioned2014-12-19T17:28:26Z-
dc.date.available2014-12-19T17:28:26Z-
dc.date.issued2012-
dc.identifier.issn1097-2765-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/91474-
dc.description.abstractCertain members of the peroxiredoxin (Prx) family undergo inactivation through hyperoxidation of the catalytic cysteine to sulfinic acid during catalysis and are reactivated by sulfiredoxin; however, the physiological significance of this reversible regulatory process is unclear. We now show that PrxIII in mouse adrenal cortex is inactivated by H2O2 produced by cytochrome P450 enzymes during corticosterone production stimulated by adrenocorticotropic hormone. Inactivation of PrxIII triggers a sequence of events including accumulation of H2O2, activation of p38 mitogen-activated protein kinase, suppression of steroidogenic acute regulatory protein synthesis, and inhibition of steroidogenesis. Interestingly, levels of inactivated PrxIII, activated p38, and sulfiredoxin display circadian oscillations. Steroidogenic tissue-specific ablation of sulfiredoxin in mice resulted in the persistent accumulation of inactive PrxIII and suppression of the adrenal circadian rhythm of corticosterone production. The coupling of CYP11B1 activity to PrxIII inactivation provides a feedback regulatory mechanism for steroidogenesis that functions independently of the hypothalamic-pituitary-adrenal axis.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfMolecular Cell-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleFeedback Control of Adrenal Steroidogenesis via H2O2-Dependent, Reversible Inactivation of Peroxiredoxin III in Mitochondria-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorIn Sup Kil-
dc.contributor.googleauthorSe Kyoung Lee-
dc.contributor.googleauthorKeun Woo Ryu-
dc.contributor.googleauthorHyun Ae Woo-
dc.contributor.googleauthorMeng-Chun Hu-
dc.contributor.googleauthorSoo Han Bae-
dc.contributor.googleauthorSue Goo Rhee-
dc.identifier.doi10.1016/j.molcel.2012.05.030-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00281-
dc.contributor.localIdA01798-
dc.contributor.localIdA02847-
dc.relation.journalcodeJ02256-
dc.contributor.alternativeNameKil, In Sup-
dc.contributor.alternativeNameBae, Soo Han-
dc.contributor.alternativeNameRhee, Sue Goo-
dc.contributor.affiliatedAuthorKil, In Sup-
dc.contributor.affiliatedAuthorBae, Soo Han-
dc.contributor.affiliatedAuthorRhee, Sue Goo-
dc.citation.volume46-
dc.citation.number5-
dc.citation.startPage584-
dc.citation.endPage594-
dc.identifier.bibliographicCitationMolecular Cell, Vol.46(5) : 584-594, 2012-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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