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Transglutaminase 2 inhibits apoptosis induced by calcium-overload through down-regulation of Bax

DC Field Value Language
dc.contributor.authorCho, Sung Yup-
dc.contributor.authorLee, Jin-Haeng-
dc.contributor.authorBae, Han-Dong-
dc.contributor.authorJeong, Eui Man-
dc.contributor.authorJang, Gi-Yong-
dc.contributor.authorKim, Chai-Wan-
dc.contributor.authorShin, Dong-Myung-
dc.contributor.authorJeon, Ju-Hong-
dc.contributor.authorKim, In-Gyu-
dc.date.accessioned2024-05-20T07:30:24Z-
dc.date.available2024-05-20T07:30:24Z-
dc.date.created2021-12-21-
dc.date.issued2010-09-
dc.identifier.citationEXPERIMENTAL AND MOLECULAR MEDICINE, Vol.42 No.9, pp.639-650-
dc.identifier.issn1226-3613-
dc.identifier.urihttps://hdl.handle.net/10371/203544-
dc.description.abstractAn abrupt increase of intracellular Ca(2+) is observed in cells under hypoxic or oxidatively stressed conditions. The dysregulated increase of cytosolic Ca(2+) triggers apoptotic cell death through mitochondrial swelling and activation of Ca(2+)-dependent enzymes. Transglutaminase 2 (TG2) is a Ca(2+)-dependent enzyme that catalyzes transamidation reaction producing cross-linked and polyaminated proteins. TG2 activity is known to be involved in the apoptotic process. However, the pro-apoptotic role of TG2 is still controversial. In this study, we investigate the role of TG2 in apoptosis induced by Ca(2+)-overload. Overexpression of TG2 inhibited the A23187-induced apoptosis through suppression of caspase-3 and -9 activities, cytochrome c release into cytosol, and mitochondria membrane depolarization. Conversely, down-regulation of TG2 caused the increases of cell death, caspase-3 activity and cytochrome c in cytosol in response to Ca(2+)-overload. Western blot analysis of Bcl-2 family proteins showed that TG2 reduced the expression level of Bax protein. Moreover, overexpression of Bax abrogated the anti-apoptotic effect of TG2, indicating that TG2-mediated suppression of Bax is responsible for inhibiting cell death under Ca(2+)-overloaded conditions. Our findings revealed a novel anti-apoptotic pathway involving TG2, and suggested the induction of TG2 as a novel strategy for promoting cell survival in diseases such as ischemia and neurodegeneration.-
dc.language영어-
dc.publisherKOREAN SOC MED BIOCHEMISTRY MOLECULAR BIOLOGY-
dc.titleTransglutaminase 2 inhibits apoptosis induced by calcium-overload through down-regulation of Bax-
dc.typeArticle-
dc.identifier.doi10.3858/emm.2010.42.9.063-
dc.citation.journaltitleEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.identifier.wosid000282598500005-
dc.identifier.scopusid2-s2.0-77957727111-
dc.citation.endpage650-
dc.citation.number9-
dc.citation.startpage639-
dc.citation.volume42-
dc.identifier.kciidART001480931-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorCho, Sung Yup-
dc.contributor.affiliatedAuthorJeon, Ju-Hong-
dc.contributor.affiliatedAuthorKim, In-Gyu-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusTISSUE TRANSGLUTAMINASE-
dc.subject.keywordPlusCELL-DEATH-
dc.subject.keywordPlusINTRACELLULAR-LOCALIZATION-
dc.subject.keywordPlusMEDIATES ACTIVATION-
dc.subject.keywordPlusMAP KINASE-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusBINDING-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusDIFFERENTIATION-
dc.subject.keywordPlusMITOCHONDRIA-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorBax-
dc.subject.keywordAuthorcalcium-
dc.subject.keywordAuthormitochondria-
dc.subject.keywordAuthortransglutaminase 2-
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