Glutaredoxin 2a, a mitochondrial isoform, plays a protective role in a human cell line under serum deprivation
DC Field | Value | Language |
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dc.contributor.author | Kim, Su-Jung | - |
dc.contributor.author | Jung, Hyun-Joo | - |
dc.contributor.author | Choi, Hojin | - |
dc.contributor.author | Lim, Chang-Jin | - |
dc.date.accessioned | 2022-07-16T15:59:28Z | - |
dc.date.available | 2022-07-16T15:59:28Z | - |
dc.date.created | 2021-05-12 | - |
dc.date.issued | 2012-04 | - |
dc.identifier.issn | 0301-4851 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/165915 | - |
dc.description.abstract | The roles of mitochondrial glutaredoxin (Grx2a) under serum deprivation were assessed using the human stable HepG2 cell lines overexpressing or down-regulating Grx2a. The Grx2a-overexpressing stable cells displayed enhanced proliferation, decreased reactive oxygen species (ROS) and caspase-3 activity levels, and increased total GSH level, compared to the vector control cells. These characteristics of the overexpressing stable cells were reversed by down-regulating Grx2a in the same cell line. In the limited serum conditions, the Grx2a-overexpressing stable pcDNA3.0/HA-Grx2a cells exhibited higher cellular viabilities and total GSH level, and showed much lower enhancement in ROS and caspase-3 activity levels than the vector control pcDNA3.0/HA cells. However, the Grx2a-down-regulating stable cells gave rise to diminished cellular viabilities and further decreased total GSH level, and contained significantly higher ROS and caspase-3 activity levels, under serum deprivation than the vector control cells. These results suggest that Grx2a plays proliferative and anti-apoptotic roles under serum deprivation. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | SPRINGER | - |
dc.title | Glutaredoxin 2a, a mitochondrial isoform, plays a protective role in a human cell line under serum deprivation | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Choi, Hojin | - |
dc.identifier.doi | 10.1007/s11033-011-1152-0 | - |
dc.identifier.scopusid | 2-s2.0-84862998387 | - |
dc.identifier.wosid | 000301108500044 | - |
dc.identifier.bibliographicCitation | MOLECULAR BIOLOGY REPORTS, v.39, no.4, pp.3755 - 3765 | - |
dc.relation.isPartOf | MOLECULAR BIOLOGY REPORTS | - |
dc.citation.title | MOLECULAR BIOLOGY REPORTS | - |
dc.citation.volume | 39 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 3755 | - |
dc.citation.endPage | 3765 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | PROTEIN S-GLUTATHIONYLATION | - |
dc.subject.keywordPlus | LENS EPITHELIAL-CELLS | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | THIOREDOXIN REDUCTASE | - |
dc.subject.keywordPlus | REDOX REGULATION | - |
dc.subject.keywordPlus | DNA-DAMAGE | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | THIOLTRANSFERASE | - |
dc.subject.keywordPlus | OVEREXPRESSION | - |
dc.subject.keywordAuthor | Glutaredoxin | - |
dc.subject.keywordAuthor | Reactive oxygen species | - |
dc.subject.keywordAuthor | Serum deprivation | - |
dc.subject.keywordAuthor | Apoptosis | - |
dc.identifier.url | https://link.springer.com/article/10.1007/s11033-011-1152-0 | - |
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