DC Field | Value | Language |
---|---|---|
dc.contributor.author | KIM, YOUNGJIN | - |
dc.date.accessioned | 2019-04-07T20:52:09Z | - |
dc.date.available | 2019-04-07T20:52:09Z | - |
dc.date.created | 2019-03-11 | - |
dc.date.issued | 2011-12 | - |
dc.identifier.issn | 0006-3002 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/96465 | - |
dc.description.abstract | Higd-1a (hypoxia induced gene domain family-1a) is a mitochondrial inner membrane protein with a conformation of N-terminal outside-C-terminal outside and loop inside. There are four Higd genes, Higd-1a, -1b, -1c and -2a, in the mouse. Higd-1a and -2a are expressed primarily in the brain, heart, kidney and leukocytes. HIF (hypoxia-inducible factor) overexpression induced the endogenous expression and promoter activity of Higd-1a. Mutation of the HRE (hypoxia-response element) site at - 32 bp in the Higd-1a promoter reduced the promoter activity, suggesting that transcription of Higd-1a is regulated by binding of the transcription factor HIF to the HRE. Higd-1a promoted cell survival under hypoxia. RAW264.7 cells stably transfected with Higd-1a underwent less apoptosis than control cells in a hypoxic condition, and hypoxia-induced apoptosis was strongly enhanced when endogenous Higd-la was silenced by siRNA. The survival effect of Higd-1a was completely abolished by deletion of the 26 N-terminal amino acids, and we showed that Higd-1a increased survival by inhibiting cytochrome C release and reducing the activities of caspases. However, expression of Bcl-2, Bax, Bad, and BNIP3 and translocation of AIF were unaffected under the same conditions. Higd-2a also enhanced cell survival under hypoxia. Cells transfected with Higd-2a underwent less apoptosis than control cells in hypoxic conditions, and hypoxia-induced apoptosis increased when endogenous Higd-2a was depleted. Together these observations indicate that Higd-1a is induced by hypoxia in a HIF-dependent manner and its anti-apoptotic effect results from inhibiting cytochrome C release and reducing caspase activities. (C) 2011 Elsevier B.V. All rights reserved. | - |
dc.language | English | - |
dc.publisher | Elsevier | - |
dc.relation.isPartOf | BIOCHIMICA ET BIOPHYSICA ACTA | - |
dc.title | The survival effect of mitochondrial Higd-1a is associated with suppression of cytochrome C release and prevention of caspase activation. | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.bbamcr.2011.07.017 | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | BIOCHIMICA ET BIOPHYSICA ACTA, v.1813, no.12, pp.2088 - 2098 | - |
dc.identifier.wosid | 000297882400012 | - |
dc.citation.endPage | 2098 | - |
dc.citation.number | 12 | - |
dc.citation.startPage | 2088 | - |
dc.citation.title | BIOCHIMICA ET BIOPHYSICA ACTA | - |
dc.citation.volume | 1813 | - |
dc.contributor.affiliatedAuthor | KIM, YOUNGJIN | - |
dc.identifier.scopusid | 2-s2.0-82555164967 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | HYPOXIA-INDUCIBLE FACTOR | - |
dc.subject.keywordPlus | INDUCED CELL-DEATH | - |
dc.subject.keywordPlus | NITRIC-OXIDE | - |
dc.subject.keywordPlus | FACTOR-I | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | TRANSCRIPTIONAL ACTIVATION | - |
dc.subject.keywordPlus | FACTOR 1-ALPHA | - |
dc.subject.keywordPlus | CANCER CELLS | - |
dc.subject.keywordPlus | ANGIOGENESIS | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordAuthor | Higd | - |
dc.subject.keywordAuthor | HIF | - |
dc.subject.keywordAuthor | HRE | - |
dc.subject.keywordAuthor | Apoptosis | - |
dc.subject.keywordAuthor | Cytochrome C | - |
dc.subject.keywordAuthor | Caspase | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Cell Biology | - |
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