HtrA2/Omi influences the stability of LON protease 1 and prohibitin, proteins involved in mitochondrial homeostasis
DC Field | Value | Language |
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dc.contributor.author | Goo, Hui-Gwan | - |
dc.contributor.author | Rhim, Hyangshuk | - |
dc.contributor.author | Kang, Seongman | - |
dc.date.accessioned | 2021-09-05T03:07:46Z | - |
dc.date.available | 2021-09-05T03:07:46Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2014-11-01 | - |
dc.identifier.issn | 0014-4827 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/96812 | - |
dc.description.abstract | High temperature requirement A2 (HtrA2)/Omi is a serine protease localized in mitochondria. In response to apoptotic stimuli, HtrA2 is released to the cytoplasm and cleaves many proteins, including XIAP, Apollon/BRUCE, WT1, and Ped/Pea-15, to promote apoptosis. However, the function of HtrA2 in mitochondria under normal conditions remains unclear. Here, we show that the mitochondrial proteins, LON protease 1 (LONP1) and prohibitin (PHB), are overexpressed in HtrA2(-/-) mouse embryonic fibroblast (MEF) cells and HtrA2 knock-down HEK293T cells. We also confirm the effect of the HtrA2 protease on the stability of the above mitochondrial quality control proteins in motor neuron degeneration 2 (mnd2) mice, which have a greatly reduced protease activity as a result of a Ser276Cys missense mutation of the HtrA2 gene. In addition, PHB interacts with and is directly cleaved by HtrA2. Luminescence assays demonstrate that the intracellular ATP level is decreased in HtrA2(-/-) cells compared to HtrA2(+/+) cells. HtrA2 deficiency causes a decrease in the mitochondrial membrane potential, and reactive oxygen species (ROS) generation is greater in HtrA2(-/-) cells than in HtrA2(+/+) cells. Our results implicate that HtrA2 might be an upstream regulator of mitochondrial homeostasis. (C) 2014 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER INC | - |
dc.subject | SERINE-PROTEASE | - |
dc.subject | CELL-DEATH | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | ATP | - |
dc.subject | BINDING | - |
dc.subject | PINK1 | - |
dc.subject | BETA | - |
dc.subject | NEURODEGENERATION | - |
dc.subject | ACCUMULATION | - |
dc.subject | APOPTOSIS | - |
dc.title | HtrA2/Omi influences the stability of LON protease 1 and prohibitin, proteins involved in mitochondrial homeostasis | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kang, Seongman | - |
dc.identifier.doi | 10.1016/j.yexcr.2014.07.032 | - |
dc.identifier.scopusid | 2-s2.0-84908237888 | - |
dc.identifier.wosid | 000343953500022 | - |
dc.identifier.bibliographicCitation | EXPERIMENTAL CELL RESEARCH, v.328, no.2, pp.456 - 465 | - |
dc.relation.isPartOf | EXPERIMENTAL CELL RESEARCH | - |
dc.citation.title | EXPERIMENTAL CELL RESEARCH | - |
dc.citation.volume | 328 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 456 | - |
dc.citation.endPage | 465 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | SERINE-PROTEASE | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | ATP | - |
dc.subject.keywordPlus | BINDING | - |
dc.subject.keywordPlus | PINK1 | - |
dc.subject.keywordPlus | BETA | - |
dc.subject.keywordPlus | NEURODEGENERATION | - |
dc.subject.keywordPlus | ACCUMULATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordAuthor | HtrA2 | - |
dc.subject.keywordAuthor | Mitochondria | - |
dc.subject.keywordAuthor | Mnd2 | - |
dc.subject.keywordAuthor | Protein quality control | - |
dc.subject.keywordAuthor | PHB | - |
dc.subject.keywordAuthor | Mitochondrial homeostasis | - |
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