DC Field | Value | Language |
---|---|---|
dc.contributor.author | Song, Sungmin | ko |
dc.contributor.author | Lee, Huikyong | ko |
dc.contributor.author | Kam, Tae-In | ko |
dc.contributor.author | Tai, Mei Ling | ko |
dc.contributor.author | Lee, Joo-Yong | ko |
dc.contributor.author | Noh, Jee-Yeon | ko |
dc.contributor.author | Shim, Sang Mi | ko |
dc.contributor.author | Seo, Soo Jung | ko |
dc.contributor.author | Kong, Young-Yun | ko |
dc.contributor.author | Nakagawa, Toshiyuki | ko |
dc.contributor.author | Chung, Chul-Woong | ko |
dc.contributor.author | Choi, Deog-Young | ko |
dc.contributor.author | Oubrahim, Hammou | ko |
dc.contributor.author | Jung, Yong-Keun | ko |
dc.date.accessioned | 2023-05-04T07:01:18Z | - |
dc.date.available | 2023-05-04T07:01:18Z | - |
dc.date.created | 2023-05-04 | - |
dc.date.created | 2023-05-04 | - |
dc.date.issued | 2008-08 | - |
dc.identifier.citation | JOURNAL OF CELL BIOLOGY, v.182, no.4, pp.675 - 684 | - |
dc.identifier.issn | 0021-9525 | - |
dc.identifier.uri | http://hdl.handle.net/10203/306630 | - |
dc.description.abstract | Amyloid-beta (A beta) neurotoxicity is believed to contribute to the pathogenesis of Alzheimer's disease (AD). Previously we found that E2-25K/Hip-2, an E2 ubiquitin-conjugating enzyme, mediates A beta neurotoxicity. Here, we report that E2-25K/Hip-2 modulates caspase-12 activity via the ubiquitin/proteasome system. Levels of endoplasmic reticulum (ER)-resident caspase-12 are strongly up-regulated in the brains of AD model mice, where the enzyme colocalizes with E2-25K/Hip-2. A beta in creases expression of E2-25K/Hip-2, which then stabilizes caspase-12 protein by inhibiting proteasome activity. This increase in E2-25K/Hip-2 also induces proteolytic activation of caspase-12 through its ability to induce calpainlike activity. Knockdown of E2-25K/Hip-2 expression suppresses neuronal cell death triggered by ER stress, and thus caspase-12 is required for the E2-25K/Hip-2-mediated cell death. Finally, we find that E2-25K/Hip-2-deficient cortical neurons are resistant to A beta toxicity and to the induction of ER stress and caspase-12 expression by A beta. E2-25K/Hip-2 is thus an essential upstream regulator of the expression and activation of caspase-12 in ER stress mediated A beta neurotoxicity. | - |
dc.language | English | - |
dc.publisher | ROCKEFELLER UNIV PRESS | - |
dc.title | E2-25K/Hip-2 regulates caspase-12 in ER stress-mediated A beta neurotoxicity | - |
dc.type | Article | - |
dc.identifier.wosid | 000259050000009 | - |
dc.identifier.scopusid | 2-s2.0-50249163706 | - |
dc.type.rims | ART | - |
dc.citation.volume | 182 | - |
dc.citation.issue | 4 | - |
dc.citation.beginningpage | 675 | - |
dc.citation.endingpage | 684 | - |
dc.citation.publicationname | JOURNAL OF CELL BIOLOGY | - |
dc.identifier.doi | 10.1083/jcb.200711066 | - |
dc.contributor.localauthor | Kam, Tae-In | - |
dc.contributor.nonIdAuthor | Song, Sungmin | - |
dc.contributor.nonIdAuthor | Lee, Huikyong | - |
dc.contributor.nonIdAuthor | Tai, Mei Ling | - |
dc.contributor.nonIdAuthor | Lee, Joo-Yong | - |
dc.contributor.nonIdAuthor | Noh, Jee-Yeon | - |
dc.contributor.nonIdAuthor | Shim, Sang Mi | - |
dc.contributor.nonIdAuthor | Seo, Soo Jung | - |
dc.contributor.nonIdAuthor | Kong, Young-Yun | - |
dc.contributor.nonIdAuthor | Nakagawa, Toshiyuki | - |
dc.contributor.nonIdAuthor | Chung, Chul-Woong | - |
dc.contributor.nonIdAuthor | Choi, Deog-Young | - |
dc.contributor.nonIdAuthor | Oubrahim, Hammou | - |
dc.contributor.nonIdAuthor | Jung, Yong-Keun | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.subject.keywordPlus | AMYLOID-BETA | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | PRION PROTEIN | - |
dc.subject.keywordPlus | CROSS-TALK | - |
dc.subject.keywordPlus | PROTEASOME | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | NEURODEGENERATION | - |
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