Control of mammalian G protein signaling by N-terminal acetylation and the N-end rule pathway
DC Field | Value | Language |
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dc.contributor.author | Park, Sang-Eun | - |
dc.contributor.author | Kim, Jeong-Mok | - |
dc.contributor.author | Seok, Ok-Hee | - |
dc.contributor.author | Cho, Hanna | - |
dc.contributor.author | Wadas, Brandon | - |
dc.contributor.author | Kim, Seon-Young | - |
dc.contributor.author | Varshavsky, Alexander | - |
dc.contributor.author | Hwang, Cheol-Sang | - |
dc.date.accessioned | 2021-08-02T18:26:18Z | - |
dc.date.available | 2021-08-02T18:26:18Z | - |
dc.date.created | 2021-05-13 | - |
dc.date.issued | 2015-03 | - |
dc.identifier.issn | 0036-8075 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/25619 | - |
dc.description.abstract | Rgs2, a regulator of G proteins, lowers blood pressure by decreasing signaling through G alpha(q). Human patients expressing Met-Leu-Rgs2 (ML-Rgs2) or Met-Arg-Rgs2 (MR-Rgs2) are hypertensive relative to people expressing wild-type Met-Gln-Rgs2 (MQ-Rgs2). We found that wild-type MQ-Rgs2 and its mutant, MR-Rgs2, were destroyed by the Ac/N-end rule pathway, which recognizes N-alpha-terminally acetylated (Nt-acetylated) proteins. The shortest-lived mutant, ML-Rgs2, was targeted by both the Ac/N-end rule and Arg/N-end rule pathways. The latter pathway recognizes unacetylated N-terminal residues. Thus, the Nt-acetylated Ac-MX-Rgs2 (X = Arg, Gln, Leu) proteins are specific substrates of the mammalian Ac/N-end rule pathway. Furthermore, the Ac/N-degron of Ac-MQ-Rgs2 was conditional, and Teb4, an endoplasmic reticulum (ER) membrane-embedded ubiquitin ligase, was able to regulate G protein signaling by targeting Ac-MX-Rgs2 proteins for degradation through their N-alpha-terminal acetyl group. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | AMER ASSOC ADVANCEMENT SCIENCE | - |
dc.title | Control of mammalian G protein signaling by N-terminal acetylation and the N-end rule pathway | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Jeong-Mok | - |
dc.identifier.doi | 10.1126/science.aaa3844 | - |
dc.identifier.scopusid | 2-s2.0-84924769665 | - |
dc.identifier.wosid | 000350824300038 | - |
dc.identifier.bibliographicCitation | SCIENCE, v.347, no.6227, pp.1249 - 1252 | - |
dc.relation.isPartOf | SCIENCE | - |
dc.citation.title | SCIENCE | - |
dc.citation.volume | 347 | - |
dc.citation.number | 6227 | - |
dc.citation.startPage | 1249 | - |
dc.citation.endPage | 1252 | - |
dc.type.rims | ART | - |
dc.type.docType | 정기학술지(Article(Perspective Article포함)) | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | UBIQUITIN LIGASE | - |
dc.subject.keywordPlus | CELLULAR-PROTEINS | - |
dc.subject.keywordPlus | DEGRADATION | - |
dc.subject.keywordPlus | RGS2 | - |
dc.subject.keywordPlus | REGULATORS | - |
dc.subject.keywordPlus | TEB4 | - |
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