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Sec16A is critical for both conventional and unconventional secretion of CFTR
DC Field | Value | Language |
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dc.contributor.author | 김주영 | - |
dc.contributor.author | 김지윤 | - |
dc.contributor.author | 노신혜 | - |
dc.contributor.author | 박학 | - |
dc.contributor.author | 이민구 | - |
dc.date.accessioned | 2017-11-02T08:06:50Z | - |
dc.date.available | 2017-11-02T08:06:50Z | - |
dc.date.issued | 2017 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/154094 | - |
dc.description.abstract | CFTR is a transmembrane protein that reaches the cell surface via the conventional Golgi mediated secretion pathway. Interestingly, ER-to-Golgi blockade or ER stress induces alternative GRASP-mediated, Golgi-bypassing unconventional trafficking of wild-type CFTR and the disease-causing ΔF508-CFTR, which has folding and trafficking defects. Here, we show that Sec16A, the key regulator of conventional ER-to-Golgi transport, plays a critical role in the ER exit of protein cargos during unconventional secretion. In an initial gene silencing screen, Sec16A knockdown abolished the unconventional secretion of wild-type and ΔF508-CFTR induced by ER-to-Golgi blockade, whereas the knockdown of other COPII-related components did not. Notably, during unconventional secretion, Sec16A was redistributed to cell periphery and associated with GRASP55 in mammalian cells. Molecular and morphological analyses revealed that IRE1α-mediated signaling is an upstream regulator of Sec16A during ER-to-Golgi blockade or ER stress associated unconventional secretion. These findings highlight a novel function of Sec16A as an essential mediator of ER stress-associated unconventional secretion. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.language | English | - |
dc.publisher | Nature Publishing Group | - |
dc.relation.isPartOf | SCIENTIFIC REPORTS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Sec16A is critical for both conventional and unconventional secretion of CFTR | - |
dc.type | Article | - |
dc.publisher.location | England | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Pharmacology | - |
dc.contributor.googleauthor | He Piao | - |
dc.contributor.googleauthor | Jiyoon Kim | - |
dc.contributor.googleauthor | Shin Hye Noh | - |
dc.contributor.googleauthor | Hee-Seok Kweon | - |
dc.contributor.googleauthor | Joo Young Kim | - |
dc.contributor.googleauthor | Min Goo Lee | - |
dc.identifier.doi | 10.1038/srep39887. | - |
dc.contributor.localId | A04545 | - |
dc.contributor.localId | A01285 | - |
dc.contributor.localId | A05131 | - |
dc.contributor.localId | A02781 | - |
dc.contributor.localId | A00942 | - |
dc.relation.journalcode | J02646 | - |
dc.identifier.eissn | 2045-2322 | - |
dc.identifier.pmid | 28067262 | - |
dc.contributor.alternativeName | Kim, Joo Young | - |
dc.contributor.alternativeName | Kim, Ji Yoon | - |
dc.contributor.alternativeName | Noh, Shin Hye | - |
dc.contributor.alternativeName | Piao, He | - |
dc.contributor.alternativeName | Lee, Min Goo | - |
dc.contributor.affiliatedAuthor | Kim, Ji Yoon | - |
dc.contributor.affiliatedAuthor | Noh, Shin Hye | - |
dc.contributor.affiliatedAuthor | Piao, He | - |
dc.contributor.affiliatedAuthor | Lee, Min Goo | - |
dc.contributor.affiliatedAuthor | Kim, Joo Young | - |
dc.citation.title | Scientific Reports | - |
dc.citation.volume | 7 | - |
dc.citation.startPage | 39887 | - |
dc.identifier.bibliographicCitation | SCIENTIFIC REPORTS, Vol.7 : 39887, 2017 | - |
dc.date.modified | 2017-11-01 | - |
dc.identifier.rimsid | 41590 | - |
dc.type.rims | ART | - |
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