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Sec16A is critical for both conventional and unconventional secretion of CFTR

DC FieldValueLanguage
dc.contributor.author김주영-
dc.contributor.author김지윤-
dc.contributor.author노신혜-
dc.contributor.author박학-
dc.contributor.author이민구-
dc.date.accessioned2017-11-02T08:06:50Z-
dc.date.available2017-11-02T08:06:50Z-
dc.date.issued2017-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/154094-
dc.description.abstractCFTR 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.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.languageEnglish-
dc.publisherNature Publishing Group-
dc.relation.isPartOfSCIENTIFIC REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleSec16A is critical for both conventional and unconventional secretion of CFTR-
dc.typeArticle-
dc.publisher.locationEngland-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Pharmacology-
dc.contributor.googleauthorHe Piao-
dc.contributor.googleauthorJiyoon Kim-
dc.contributor.googleauthorShin Hye Noh-
dc.contributor.googleauthorHee-Seok Kweon-
dc.contributor.googleauthorJoo Young Kim-
dc.contributor.googleauthorMin Goo Lee-
dc.identifier.doi10.1038/srep39887.-
dc.contributor.localIdA04545-
dc.contributor.localIdA01285-
dc.contributor.localIdA05131-
dc.contributor.localIdA02781-
dc.contributor.localIdA00942-
dc.relation.journalcodeJ02646-
dc.identifier.eissn2045-2322-
dc.identifier.pmid28067262-
dc.contributor.alternativeNameKim, Joo Young-
dc.contributor.alternativeNameKim, Ji Yoon-
dc.contributor.alternativeNameNoh, Shin Hye-
dc.contributor.alternativeNamePiao, He-
dc.contributor.alternativeNameLee, Min Goo-
dc.contributor.affiliatedAuthorKim, Ji Yoon-
dc.contributor.affiliatedAuthorNoh, Shin Hye-
dc.contributor.affiliatedAuthorPiao, He-
dc.contributor.affiliatedAuthorLee, Min Goo-
dc.contributor.affiliatedAuthorKim, Joo Young-
dc.citation.titleScientific Reports-
dc.citation.volume7-
dc.citation.startPage39887-
dc.identifier.bibliographicCitationSCIENTIFIC REPORTS, Vol.7 : 39887, 2017-
dc.date.modified2017-11-01-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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