| http://purl.uniprot.org/citations/28067262 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28067262 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28067262 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.org/dc/terms/identifier | "doi:10.1038/srep39887"xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.org/dc/terms/identifier | "doi:10.1038/srep39887"xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Kim J."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Kim J."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Kim J.Y."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Kim J.Y."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Lee M.G."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Lee M.G."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Kweon H.S."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Kweon H.S."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Noh S.H."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Noh S.H."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Piao H."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/author | "Piao H."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/name | "Sci. Rep."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/name | "Sci. Rep."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/pages | "39887"xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/pages | "39887"xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/title | "Sec16A is critical for both conventional and unconventional secretion of CFTR."xsd:string |
| http://purl.uniprot.org/citations/28067262 | http://purl.uniprot.org/core/title | "Sec16A is critical for both conventional and unconventional secretion of CFTR."xsd:string |