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Here, we examined the effects of <jats:styled-content style=\"fixed-case\">NSF<\/jats:styled-content> knockdown on Golgi structure and different vesicle trafficking pathways in mammalian cells. <jats:styled-content style=\"fixed-case\">NSF<\/jats:styled-content> knockdown caused Golgi fragmentation and abolished transferrin receptor exocytosis, defects that were rescued by <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>i\u2010resistant <jats:styled-content style=\"fixed-case\">NSF<\/jats:styled-content>. Strikingly, <jats:styled-content style=\"fixed-case\">NSF<\/jats:styled-content> deficiency in HeLa cells barely affected cell viability, anterograde trafficking of vesicular stomatitis virus glycoprotein G and transferrin endocytosis. These results confirm the central role of <jats:styled-content style=\"fixed-case\">NSF<\/jats:styled-content> in Golgi structure and reveal differential requirement of <jats:styled-content style=\"fixed-case\">NSF<\/jats:styled-content> for exocytic recycling and constitutive trafficking pathways.<\/jats:p>","DOI":"10.1002\/1873-3468.12532","type":"journal-article","created":{"date-parts":[[2016,12,20]],"date-time":"2016-12-20T07:43:01Z","timestamp":1482219781000},"page":"273-281","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Differential requirement for <i>N<\/i>\u2010ethylmaleimide\u2010sensitive factor in endosomal trafficking of transferrin receptor from anterograde trafficking of vesicular stomatitis virus glycoprotein G"],"prefix":"10.1002","volume":"591","author":[{"given":"Jiannan","family":"Fan","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering Key Laboratory of Biomedical 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