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dc.contributor.authorMorishita, Hideaki
dc.contributor.authorZhao, Yan G.
dc.contributor.authorTamura, Norito
dc.contributor.authorNishimura, Taki
dc.contributor.authorKanda, Yuki
dc.contributor.authorSakamaki, Yuriko
dc.contributor.authorOkazaki, Mitsuyo
dc.contributor.authorLi, Dongfang
dc.contributor.authorMizushima, Noboru
dc.date2022-08-11T08:09:54.000
dc.date.accessioned2022-08-23T16:48:00Z
dc.date.available2022-08-23T16:48:00Z
dc.date.issued2019-09-17
dc.date.submitted2019-10-15
dc.identifier.citation<p>Elife. 2019 Sep 17;8. pii: 48834. doi: 10.7554/eLife.48834. <a href="https://doi.org/10.7554/eLife.48834">Link to article on publisher's site</a></p>
dc.identifier.issn2050-084X (Linking)
dc.identifier.doi10.7554/eLife.48834
dc.identifier.pmid31526472
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41189
dc.description.abstractLipoproteins are lipid-protein complexes that are primarily generated and secreted from the intestine, liver, and visceral endoderm and delivered to peripheral tissues. Lipoproteins, which are assembled in the endoplasmic reticulum (ER) membrane, are released into the ER lumen for secretion, but its mechanism remains largely unknown. Here, we show that the release of lipoproteins from the ER membrane requires VMP1, an ER transmembrane protein essential for autophagy and certain types of secretion. Loss of vmp1, but not other autophagy-related genes, in zebrafish causes lipoprotein accumulation in the intestine and liver. Vmp1 deficiency in mice also leads to lipid accumulation in the visceral endoderm and intestine. In VMP1-depleted cells, neutral lipids accumulate within lipid bilayers of the ER membrane, thus affecting lipoprotein secretion. These results suggest that VMP1 is important for the release of lipoproteins from the ER membrane to the ER lumen in addition to its previously known functions.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=31526472&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2019, Morishita et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectVMP1
dc.subjectautophagy-related gene
dc.subjectcell biology
dc.subjectendoplasmic reticulum
dc.subjecthuman
dc.subjectlipoprotein
dc.subjectmouse
dc.subjectzebrafish
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectLipids
dc.titleA critical role of VMP1 in lipoprotein secretion
dc.typeJournal Article
dc.source.journaltitleeLife
dc.source.volume8
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4994&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3977
dc.identifier.contextkey15556538
refterms.dateFOA2022-08-23T16:48:00Z
html.description.abstract<p>Lipoproteins are lipid-protein complexes that are primarily generated and secreted from the intestine, liver, and visceral endoderm and delivered to peripheral tissues. Lipoproteins, which are assembled in the endoplasmic reticulum (ER) membrane, are released into the ER lumen for secretion, but its mechanism remains largely unknown. Here, we show that the release of lipoproteins from the ER membrane requires VMP1, an ER transmembrane protein essential for autophagy and certain types of secretion. Loss of vmp1, but not other autophagy-related genes, in zebrafish causes lipoprotein accumulation in the intestine and liver. Vmp1 deficiency in mice also leads to lipid accumulation in the visceral endoderm and intestine. In VMP1-depleted cells, neutral lipids accumulate within lipid bilayers of the ER membrane, thus affecting lipoprotein secretion. These results suggest that VMP1 is important for the release of lipoproteins from the ER membrane to the ER lumen in addition to its previously known functions.</p>
dc.identifier.submissionpathoapubs/3977
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pagese48834


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Copyright © 2019, Morishita et al.  This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright © 2019, Morishita et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.