Abstract
Production of a vesicular stomatitis virus spike protein G (VSVG)-pseudotyped lentiviral expression vector in HEK293 cells decreased on overexpression of low-density lipoprotein receptor (LDLR) but not that of ICAM1 or TfR1. Reverse transcription-quantitative PCR (RT-qPCR) revealed a reduction in vector RNA as a function of LDLR expression. Decreased syncytium formation suggested diminished surface expression of VSVG. Intracellular VSVG granules colocalized with LDLR, ER-Golgi intermediate compartment protein 53 (ERGIC53), LAMP2, and vimentin but not with GM130 or calnexin, suggesting that VSVG interacts with LDLR within the ERGIC, resulting in rerouting into the aggresome/autophagosome pathway.
Copyright © 2015, American Society for Microbiology. All Rights Reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigens, CD / biosynthesis
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Autoantigens / metabolism
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Calnexin / metabolism
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Cell Line
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Giant Cells / cytology
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HEK293 Cells
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Humans
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Intercellular Adhesion Molecule-1 / biosynthesis
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Lentivirus / genetics
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Lentivirus / metabolism
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Lysosomal-Associated Membrane Protein 2 / metabolism
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Mannose-Binding Lectins / metabolism
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Membrane Glycoproteins / biosynthesis*
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Membrane Glycoproteins / genetics
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Membrane Proteins / metabolism
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Receptors, LDL / biosynthesis*
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Receptors, Transferrin / biosynthesis
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Vesicular stomatitis Indiana virus / metabolism*
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Vimentin / metabolism
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Viral Envelope Proteins / biosynthesis*
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Viral Envelope Proteins / genetics
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Virus Release / physiology*
Substances
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Antigens, CD
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Autoantigens
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CD71 antigen
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G protein, vesicular stomatitis virus
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Golgin subfamily A member 2
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ICAM1 protein, human
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LAMP2 protein, human
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LMAN1 protein, human
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Lysosomal-Associated Membrane Protein 2
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Mannose-Binding Lectins
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Membrane Glycoproteins
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Membrane Proteins
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Receptors, LDL
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Receptors, Transferrin
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Vimentin
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Viral Envelope Proteins
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Intercellular Adhesion Molecule-1
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Calnexin