Abstract
Human HRD1 and SEL1 are components of endoplasmic reticulum-associated degradation (ERAD), which is a retrograde transport mechanism from the ER to the cytosol for removing unfolded proteins. The expression of HRD1 and SEL1 was induced by ER stress-inducing agents and overexpression of both ER stress-responsive transcription factors, ATF6 and XBP1. Inhibition of IRE1 and ATF6 revealed that ER stress-induced HRD1 and SEL1 expressions are mediated by IRE1-XBP1- and ATF6-dependent pathways, respectively. These results suggest that the ER stress-induced ERAD gene expressions are mediated by different pathways, which are attributed to the differences in the promoter regions.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line
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Endoplasmic Reticulum / metabolism*
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Endoribonucleases / antagonists & inhibitors
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Endoribonucleases / metabolism
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Gene Deletion
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Gene Expression Regulation*
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Humans
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Membrane Proteins / antagonists & inhibitors
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Membrane Proteins / metabolism
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Mutation / genetics
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Promoter Regions, Genetic / genetics
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Protein Serine-Threonine Kinases / antagonists & inhibitors
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Protein Serine-Threonine Kinases / metabolism
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Proteins / genetics
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Proteins / metabolism*
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Signal Transduction*
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Ubiquitin-Protein Ligases / genetics
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Ubiquitin-Protein Ligases / metabolism*
Substances
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Membrane Proteins
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Proteins
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SEL1L protein, human
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SYVN1 protein, human
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Ubiquitin-Protein Ligases
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ERN2 protein, human
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Protein Serine-Threonine Kinases
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Endoribonucleases