A different pathway in the endoplasmic reticulum stress‐induced expression of human HRD1 and SEL1 genes
Copyright policy )A different pathway in the endoplasmic reticulum stress‐induced expression of human HRD1 and SEL1 genes
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.
- Yokohama College of Pharmacy Japan
- Hokkaido University Japan
- Chiba Institute of Science Japan
- Yokohama University of Pharmacy Japan
- Hokkaido Bunkyo University Japan
Ubiquitin-Protein Ligases, Membrane Proteins, Proteins, ERAD, Protein Serine-Threonine Kinases, Endoplasmic Reticulum, 499, XBP1, Cell Line, HRD1, Gene Expression Regulation, Endoribonucleases, Mutation, SEL1, Humans, ER stress, ATF6, Promoter Regions, Genetic, Gene Deletion, Signal Transduction
Ubiquitin-Protein Ligases, Membrane Proteins, Proteins, ERAD, Protein Serine-Threonine Kinases, Endoplasmic Reticulum, 499, XBP1, Cell Line, HRD1, Gene Expression Regulation, Endoribonucleases, Mutation, SEL1, Humans, ER stress, ATF6, Promoter Regions, Genetic, Gene Deletion, Signal Transduction
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