Randomized trial reveals different pathways induce HRD1 and SEL1 gene expression during ER stress, indicating complexity in cellular responses.
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.
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Kaneko et al. (2007) studied this question.
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