A different pathway in the endoplasmic reticulum stress-induced expression of human HRD1 and SEL1 genes

FEBS Lett. 2007 Nov 27;581(28):5355-60. doi: 10.1016/j.febslet.2007.10.033. Epub 2007 Oct 29.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Endoplasmic Reticulum / metabolism*
  • Endoribonucleases / antagonists & inhibitors
  • Endoribonucleases / metabolism
  • Gene Deletion
  • Gene Expression Regulation*
  • Humans
  • Membrane Proteins / antagonists & inhibitors
  • Membrane Proteins / metabolism
  • Mutation / genetics
  • Promoter Regions, Genetic / genetics
  • Protein Serine-Threonine Kinases / antagonists & inhibitors
  • Protein Serine-Threonine Kinases / metabolism
  • Proteins / genetics
  • Proteins / metabolism*
  • Signal Transduction*
  • Ubiquitin-Protein Ligases / genetics
  • Ubiquitin-Protein Ligases / metabolism*

Substances

  • Membrane Proteins
  • Proteins
  • SEL1L protein, human
  • SYVN1 protein, human
  • Ubiquitin-Protein Ligases
  • ERN2 protein, human
  • Protein Serine-Threonine Kinases
  • Endoribonucleases