Transcriptomic responses to SEL1L-HRD1 ERAD deficiency in HEK293T cells and mouse brown adipose tissue
The mamallian SEL1L-HRD1 endoplasmic reticulum-associated degradation (ERAD) complex is essential for retrotranslocation and degradatin of misfolded proteins in the ER. HRD1 is an E3-ligase with multiple transmembrane domains that consititute the retrotranslocation channel, while its cofactor SEL1L is responsible for the stability of the complex and for substrate recruitment. This study aims to identify transcriptionally-regulated genes responding to SEL1L-HRD1 ERAD deficiency in two different mammalian cell types. Overall design: Transcript abundance in wildtype, SEL1L and HRD1 (SYVN1) knockout HEK293T cells generated using CRISPR-Cas9 technology and in brown adipose tissue (BAT) from 12-week-old wildtype, Sel1l flox/flox;Ucp1-Cre and Syvn1 flox/flox;Ucp1-Cre C57BL/6J mice measured by RNA-seq.