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- W2275023455 abstract "Endoplasmic reticulum-associated degradation (ERAD) is an essential quality control mechanism of the folding state of proteins in the secretory pathway that targets unfolded/misfolded polypeptides for proteasomal degradation. The cytosolic p97/valosin-containing protein is an essential ATPase for degradation of ERAD substrates. It has been considered necessary during retro-translocation to extract proteins from the endoplasmic reticulum that are otherwise supposed to accumulate in the endoplasmic reticulum lumen. The activity of the p97-associated deubiquitinylase YOD1 is also required for substrate disposal. We used the in vivo biotinylation retro-translocation assay in mammalian cells under conditions of impaired p97 or YOD1 activity to directly discriminate their requirements and diverse functions in ERAD. Using different ERAD substrates, we found that both proteins participate in two distinct retro-translocation steps. For CD4 and MHC-Iα, which are induced to degradation by the HIV-1 protein Vpu and by the CMV immunoevasins US2 and US11, respectively, p97 and YOD1 have a retro-translocation-triggering role. In contrast, for three other spontaneous ERAD model substrates (NS1, NHK-α1AT, and BST-2/Tetherin), p97 and YOD1 are required in the downstream events of substrate deglycosylation and proteasomal degradation." @default.
- W2275023455 created "2016-06-24" @default.
- W2275023455 creator A5001029192 @default.
- W2275023455 creator A5040546254 @default.
- W2275023455 creator A5045650524 @default.
- W2275023455 creator A5067832764 @default.
- W2275023455 date "2015-11-01" @default.
- W2275023455 modified "2023-10-18" @default.
- W2275023455 title "The VCP/p97 and YOD1 Proteins Have Different Substrate-dependent Activities in Endoplasmic Reticulum-associated Degradation (ERAD)" @default.
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- W2275023455 doi "https://doi.org/10.1074/jbc.m115.656660" @default.
- W2275023455 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4653676" @default.
- W2275023455 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26463207" @default.
- W2275023455 hasPublicationYear "2015" @default.
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