ArticleThe Journal of biological chemistry2015
The VCP/p97 and YOD1 Proteins Have Different Substrate-dependent Activities in Endoplasmic Reticulum-associated Degradation (ERAD).
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- OTU deubiquitinases in disease: roles and targeting.Trends in molecular medicine · 2026Review
- The Immunoregulatory Mechanisms of Human Cytomegalovirus from Primary Infection to Reactivation.Pathogens (Basel, Switzerland) · 2025Review
- Role of Endoplasmic Reticulum Stress-Associated Genes in Septic Neonatal Foals.Antioxidants (Basel, Switzerland) · 2025Article
- Regulation of disease signaling by YOD1: potential implications for therapeutic strategies.Cancer cell international · 2025Review
- YOD1 sustains NOD2-mediated protective signaling in colitis by stabilizing RIPK2.EMBO reports · 2024Article
- Endoplasmic reticulum stress and quality control in relation to cisplatin resistance in tumor cells.Frontiers in pharmacology · 2024Review
- The ubiquitin thioesterase YOD1 ameliorates mutant Huntingtin induced pathology in Drosophila.Scientific reports · 2023Article
- Valosin containing protein (VCP): initiator, modifier, and potential drug target for neurodegenerative diseases.Molecular neurodegeneration · 2023Review
- Ubiquitin-modifying enzymes in Huntington's disease.Frontiers in molecular biosciences · 2023Review
- Identification of potential diagnostic and prognostic biomarkers for sepsis based on machine learning.Computational and structural biotechnology journal · 2023Article
- p97/UBXD1 Generate Ubiquitylated Proteins That Are Sequestered into Nuclear Envelope Herniations in Torsin-Deficient Cells.International journal of molecular sciences · 2022Article
- Article
- Identification of two rate-limiting steps in the degradation of partially folded immunoglobulin light chains.Frontiers in cell and developmental biology · 2022Article
- How Viruses Use the VCP/p97 ATPase Molecular Machine.Viruses · 2021Review
- Mutations and Protein Interaction Landscape Reveal Key Cellular Events Perturbed in Upper Motor Neurons with HSP and PLS.Brain sciences · 2021Article
- Increased BST-2 expression by HBV infection promotes HBV-associated HCC tumorigenesis.Journal of gastrointestinal oncology · 2021Article
- Long Non-coding RNA FIRRE Acts as a miR-520a-3p Sponge to Promote Gallbladder Cancer Progression via Mediating YOD1 Expression.Frontiers in genetics · 2021Article
- BiP/GRP78 Mediates ERAD Targeting of Proteins Produced by Membrane-Bound Ribosomes Stalled at the STOP-Codon.Journal of molecular biology · 2019Article
- Isolation of secreted proteins from Drosophila ovaries and embryos through in vivo BirA-mediated biotinylation.PloS one · 2019Article
- Valosin-Containing Protein/p97 as a Novel Therapeutic Target in Acute Lymphoblastic Leukemia.Neoplasia (New York, N.Y.) · 2017Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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