ArticleMolecular biology of the cell2013
A deubiquitinase negatively regulates retro-translocation of nonubiquitinated substrates.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Renal Ischemia Induces Endoplasmic Reticulum Stress and Impairs the Reparative Potency of Scattered Tubular-Like Cells.American journal of nephrology · 2025Article
- Elucidation of the late steps in the glycan-dependent ERAD of soluble misfolded glycoproteins.The Plant journal : for cell and molecular biology · 2025Article
- The role of ubiquitination in health and disease.MedComm · 2024Review
- The ubiquitin thioesterase YOD1 ameliorates mutant Huntingtin induced pathology in Drosophila.Scientific reports · 2023Article
- The deubiquitinase OTUD1 regulates immunoglobulin production and proteasome inhibitor sensitivity in multiple myeloma.Nature communications · 2022Article
- Deubiquitinases in Neurodegeneration.Cells · 2022Review
- The Roles of the Ubiquitin-Proteasome System in the Endoplasmic Reticulum Stress Pathway.International journal of molecular sciences · 2021Review
- 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
- Article
- Toxins Utilize the Endoplasmic Reticulum-Associated Protein Degradation Pathway in Their Intoxication Process.International journal of molecular sciences · 2019Review
- Crosstalk Between Mammalian Autophagy and the Ubiquitin-Proteasome System.Frontiers in cell and developmental biology · 2018Review
- Article
- The evolving role of ubiquitin modification in endoplasmic reticulum-associated degradation.The Biochemical journal · 2017Review
- Intracellular trafficking of bacterial toxins.Current opinion in cell biology · 2016Review
- Endoplasmic Reticulum-Associated Degradation and Lipid Homeostasis.Annual review of nutrition · 2016Review
- The VCP/p97 and YOD1 Proteins Have Different Substrate-dependent Activities in Endoplasmic Reticulum-associated Degradation (ERAD).The Journal of biological chemistry · 2015Article
- A bacterial toxin and a nonenveloped virus hijack ER-to-cytosol membrane translocation pathways to cause disease.Critical reviews in biochemistry and molecular biology · 2015Review
- Ongoing controversies surrounding cardiac remodeling: is it black and white-or rather fifty shades of gray?Frontiers in physiology · 2015Review
- Co- and post-translocation roles for HSP90 in cholera Intoxication.The Journal of biological chemistry · 2014Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) membrane-bound E3 ubiquitin ligases promote ER-associated degradation (ERAD) by ubiquitinating a retro-translocated substrate that reaches the cytosol from the ER, targeting it to the proteasome for destruction. Recent findings implicate ERAD-associated deubiquitinases (DUBs) as positive and negative regulators during ERAD, reflecting the different consequences of deubiquitinating a substrate prior to proteasomal degradation. These observations raise the question of whether a DUB can control the fate of a nonubiquitinated ERAD substrate. In this study, we probed the role of the ERAD-associated DUB, YOD1, during retro-translocation of the nonubiquitinated cholera toxin A1 (CTA1) peptide, a critical intoxication step. Through combining knockdown, overexpression, and binding studies, we demonstrated that YOD1 negatively controls CTA1 retro-translocation, likely by deubiquitinating and inactivating ubiquitinated ERAD components that normally promote toxin retro-translocation. YOD1 also antagonizes the proteasomal degradation of nonglycosylated pro-α factor, a postulated nonubiquitinated yeast ERAD substrate, in mammalian cells. Our findings reveal that a cytosolic DUB exerts a negative function during retro-translocation of nonubiquitinated substrates, potentially by acting on elements of the ERAD machinery.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.