ArticleeLife2019
Cycles of autoubiquitination and deubiquitination regulate the ERAD ubiquitin ligase Hrd1.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- ERO1L induces macrophage infiltration to potentiate KrasCell & bioscience · 2026Article
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- Competition between Der1 and ERAD-M substrates controls Hrd1 complex function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Lipid bilayer thinning near a ubiquitin ligase selects ER membrane proteins for degradation.bioRxiv : the preprint server for biology · 2025Article
- Article
- SEL1L-HRD1-mediated ERAD in mammals.Nature cell biology · 2025Review
- Phase Separation Clustering of Poly Ubiquitin Cargos on Ternary Mixture Lipid Membranes by Synthetically Cross-Linked Ubiquitin Binder Peptides.Biochemistry · 2025Article
- Ubiquitin protease Ubp1 cooperates with Ubp10 and Ubp12 to revert lysine-164 PCNA ubiquitylation at replication forks.Nucleic acids research · 2025Article
- Ubiquitination and De-Ubiquitination in the Synthesis of Cow Milk Fat: Reality and Prospects.Molecules (Basel, Switzerland) · 2024Review
- TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation.Cancer medicine · 2024Article
- Advances in the study of protein folding and endoplasmic reticulum-associated degradation in mammal cells.Journal of Zhejiang University. Science. B · 2024Review
- Direct observation of autoubiquitination for an integral membrane ubiquitin ligase in ERAD.Nature communications · 2024Article
- Hypomorphic variants of SEL1L-HRD1 ER-associated degradation are associated with neurodevelopmental disorders.The Journal of clinical investigation · 2024Article
- Navigating the landscape of mitochondrial-ER communication in health and disease.Frontiers in molecular biosciences · 2024Review
- Deep mutational scanning highlights a role for cytosolic regions in Hrd1 function.Cell reports · 2023Article
- Mechanisms of substrate processing during ER-associated protein degradation.Nature reviews. Molecular cell biology · 2023Review
- Involvement of Proteasomal and Endoplasmic Reticulum Stress in Neurodegeneration After Global Brain Ischemia.Molecular neurobiology · 2023Article
- Real-time bio-layer interferometry ubiquitination assays as alternatives to western blotting.Analytical biochemistry · 2023Article
- Lhs1 dependent ERAD is determined by transmembrane domain context.The Biochemical journal · 2023Article
- Accumulated precursors of specific GPI-anchored proteins upregulate GPI biosynthesis with ARV1.The Journal of cell biology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Misfolded proteins in the lumen of the endoplasmic reticulum (ER) are retrotranslocated into the cytosol and polyubiquitinated before being degraded by the proteasome. The multi-spanning ubiquitin ligase Hrd1 forms the retrotranslocation channel and associates with three other membrane proteins (Hrd3, Usa1, Der1) of poorly defined function. The Hrd1 channel is gated by autoubiquitination, but how Hrd1 escapes degradation by the proteasome and returns to its inactive ground state is unknown. Here, we show that autoubiquitination of Hrd1 is counteracted by Ubp1, a deubiquitinating enzyme that requires its N-terminal transmembrane segment for activity towards Hrd1. The Hrd1 partner Hrd3 serves as a brake for autoubiquitination, while Usa1 attenuates Ubp1's deubiquitination activity through an inhibitory effect of its UBL domain. These results lead to a model in which the Hrd1 channel is regulated by cycles of autoubiquitination and deubiquitination, reactions that are modulated by the other components of the Hrd1 complex.
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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.