ReviewBiochemical Society transactions2021
It's not just a phase; ubiquitination in cytosolic protein quality control.
Review in Biochemical Society transactions, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
13 citing papers in PubMed, 20 citations in OpenAlex.
- Turnover of missense mutant cytosolic proteins proceeds in the absence of major quality control E3 ligases.microPublication biology · 2026Article
- Linked-domain inhibitors designed to block UBE2D induce the unfolded protein response.Cell chemical biology · 2025Article
- Proteostasis and protein quality control in chloroplasts: mechanisms and novel insights related to protein mislocalization.Journal of experimental botany · 2025Review
- Challenges and opportunities in mRNA vaccine development against bacteria.Nature microbiology · 2025Review
- Design of linked-domain protein inhibitors of UBE2D as tools to study cellular ubiquitination.bioRxiv : the preprint server for biology · 2024Article
- Cytoplasmic redox imbalance in the thioredoxin system activates Hsf1 and results in hyperaccumulation of the sequestrase Hsp42 with misfolded proteins.Molecular biology of the cell · 2024Article
- UBE2J1 is the E2 ubiquitin-conjugating enzyme regulating androgen receptor degradation and antiandrogen resistance.Oncogene · 2024Article
- An Overview of the Deubiquitinase USP53: A Promising Diagnostic Marker and Therapeutic Target.Current protein & peptide science · 2024Review
- Elucidation of Site-Specific Ubiquitination on Chaperones in Response to Mutant Huntingtin.Cellular and molecular neurobiology · 2023Article
- Linear ubiquitination induces NEMO phase separation to activate NF-κB signaling.Life science alliance · 2023Article
- Top-Down Proteomics and Comparative 2D-DIGE Analysis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Modulating the Ubiquitin-Proteasome System: A Therapeutic Strategy for Autoimmune Diseases.Cells · 2022Review
- The San1 Ubiquitin Ligase Avidly Recognizes Misfolded Proteins through Multiple Substrate Binding Sites.Biomolecules · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
The accumulation of misfolded proteins is associated with numerous degenerative conditions, cancers and genetic diseases. These pathological imbalances in protein homeostasis (termed proteostasis), result from the improper triage and disposal of damaged and defective proteins from the cell. The ubiquitin-proteasome system is a key pathway for the molecular control of misfolded cytosolic proteins, co-opting a cascade of ubiquitin ligases to direct terminally damaged proteins to the proteasome via modification with chains of the small protein, ubiquitin. Despite the evidence for ubiquitination in this critical pathway, the precise complement of ubiquitin ligases and deubiquitinases that modulate this process remains under investigation. Whilst chaperones act as the first line of defence against protein misfolding, the ubiquitination machinery has a pivotal role in targeting terminally defunct cytosolic proteins for destruction. Recent work points to a complex assemblage of chaperones, ubiquitination machinery and subcellular quarantine as components of the cellular arsenal against proteinopathies. In this review, we examine the contribution of these pathways and cellular compartments to the maintenance of the cytosolic proteome. Here we will particularly focus on the ubiquitin code and the critical enzymes which regulate misfolded proteins in the cytosol, the molecular point of origin for many neurodegenerative and genetic diseases.
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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.