ArticleNature communications2018
TRIM11 activates the proteasome and promotes overall protein degradation by regulating USP14.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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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.
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Who cites it
49 citing papers in PubMed, 70 citations in OpenAlex.
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- TRIM11 potentiates antitumor immunity via inhibition of the IFN-γ/PD-L1 axis.Cell death and differentiation · 2026Article
- Ubiquitination and deubiquitination as critical modulators of NSCLC tumorigenesis and drug resistance.Discover oncology · 2026Review
- Targeted Delivery of Schisandrin A to Cardiac Endothelium Alleviates Myocardial Ischemia-Reperfusion Injury via Suppression of Ferroptosis.International journal of nanomedicine · 2026Article
- TRIM family proteins: dual roles in tumor immunity.Frontiers in cell and developmental biology · 2026Review
- Identification of common variants influencing risk of the three-repeat tauopathy Pick's disease: a genome wide association study.medRxiv : the preprint server for health sciences · 2025Article
- Astaxanthin inhibits hepatocellular carcinoma by targeting USP39-mediated β-catenin stabilization through deubiquitination.Scientific reports · 2025Article
- USP47 Regulates Excitatory Synaptic Plasticity and Modulates Seizures in Murine Models by Blocking Ubiquitinated AMPAR Degradation.Neuroscience bulletin · 2025Article
- A No-Brainer! The Therapeutic Potential of TRIM Proteins in Viral and Central Nervous System Diseases.Viruses · 2025Review
- Activation of the 26S Proteasome to Reduce Proteotoxic Stress and Improve the Efficacy of PROTACs.ACS pharmacology & translational science · 2025Review
- TRIM22 functions as a scaffold protein for autophagy initiation.Animal cells and systems · 2025Article
- USP14 inhibition enhances Parkin-independent mitophagy in iNeurons.Pharmacological research · 2024Article
- Emerging roles of tripartite motif family proteins (TRIMs) in breast cancer.Cancer medicine · 2024Review
- Proteotoxic stress and the ubiquitin proteasome system.Seminars in cell & developmental biology · 2024Review
- Friend or foe? Reciprocal regulation between E3 ubiquitin ligases and deubiquitinases.Biochemical Society transactions · 2024Review
- Identifying TRIM11 Upregulators as Therapeutic Targets in Alzheimer's Disease: A Bayesian Network Approach.AMIA ... Annual Symposium proceedings. AMIA Symposium · 2024Article
- Review
- Tripartite Motif Protein Family in Central Nervous System Diseases.Cellular and molecular neurobiology · 2023Review
- TRIM11 protects against tauopathies and is down-regulated in Alzheimer's disease.Science (New York, N.Y.) · 2023Article
- EETs alleviate alveolar epithelial cell senescence by inhibiting endoplasmic reticulum stress through the Trim25/Keap1/Nrf2 axis.Redox biology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The proteasome is a complex protease critical for protein quality control and cell regulation, and its dysfunction is associated with cancer and other diseases. However, the mechanisms that control proteasome activity in normal and malignant cells remain unclear. Here we report that TRIM11 enhances degradation of aberrant and normal regulatory proteins, and augments overall rate of proteolysis. Mechanistically, TRIM11 binds to both the proteasome and USP14, a deubiquitinase that prematurely removes ubiquitins from proteasome-bound substrates and also noncatalytically inhibits the proteasome, and precludes their association, thereby increasing proteasome activity. TRIM11 promotes cell survival and is upregulated upon heat shock. Moreover, TRIM11 is required for tumor growth, and increased expression of TRIM11 correlates with poor clinical survival. These findings identify TRIM11 as an important activator of the proteasome, define a pathway that adjusts proteasome activity, and reveal a mechanism by which tumor cells acquire higher degradative power to support oncogenic growth.
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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.