ReviewCell death and differentiation2020
TRIM proteins in autophagy: selective sensors in cell damage and innate immune responses.
Review in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
116 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.
- [Advances of TRIM superfamily proteins in chronic liver disease and hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022Pooled it
- The microbiota-proteostasis axis: implications in neurodegenerative diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- TRIM37 interacts with TRIM28 to maintain primordial germ cell identity during migration.Cell research · 2026Article
- A role for CASM in the repair of damaged Golgi architecture.Autophagy · 2026Article
- [CHOP promotes hepatocyte pyroptosis by downregulating endoplasmic reticulophagy and enhancing endoplasmic reticulum-mitochondria interaction].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- TRIM Expression and Its Association With Disease Activity in Systemic Lupus Erythematosus.The Kaohsiung journal of medical sciences · 2026Article
- Elevated TRIM25 Impairs Poly (ADP-ribose) Metabolism via PARG Degradation and Mediates Compression-Induced Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TRIM11 potentiates antitumor immunity via inhibition of the IFN-γ/PD-L1 axis.Cell death and differentiation · 2026Article
- TRIM21 promotes astrocyte-mediated neuroinflammation in experimental autoimmune encephalomyelitis by stabilizing RGMa via K33-linked ubiquitination.Journal of neuroinflammation · 2026Article
- TRIM7-mediated autophagy-lysosomal signaling is essential for preimplantation development in mice.Journal of translational medicine · 2026Article
- P2X7R deficiency alleviates cardiac senescence by enhancing mitophagy via the HuR/TRIM26/NR4A1 axis.Clinical and translational medicine · 2026Article
- TRIM38 Suppresses Breast Cancer Progression via Modulating SQSTM1 Ubiquitination and Autophagic Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tenuigenin targets Trim31 and NF-κB pathway to protect dopaminergic neurons in Parkinson's disease mice.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- MacrophageAutophagy · 2025Article
- The role of TRIM proteins in the pathogenesis of mycobacterium tuberculosis.Biology direct · 2025Review
- The dynamic role of TRIM8, a novel ciliary protein, during various stages of mitosis.Cell death & disease · 2025Article
- IRGM Inhibits the AKT/mTOR Signaling Pathway by Interacting with TRIM21 to Alleviate Sepsis-Induced Acute Lung Injury.Inflammation · 2025Article
- A role for CASM in the repair of damaged Golgi architecture.bioRxiv : the preprint server for biology · 2025Article
- Research and development prospects of TRIM65.Journal of cancer research and clinical oncology · 2025Review
- TRIM21-driven K63-linked ubiquitination of RBM38c, as a novel interactor of BECN1, contributes to DNA damage-induced autophagy.Cell death and differentiation · 2025Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy, a main intracellular catabolic process, is induced in response to a variety of cellular stresses to promptly degrade harmful agents and to coordinate the activity of prosurvival and prodeath processes in order to determine the fate of the injured cells. While the main components of the autophagy machinery are well characterized, the molecular mechanisms that confer selectivity to this process both in terms of stress detection and cargo engulfment have only been partly elucidated. Here, we discuss the emerging role played by the E3 ubiquitin ligases of the TRIM family in regulating autophagy in physiological and pathological conditions, such as inflammation, infection, tumorigenesis, and muscle atrophy. TRIM proteins employ different strategies to regulate the activity of the core autophagy machinery, acting either as scaffold proteins or via ubiquitin-mediated mechanisms. Moreover, they confer high selectivity to the autophagy-mediated degradation as described for the innate immune response, where TRIM proteins mediate both the engulfment of pathogens within autophagosomes and modulate the immune response by controlling the stability of signaling regulators. Importantly, the elucidation of the molecular mechanisms underlying the regulation of autophagy by TRIMs is providing important insights into how selective types of autophagy are altered under pathological conditions, as recently shown in cancer and muscular dystrophy.
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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.