Evidence map›Paper›PMID 42242206›Full record

ArticleMolecular cell2026

TRIM21 induces selective autophagy of viruses and bacteria.

Tyler Rhinesmith, Anna Albecka, Marina Vaysburd, Claudia Puri, Jakub Luptak, Jerome Boulanger, Quynh-Mai Nguyen Le, Matthew J Gratian, Kevin O'Connell, Lara Few and 4 more

Abstract read
In one paragraph

Article in Molecular cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Tyler RhinesmithMRC Laboratory of Molecular Biology, Cambridge, UK. Electronic address: rhinesmith@mrclmb.ac.uk.
Anna AlbeckaMRC Laboratory of Molecular Biology, Cambridge, UK.
Marina VaysburdMRC Laboratory of Molecular Biology, Cambridge, UK.
Claudia PuriCambridge Institute for Medical Research, Cambridge, UK; UK Dementia Research Institute, Cambridge, UK.
Jakub LuptakMRC Laboratory of Molecular Biology, Cambridge, UK.
Jerome BoulangerMRC Laboratory of Molecular Biology, Cambridge, UK.
Quynh-Mai Nguyen LeMRC Laboratory of Molecular Biology, Cambridge, UK.
Matthew J GratianCambridge Institute for Medical Research, Cambridge, UK.
Kevin O'ConnellMRC Laboratory of Molecular Biology, Cambridge, UK.
Lara FewMRC Laboratory of Molecular Biology, Cambridge, UK.
Mark Donaldson-WingMRC Laboratory of Molecular Biology, Cambridge, UK.
Patrycja KozikMRC Laboratory of Molecular Biology, Cambridge, UK.
David C RubinszteinCambridge Institute for Medical Research, Cambridge, UK; UK Dementia Research Institute, Cambridge, UK.
Leo C JamesMRC Laboratory of Molecular Biology, Cambridge, UK. Electronic address: lcj@mrclmb.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TRIM21 is an exceptionally versatile ubiquitin ligase that can be directed by antibodies to target oligomeric protein scaffolds, viral capsids, and proteopathic aggregates for intracellular degradation. How the cell degrades these typically resistant substrates remains poorly understood. To address this, we used TRIM21 viral restriction to create a genome-wide phenotypic screen for antibody-dependent capsid degradation. We identify an antimicrobial selective macroautophagy pathway in mammalian cells, which we term "antibody-directed xenophagy" (ADX). We show that this mechanism restricts structurally diverse pathogens, including adenovirus and Salmonella. Using quantitative microscopy, we demonstrate that TRIM21 rapidly intercepts antibody-pathogen complexes, leading to ubiquitin ligase activation. Following this, selective autophagy adaptors are recruited, and viral cargoes are delivered to lysosomes. This process reduces Salmonella pathology and bacterial tissue invasion in mice. We propose that TRIM21 evolved through competition with pathogens to induce autophagy of diverse and complex substrates, potentially explaining its versatility for targeted protein degradation.

Indexed as

AutophagyMacroautophagyRibonucleoproteinsAnimalsHEK293 CellsHeLa CellsHost-Pathogen InteractionsHumansLysosomesMiceProteolysisSalmonellaSalmonella InfectionsSS-A AntigenTRIM21 ProteinRibonucleoproteinsSS-A AntigenTRIM21 Proteinantibodyantimicrobial responseantiviral immunityautophagyinnate immunityprotein degradationtargeted protein degradationubiquitin ligaseubiquitin proteasome systemxenophagy

Identifiers

PMID42242206
PMCPMC7619466

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.