Evidence map›Paper›PMID 39205302›Full record

ReviewViruses2024

TRIM Proteins and Antiviral Microtubule Reorganization: A Novel Component in Innate Immune Responses?

Charlotte Vadon, Maria Magda Magiera, Andrea Cimarelli

Abstract readReview
In one paragraph

Review in Viruses, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Machine Learning-Driven Discovery of TRIM Genes as Diagnostic Biomarkers for Idiopathic Pulmonary Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Article
  5. Article
  6. Review
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

3 authors.

Charlotte VadonCentre International de Recherche en Infectiologie (CIRI), Univ Lyon, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, ENS de Lyon, F-69364 Lyon, France.
Maria Magda MagieraInstitut Curie, CNRS, UMR3348, Centre Universitaire, Bat 110, F-91405 Orsay, France.
Andrea CimarelliCentre International de Recherche en Infectiologie (CIRI), Univ Lyon, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, ENS de Lyon, F-69364 Lyon, France.ORCID 0000-0003-0892-0488

Funding

Agence Nationale de Recherches sur le Sida et les Hépatites Virales AO-2019-1 and AO-2024-2, n°ANRS0644Sidaction AAP34-1 - 13904
6 · The paper itself

Abstract

TRIM proteins are a family of innate immune factors that play diverse roles in innate immunity and protect the cell against viral and bacterial aggression. As part of this special issue on TRIM proteins, we will take advantage of our findings on TRIM69, which acts by reorganizing the microtubules (MTs) in a manner that is fundamentally antiviral, to more generally discuss how host-pathogen interactions that take place for the control of the MT network represent a crucial facet of the struggle that opposes viruses to their cell environment. In this context, we will present several other TRIM proteins that are known to interact with microtubules in situations other than viral infection, and we will discuss evidence that may suggest a possible contribution to viral control. Overall, the present review will highlight the importance that the control of the microtubule network bears in host-pathogen interactions.

Indexed as

Host-Pathogen InteractionsImmunity, InnateMicrotubulesTripartite Motif ProteinsAnimalsHumansVirus DiseasesTripartite Motif ProteinscytoskeletoninfectioninterferonmicrotubuleTRIMvirus

Identifiers

PMID39205302
PMCPMC11359181

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.