Evidence map›Paper›PMID 42377665›Full record

ReviewImmunologic research2026

TRIM28 and TRIM32: multifaceted regulators of innate immunity and antiviral defence.

Sreya Sherin Biju, Ravi Prakash Arya, Anismrita Lahon

Abstract readReview
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In one paragraph

Review in Immunologic research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Sreya Sherin BijuDepartment of Viral Vaccines, Institute of Advanced Virology, Thiruvananthapuram, Kerala, India.
Ravi Prakash AryaDepartment of Biotechnology, Assam University, Silchar, Assam, India. ravi.arya82@gmail.com.
Anismrita LahonDepartment of Viral Vaccines, Institute of Advanced Virology, Thiruvananthapuram, Kerala, India. anismrita.niv@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As versatile E3 ubiquitin ligases, Tripartite Motif (TRIM) proteins are essential elements of the innate immune response. The antiviral roles of TRIM28 and TRIM32 have been well documented, and they function in different ways. TRIM28 regulates the transcriptional expression of antiviral genes, while TRIM32 ubiquitinates host or viral proteins and directs their proteasomal breakdown. When taken together, they represent complementary transcriptional and post-translational host defence mechanisms. While TRIM28 primarily acts as a transcriptional repressor and TRIM32 as an E3 ubiquitin ligase, both proteins also play opposing roles in cell differentiation and immunity. Given the large number of TRIM family members, focusing on these two allows us to present representative transcriptional and ubiquitination-mediated regulatory mechanisms in depth. This review focuses on the regulatory differences in TRIM28 and TRIM32 in RIG-like receptor (RLR) signalling, Stimulator of Interferon Genes (STING) pathways, Toll-like receptor (TLR) signalling, and NOD-like receptors (NLR)-mediated inflammation, which are key to the host's immune response. These protein interactomes exhibit a significant interaction with other cellular pathways, broadening their significance beyond antiviral responses to encompass broader genetic and therapeutic implications.

Indexed as

Transcription FactorsTripartite Motif-Containing Protein 28Tripartite Motif ProteinsUbiquitin-Protein LigasesVirus DiseasesAnimalsHumansImmunity, InnateMembrane ProteinsSignal TransductionToll-Like ReceptorsUbiquitinationMembrane ProteinsToll-Like ReceptorsTranscription FactorsTRIM32 protein, humanTripartite Motif-Containing Protein 28Tripartite Motif ProteinsUbiquitin-Protein LigasesAntiviral ResponsesInnate ImmunitySignalling PathwayTRIM28TRIM32

Identifiers

PMID42377665

What OpenQuestion holds

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Registered trials

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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.