Evidence map›Paper›PMID 41303552›Full record

ArticleInternational journal of molecular sciences2025

Deubiquitinating Enzymes Ubiquitin-Specific Proteases 7 and 10 Regulate TAU Aggregation.

Christiane Volbracht, Karina Fog

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

2 authors.

Christiane VolbrachtNeuroscience, H. Lundbeck A/S, 2500 Valby, Denmark.ORCID 0000-0002-5748-9981
Karina FogNeuroscience, H. Lundbeck A/S, 2500 Valby, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulation of the microtubule-associated protein TAU into inclusions is a hallmark of tauopathies including Alzheimer's disease (AD), potentially driven by impaired protein degradation and dysregulated ubiquitination. To explore the role of deubiquitinating enzymes (DUBs), we performed siRNA knockdown screens targeting 93 murine DUBs in rTg4510 cortical cultures. Knockdown and pharmacological inhibition of the ubiquitin-specific proteases 7 (Usp7) and 10 (Usp10) significantly reduced seeded TAU aggregation without affecting soluble TAU levels. These effects were observed in both cortical and organotypic hippocampal slice cultures from rTg4510 mice, as well as in wildtype neurons seeded with AD-derived pathological TAU. Inhibition of Usp7 and Usp10 was associated with increased polyubiquitination of residual TAU inclusions in rTg4510 cortical cultures. These findings suggest that Usp7 and Usp10 contribute to pathological TAU accumulation by modulating ubiquitin-dependent degradation pathways. Targeting USP7 and USP10 may offer a novel therapeutic strategy for AD and related tauopathies.

Indexed as

Protein Aggregation, Pathologicaltau ProteinsUbiquitin-Specific Peptidase 7Ubiquitin ThiolesteraseAlzheimer DiseaseAnimalsHippocampusHumansMiceNeuronsProtein AggregatesUbiquitinationProtein Aggregatestau ProteinsUbiquitin-Specific Peptidase 7Ubiquitin ThiolesteraseUSP10 protein, mouseUsp7 protein, mouseAlzheimer’s diseaserTg4510tauopathyubiquitinUSP10USP7

Identifiers

PMID41303552
PMCPMC12652193

What OpenQuestion 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 OpenQuestion graph.