Evidence map›Paper›PMID 40699434›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2025

Screening Methods for NMD Inhibitors or Readthrough Activators.

Selma Nedjma, Fabrice Lejeune

Abstract read
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Article in Methods in molecular biology (Clifton, N.J.), 2025. 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

2 authors.

Selma NedjmaUniversity of Lille, CNRS, Inserm, UMR9020-U1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, Lille, France.
Fabrice LejeuneUniversity of Lille, CNRS, Inserm, UMR9020-U1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, Lille, France. fabrice.lejeune@inserm.fr.ORCID https://orcid.org/0000-0002-5132-3585

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonsense mutations cause approximately 10% of genetic disease cases. Certain molecules can rescue the expression of genes carrying a nonsense mutation, either by activating readthrough of the premature termination codon or by inhibiting the mRNA surveillance mechanism called nonsense-mediated mRNA decay (NMD). In the first approach, a full-length protein will be synthesized, differing by at most one amino acid from the wild-type protein. In the second approach, a truncated protein will be synthesized, which sometimes retains partially or completely the function of the wild-type protein. Here we describe methods for identifying, by screening, molecules having the capacity either to inhibit NMD or to activate readthrough.

Indexed as

Codon, NonsenseNonsense Mediated mRNA DecayProtein BiosynthesisDrug Evaluation, PreclinicalHumansRNA, MessengerCodon, NonsenseRNA, MessengerNonsense-mediated mRNA decay (NMD)ReadthroughScreening methodSmall molecules

Identifiers

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.