Evidence map›Paper›PMID 30992545›Full record

ReviewNature reviews. Molecular cell biology2019

Quality and quantity control of gene expression by nonsense-mediated mRNA decay.

Tatsuaki Kurosaki, Maximilian W Popp, Lynne E Maquat

Erratum issuedOpen access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 491 papers.

0numbers the graph read from it
0cells of the map it votes in
491citing papers in PubMed
32.4field-weighted citation impact, top 1% of its field
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

491 citing papers in PubMed, 808 citations in OpenAlex.

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  7. Targeted gene editing ofMolecular therapy. Nucleic acids · 2026
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  11. TargetingGenes & development · 2026
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  13. RNAViruses · 2026
    Review
  14. Article
  15. Article
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  17. Article
  18. Article
  19. Article
  20. Article

431 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Tatsuaki Kurosaki *Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA.ORCID http://orcid.org/0000-0003-3231-1359
Maximilian W Popp *Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA.
Lynne E MaquatDepartment of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. lynne_maquat@urmc.rochester.edu.
University of Rochester · USUniversity of Rochester Medical Center · US

Funding

REGULATION OF SELENOPROTEIN RNA METABOLISMR01GM059614 · NIGMS · UNIVERSITY OF ROCHESTER · PI MAQUAT, LYNNE E · 1999 to 2022
$9.1M
NIGMS NIH HHS R01 GM059614
6 · The paper itself

Abstract

Nonsense-mediated mRNA decay (NMD) is one of the best characterized and most evolutionarily conserved cellular quality control mechanisms. Although NMD was first found to target one-third of mutated, disease-causing mRNAs, it is now known to also target ~10% of unmutated mammalian mRNAs to facilitate appropriate cellular responses - adaptation, differentiation or death - to environmental changes. Mutations in NMD genes in humans are associated with intellectual disability and cancer. In this Review, we discuss how NMD serves multiple purposes in human cells by degrading both mutated mRNAs to protect the integrity of the transcriptome and normal mRNAs to control the quantities of unmutated transcripts.

Indexed as

Gene Expression Regulation, NeoplasticMutationNonsense Mediated mRNA DecayTranscriptomeAnimalsHumansIntellectual DisabilityNeoplasmsRNA, MessengerRNA, NeoplasmRNA, MessengerRNA, Neoplasm

Identifiers

PMID30992545
PMCPMC6855384
OpenAlexW2939923831

What OpenQuestion holds

Textmetadata
LicenceTDM
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.