Evidence map›Paper›PMID 32940403›Full record

ArticleThe FEBS journal2021

Evidence for a dominant-negative mechanism in HARS1-mediated peripheral neuropathy.

Rebecca Meyer-Schuman, Anthony Antonellis

Open access · bronzeAbstract readComment
PubMed Full text at PMC Publisher
In one paragraph

Article in The FEBS journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Usher Syndrome: Genetics of a Human Ciliopathy.International journal of molecular sciences · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Rebecca Meyer-SchumanDepartment of Human Genetics, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0002-2004-3505
Anthony AntonellisDepartment of Human Genetics, University of Michigan, Ann Arbor, MI, USA.
University of Michigan · US

Funding

PREDOCTORAL TRAINING IN GENETICST32GM007544 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORAN, JOHN V. · 1985 to 2022
$11.3M
Defining the Role of Aminoacyl-tRNA Synthetases in Human Health and DiseaseR35GM136441 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Anthony Antonellis · 2020 to 2026
$2.8M
Aminoacyl-tRNA synthetases and human inherited diseaseR01GM118647 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ANTONELLIS, ANTHONY · 2016 to 2019
$1.6M
Defining the Molecular Pathology of Neuropathy-associated Aminoacyl-tRNA Synthetase MutationsF31NS108510 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCHUMAN, REBECCA MEYER · 2018 to 2020
$74k
NIGMS NIH HHS R01 GM118647NIGMS NIH HHS R35 GM136441NIGMS NIH HHS T32 GM007544NINDS NIH HHS F31 NS108510
6 · The paper itself

Abstract

The pathogenic mechanism of neuropathy-associated aminoacyl-tRNA synthetase (ARS) gene variants is poorly defined. Mullen et al. generate new models of pathogenic, dominant HARS1 mutations and show that they increase eIF2α phosphorylation and decrease protein translation in neurons. These results are consistent with a dominant-negative mechanism of ARS-mediated peripheral neuropathy. Comment on: https://doi.org/10.1111/febs.15449.

Indexed as

Histidine-tRNA LigasePeripheral Nervous System DiseasesAnimalsMutationNeuronal OutgrowthProtein BiosynthesisZebrafishHistidine-tRNA Ligaseaminoacyl-tRNA synthetasedominant-negativeHARS1peripheral neuropathyprotein translation

Identifiers

PMID32940403
PMCPMC8027917
OpenAlexW3087295704

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.