Evidence map›Paper›PMID 37024942›Full record

ArticleAmerican journal of medical genetics. Part A2023

Pontocerebellar hypoplasia associated with p.Arg183Trp homozygous variant in EXOSC1 gene: A case report.

Nadirah S Damseh, Ali N Obeidat, Khondakar Sayef Ahammed, Motee Al-Ashhab, Motee Abu Awad, Ambro van Hoof

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in American journal of medical genetics. Part A, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Built differently or defective: can RNA exosomopathies cause ribosome heterogeneity?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  7. Article
  8. A Biallelic Variant of the RNA Exosome GenemedRxiv : the preprint server for health sciences · 2023
    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

6 authors at 2 institutions in 4 countries.

Nadirah S DamsehDepartment of Pediatrics and Genetics, Al Makassed Hospital, East Jerusalem, Palestine.
Ali N ObeidatFaculty of Medicine, Al-Quds University, Abu Deis, Palestine.
Khondakar Sayef AhammedDepartment of Microbiology and Molecular Genetics, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Motee Al-AshhabDepartment of Pediatrics and Genetics, Al Makassed Hospital, East Jerusalem, Palestine.
Motee Abu AwadDepartment of Pediatrics and Genetics, Al Makassed Hospital, East Jerusalem, Palestine.
Ambro van HoofDepartment of Microbiology and Molecular Genetics, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Al-Quds University · PSThe University of Texas MD Anderson Cancer Center · US

Funding

RNAse functions in post-transcriptional gene regulationR35GM141710 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI VAN HOOF, AMBRO · 2021 to 2025
$2.4M
NIGMS NIH HHS R35 GM141710
6 · The paper itself

Abstract

Pontocerebellar hypoplasia (PCH) is a heterogeneous group of rare neurodegenerative disorders characterized by a wide phenotypic range including severe motor and cognitive impairments, microcephaly, distinctive facial features, and other features according to the type. Several classes of PCH1 have been linked to mutations in the evolutionarily conserved RNA exosome complex that consists of nine subunits (EXOSC1 to EXOSC9) and facilitates the degradation and processing of cytoplasmic and nuclear RNA from the 3' end. Only a single individual with an EXOSC1 mutation was reported with clinical features of PCH type 1 (PCH1F). Here, we report a 3-month-old female with PCH and additional clinical features not previously reported to be associated with PCH1, including dilated cardiomyopathy. On assessment, failure to thrive, microcephaly, distinctive facial features, and bluish sclera, were noted. Whole-exome sequencing was performed and revealed a novel homozygous missense variant c.547C > T (p.Arg183Trp) in the EXOSC1 gene. Functional studies in a budding yeast model that expresses the human EXOSC1 variant Arg183Trp show a slow-growth phenotype, whereas the previously identified PCH1F allele EXOSC1-Ser35Leu is lethal, indicating impaired exosome function for both of these variants. The protein levels of both EXOSC1 variants are reduced compared with wild-type when expressed in budding yeast. Herein, we ascertain the second case of PCH associated with a EXOSC1 variant that causes defects in RNA exosome function and provide a model organism system to distinguish between benign and pathogenic variants in EXOSC1.

Indexed as

Cerebellar DiseasesMicrocephalyNervous System MalformationsOlivopontocerebellar AtrophiesExosome Multienzyme Ribonuclease ComplexFemaleHumansInfantMutationRNA-Binding ProteinsEXOSC1 protein, humanExosome Multienzyme Ribonuclease ComplexRNA-Binding Proteinsdilated cardiomyopathyEXOSC1exosomopathypontocerebellar hypoplasia type 1

Identifiers

PMID37024942
PMCPMC10942657
OpenAlexW4362693002

What OpenQuestion holds

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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.