Evidence map›Paper›PMID 33231815›Full record

ArticleMolecular biology reports2020

Identification and computational analysis of USH1C, and SLC26A4 variants in Pakistani families with prelingual hearing loss.

Muhammad Noman, Shazia A Bukhari, Sakina Rehman, Muhammad Qasim, Muhammad Ali, Saima Riazuddin, Zubair M Ahmed

Open access · greenAbstract read
In one paragraph

Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 52% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Identification of Hearing Loss-Associated Variants ofBioMed research international · 2021
    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

7 authors at 3 institutions in 2 countries.

Muhammad NomanDepartment of Biochemistry, Government College University, Faisalabad, 38000, Pakistan.
Shazia A BukhariDepartment of Biochemistry, Government College University, Faisalabad, 38000, Pakistan. shaziabukhari@gcuf.edu.pk.
Sakina RehmanDepartment of Otorhinolaryngology Head and Neck Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Muhammad QasimDepartment of Biotechnology, Government College University, Faisalabad, 38000, Pakistan.
Muhammad AliDepartment of Animal Sciences, Quaid Azam University, Islamabad, 46000, Pakistan.
Saima RiazuddinDepartment of Otorhinolaryngology Head and Neck Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Zubair M AhmedDepartment of Otorhinolaryngology Head and Neck Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Government College University, Faisalabad · PKUniversity of Maryland, Baltimore · USQuaid-i-Azam University · PK

Funding

Molecular Determinants of Usher Syndrome Disorder in HumansR01DC016295 · NIDCD · UNIVERSITY OF MARYLAND BALTIMORE · PI AHMED, ZUBAIR M. · 2018 to 2022
$2.7M
Identifying Genes for Non-Syndromic Recessive Deafness-A Collaborative StudyR56DC011803 · NIDCD · UNIVERSITY OF MARYLAND BALTIMORE · PI RIAZUDDIN, SAIMA · 2017 to 2017
$638k
NIDCD NIH HHS R01 DC016295NIDCD NIH HHS R56 DC011803
6 · The paper itself

Abstract

Hearing loss (HL) is clinically and genetically heterogeneous disorder and is the most frequent occurring sensory deficit in humans. This study was conducted to decipher the genetic cause of HL occurring in two large consanguineous Pakistani families (GCNF-01, GCNF-03). Family history and pure tone audiometry of both families suggested prelingual HL, while the affected individuals of GCNF-01 also had low vision and balance problems, consistent with cardinal features of Usher syndrome type I (USH1). Exome sequencing followed by segregating analysis revealed a novel splice site variant (c.877-1G > A) of USH1C occurring with USH1 phenotype in family GCNF01. While the affected individual of family GCNF-03 were homozygous for the c.716 T > A, p.(Val239Asp) previously reported pathogenic variant of SLC26A4. Both variants have very low frequencies in control database. In silico mutagenesis and 3-dimensional simulation analyses revealed that both variants have deleterious impact on the proteins folding and secondary structures. Our study expands the mutation spectrum of the HL genes and emphasizes the utility of exome sequencing coupled with bioinformatics tools for clinical genetic diagnosis, prognosis, and family counseling.

Indexed as

AdolescentAdultCell Cycle ProteinsChildChild, PreschoolCytoskeletal ProteinsExome SequencingFemaleGenetic VariationHumansMalePakistanSulfate TransportersUsher SyndromesCell Cycle ProteinsCytoskeletal ProteinsSLC26A4 protein, humanSulfate TransportersUSH1C protein, humanExome sequencingGenetic heterogeneityPrelingual hearing impairmentSensorineural hearing lossSLC26A4USH1CUsher syndrome

Identifiers

PMID33231815
PMCPMC10680121
OpenAlexW3109707792

What OpenQuestion holds

Textmetadata
LicenceTDM
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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.