Evidence map›Paper›PMID 30272292›Full record

ArticleMolecular medicine reports2018

A family with hypothyroidism caused by fatty acid synthase and apolipoprotein B receptor mutations.

Jianhua Sun, Lizhi Sun, Weijie Chen, Xiao Yin, Yong Lu, Qiang Jiang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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 3 institutions in 1 country.

Jianhua SunDepartment of Oncology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Lizhi SunCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.
Weijie ChenDepartment of Endocrinology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.
Xiao YinDepartment of Endocrinology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.
Yong LuDepartment of Endocrinology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.
Qiang JiangDepartment of Endocrinology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.
Shandong University · CNJinan Central Hospital · CNSecond Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypothyroidism is a disease with a genetic component. The present study aimed to identify the potential causative gene mutation in a family with hypothyroidism and to investigate its potential pathology. DNA was extracted from the affected individual and his parents, maternal aunt and maternal grandmother. Whole exome sequencing was used to examine their exomes. The potential causative genes that may have an autosomal dominant mode of inheritance were selected after variant calling and filtering. Bioinformatics analysis was utilized to predict the deleteriousness of the identified variants, and multiple sequence alignment and conserved protein domain analyses were performed using online software. Finally, Sanger sequencing was used to validate the identified variants. In the present study, a total of 50 variants were screened based on the autosomal dominant mode of inheritance. Two variants, the fatty acid synthase (FASN) and apolipoprotein B receptor (APOBR) genes, were further analyzed, as they were highly associated with hypothyroidism. Genotyping results revealed that two mutations, c.G7192T (p.A2398S) in the FASN gene and c.C1883G (p.T628R) in the APOBR gene, were fully co‑segregated with established hypothyroidism phenotypes in the family. These mutations were located in the conserved α/β‑hydrolase fold and Na+/Ca2+ exchanger superfamily domain of FASN and APOBR, respectively. In conclusion, the present study demonstrated that the FASN c.G7192T and APOBR c.C1883G mutations may be the potential causative variants in this Chinese hypothyroidism pedigree.

Indexed as

MutationAdultAgedAllelesAmino Acid SequenceBiomarkersChild, PreschoolComputational BiologyDNA Mutational AnalysisExome SequencingFatty Acid SynthasesFemaleGenotypeHumansHypothyroidismMaleapolipoprotein B receptorBiomarkersFatty Acid SynthasesReceptors, LipoproteinAPOBRFASNhypothyroidismWES

Identifiers

PMID30272292
PMCPMC6236273
OpenAlexW2889771984

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.