Evidence map›Paper›PMID 31746411›Full record

ArticleMolecular medicine reports2020

A novel gross deletion and breakpoint junction sequence analysis of ATP7B in a Chinese family with Wilson disease using next‑generation sequencing and Sanger sequencing.

Wei-Liang Liu, Fang Li, Lu Liu, Wei Chen, Zhi-Xu He, Hao Gu, Rong Ai

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

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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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Missing heritability of Wilson disease: a search for the uncharacterized mutations.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Review
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 2 institutions in 1 country.

Wei-Liang Liu *Department of Pediatrics, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Fang Li *Department of Ophthalmology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Lu Liu *Department of Ophthalmology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Wei ChenDepartment of Ophthalmology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Zhi-Xu HeDepartment of Pediatrics, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Hao GuDepartment of Ophthalmology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Rong AiDepartment of Pediatrics, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Guiyang Medical University · CNAffiliated Hospital of Guizhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wilson disease (WD) is a rare autosomal recessive genetic disorder that causes abnormal copper metabolism, resulting in pathological accumulation of copper in the liver, brain and other organs. Mutations in the ATPase copper transporter 7B (ATP7B) gene, which encodes a membrane P‑type adenosine triphosphatase, have been identified as being responsible for WD. The present study analyzed clinical data and collected DNA samples from a pediatric patient with WD and her healthy parents. Mutation screening for ATP7B was performed using direct sequencing, multiplex ligation‑dependent probe amplification(MLPA), next‑generation sequencing (NGS) and Sanger sequencing of the breakpoint junction sequence. The patient (age, 2.7 years) presented with early‑onset hepatic disease. The present study identified compound heterozygous mutations of ATP7B, including a heterozygous mutation (p.Arg1,041Trp) and a novel heterozygous gross deletion of a 57,771 bp fragment (chr13: 52490972‑52548742) (GRCh37) from partial exon2‑ exon21 to external ATP7B sequence (15.833bp) in the patient. Analysis of the family members of the patient showed that the missense mutation and the gross deletion mutation were inherited from her mother and father, respectively. Microhomology and inverted repeat sequences, which may mediate the deletion mutation, were identified through sequence analysis on both sides of the breakpoints of this deletion. The present study provided additional information on the genotypic spectrum of the ATP7B gene, particularly with regard to early onset hepatic disease, as observed in the present patient with WD. The identification of the precise breakpoint junction sequence warrants further investigation of DNA break and recombination mechanisms. In detecting precise deletions, the NGS associated with Sanger sequencing of breakpoint junction sequence have been found to have more advantages than MLPA.

Indexed as

Genetic Predisposition to DiseaseAdultAge of OnsetChild, PreschoolCopperCopper-Transporting ATPasesFemaleHepatolenticular DegenerationHeterozygoteHigh-Throughput Nucleotide SequencingHumansMaleMutationPedigreeSequence DeletionATP7B protein, humanCopperCopper-Transporting ATPasesaTPase copper transporter Bchildmutationnext-generation sequencingWilson disease

Identifiers

PMID31746411
PMCPMC6896306
OpenAlexW2990641798

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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.