Evidence map›Paper›PMID 24830959›Full record

ArticleJournal of human genetics2014

A labor- and cost-effective non-optical semiconductor (Ion Torrent) next-generation sequencing of the SLC12A3 and CLCNKA/B genes in Gitelman's syndrome patients.

Beatriz Tavira, Juan Gómez, Fernando Santos, Helena Gil, Victoria Alvarez, Eliecer Coto

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2014. 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
1.1field-weighted citation impact, top 23% 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, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. NewWorld journal of nephrology · 2016
    Article
  8. 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.

Beatriz TaviraGenética Molecular-Laboratorio de Medicina-Fundación Renal (IRSIN-FRIAT), Hospital Universitario Central Asturias, Oviedo, Spain.
Juan GómezGenética Molecular-Laboratorio de Medicina-Fundación Renal (IRSIN-FRIAT), Hospital Universitario Central Asturias, Oviedo, Spain.
Fernando Santos1] Pediatría, Hospital Universitario Central Asturias, Oviedo, Spain [2] Departamento de Medicina, Universidad de Oviedo, Oviedo, Spain.
Helena GilPediatría, Hospital Universitario Central Asturias, Oviedo, Spain.
Victoria AlvarezGenética Molecular-Laboratorio de Medicina-Fundación Renal (IRSIN-FRIAT), Hospital Universitario Central Asturias, Oviedo, Spain.
Eliecer Coto1] Genética Molecular-Laboratorio de Medicina-Fundación Renal (IRSIN-FRIAT), Hospital Universitario Central Asturias, Oviedo, Spain [2] Departamento de Medicina, Universidad de Oviedo, Oviedo, Spain [3] Red de Investigación Renal (REDINREN), Madrid, Spain.
Fundación Renal Española · ESHospital Universitario Central de Asturias · ESUniversidad de Oviedo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gitelman's syndrome (GS) is a rare recessive disorder caused by mutations in the renal salt-handling genes SLC12A3 and CLCNKB. Our aim was to develop a next-generation sequencing (NGS) procedure for these genes based on two-tubes multiplex amplification of DNA pools and semiconductor sequencing with the Ion Torrent Personal Genome Machine (PGM). We created one pool with DNA from 20 GS patients previously Sanger sequenced for the coding exons of SLC12A3. A total of 13 mutations present in 11 of these patients were used as control variants to validate the NGS procedure. The full coding sequence of SLC12A3, CLCNKB and CLCNKA was amplified in only two Ampliseq tubes and processed and sequenced with the PGM. Large SLC12A3 and CLCNKB deletions were ascertained through multiplex ligation-dependent probe amplification in some patients. With the exception of the SLC12A3 exon 9, all the amplicons were successfully read and 12 of the 13 control variants were detected. The analysis of CLCNKB showed four putative mutations in the GS pool that were further assigned to specific patients. Two patients were heterozygous compounds for a single-nucleotide mutation and a large deletion at SLC12A3 or CLCNKB. We reported a NGS procedure that would facilitate the rapid and cost-effective large-scale screening of the three renal salt-handling genes. In addition to characterize the mutational spectrum of GS patients, the described procedure would facilitate the rapid and cost-effective screening of these genes at a population scale.

Indexed as

High-Throughput Nucleotide SequencingAllelesChloride ChannelsExonsGenotypeGitelman SyndromeHumansINDEL MutationIntronsMutationSolute Carrier Family 12, Member 3Chloride ChannelsCLCNKA protein, humanCLCNKB protein, humanSolute Carrier Family 12, Member 3

Identifiers

PMID24830959
OpenAlexW1990218861

What OpenQuestion holds

Textmetadata
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.