Evidence map›Paper›PMID 29449639›Full record

ArticleScientific reports2018

A hERG mutation E1039X produced a synergistic lesion on I

Jie Wu, Yuka Mizusawa, Seiko Ohno, Wei-Guang Ding, Takashi Higaki, Qi Wang, Hirohiko Kohjitani, Takeru Makiyama, Hideki Itoh, Futoshi Toyoda and 4 more

Open access · goldAbstract readCase Reports
In one paragraph

Article in Scientific reports, 2018. 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
0.3field-weighted citation impact, top 37% 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, 6 citations in OpenAlex.

  1. Article
  2. Identification and functional assessment of a KCNH2 compound heterozygosity in a patient with presumed idiopathic ventricular fibrillation ascertains the diagnosis of long QT syndrome type 2.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Article
  3. 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

14 authors at 4 institutions in 3 countries.

Jie WuDepartment of Pharmacology, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Yuka MizusawaDepartment of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan.
Seiko OhnoDepartment of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan.
Wei-Guang DingDepartment of Physiology, Shiga University of Medical Science, Shiga, Japan.
Takashi HigakiDepartment of Pediatrics, Ehime University School of Medicine, Ehime, Japan.
Qi WangDepartment of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan.
Hirohiko KohjitaniDepartment of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takeru MakiyamaDepartment of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hideki ItohDepartment of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan.
Futoshi ToyodaDepartment of Physiology, Shiga University of Medical Science, Shiga, Japan.ORCID 0000-0002-8412-6481
Andrew F JamesSchool of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, United Kingdom.
Jules C HancoxSchool of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, United Kingdom.
Hiroshi MatsuuraDepartment of Physiology, Shiga University of Medical Science, Shiga, Japan.
Minoru HorieDepartment of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Shiga, Japan. horie@belle.shiga-med.ac.jp.
Shiga University of Medical Science · JPKyoto University · JPUniversity of Bristol · GBEhime University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congenital long QT syndrome (LQTS) caused by compound mutations is usually associated with more severe clinical phenotypes. We identified a LQTS family harboring three compound mutations in different genes (KCNQ1-R174C, hERG-E1039X and SCN5A-E428K). KCNQ1-R174C, hERG-E1039X and SCN5A-E428K mutations and/or relevant wild-type (WT) cDNAs were respectively expressed in mammalian cells. I

Indexed as

AdultAgedAnimalsArrhythmias, CardiacChildChild, PreschoolCHO CellsCricetulusERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsFemaleHeartHumansKCNQ1 Potassium ChannelLong QT SyndromeMaleERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsKCNH2 protein, humanKCNQ1 Potassium ChannelKCNQ1 protein, humanNAV1.5 Voltage-Gated Sodium ChannelSCN5A protein, human

Identifiers

PMID29449639
PMCPMC5814447
OpenAlexW2802840823

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.