Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

SIDS: genetic and environmental influences may cause arrhythmia in this silent killer.

The Journal of clinical investigation - 1 Feb 2006

Makielski Jonathan C

Abstract excerpt

In this issue of the JCI, Bowers et al. show that the common polymorphism of the cardiac voltage-gated sodium channel, type Valpha (SCN5A), designated S1103Y, found in African Americans is associated with an increased risk of sudden infant death syndrome (SIDS). Wild-type and mutant SCN5A channels both functioned typically under normal conditions in vitro, but exposure to acidic intracellular pH levels such as...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Arrhythmias, Cardiac
Share to Environment
Share to Genetic Predisposition to Disease

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Infant

Share to Muscle Proteins

Share to NAV1.5 Voltage-Gated Sodium Channel

Share to Sodium Channels

Share to Sudden Infant Death

Source

Open in PubMed Open full text

Identifiers

PMID: 16453014
DOI: 10.1172/JCI27689
PMCID: PMC1359061

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SIDS: genetic and environmental influences may cause arrhythmia in this silent killer.PMID 16453014Read ↗

A common cardiac sodium channel variant associated with sudden infant death in African Americans, SCN5A S1103Y.Semantic proximity Read ↗

The common African American polymorphism SCN5A-S1103Y interacts with mutation SCN5A-R680H to increase late Na current.Semantic proximity Read ↗

Biophysical characterization of a new SCN5A mutation S1333Y in a SIDS infant linked to long QT syndrome.Semantic proximity Read ↗

Variant of SCN5A sodium channel implicated in risk of cardiac arrhythmia.Semantic proximity Read ↗

Overrepresentation of the proarrhythmic, sudden death predisposing sodium channel polymorphism S1103Y in a population-based cohort of African-American sudden infant death syndrome.Semantic proximity Read ↗

Sudden infant death syndrome: how significant are the cardiac channelopathies?Semantic proximity Read ↗

Postmortem molecular analysis of SCN5A defects in sudden infant death syndrome.Semantic proximity Read ↗

A mechanism for sudden infant death syndrome (SIDS): stress-induced leak via ryanodine receptors.Semantic proximity Read ↗

SCN1A variants associated with sudden infant death syndrome.Semantic proximity Read ↗

Cardiac ion channel mutations in the sudden infant death syndrome.Semantic proximity Read ↗

Novel mechanism for sudden infant death syndrome: persistent late sodium current secondary to mutations in caveolin-3.Semantic proximity Read ↗

Dysfunction of NaV1.4, a skeletal muscle voltage-gated sodium channel, in sudden infant death syndrome: a case-control study.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.