TRDN (Triadin) variants and mutations

TRDN (also known as Triadin) is a human protein-coding gene encoding a triadin protein. It organizes the sarcoplasmic-reticulum calcium-release complex and helps couple calsequestrin and ryanodine receptors in cardiac and skeletal muscle. Biallelic loss-of-function variants cause triadin knockout syndrome with severe exercise- or stress-triggered ventricular arrhythmias. This analysis covers 1,235 TRDN variants and mutations. Of these, 90% have computational variant effect predictions. Disease context includes catecholaminergic polymorphic ventricular tachycardia, catecholaminergic polymorphic ventricular tachycardia 1, and Abnormality of the cardiovascular system. Example TRDN variants include M1?, M1T, and T2S.

Variant analysis overview

Variant and mutation evidence

Clinical, disease, and population context

Protein structure and variant hotspots

Data sources

Evidence in this analysis draws on EBI Proteins Variation, UniProt, gnomAD v4, EuropePMC, 3D Hotspot Analysis, Interaction Network Analysis, AlphaFold DB, gnomAD constraint, Open Targets, ClinGen, MaveDB, LitVar.

Notable TRDN variants

Examples include M1?, M1T, T2S, E3D, E3V, T5I, T5S, A6V. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.