ArticleClinical genetics2026
Clinical Variability Including Non-Dilated Left Ventricular and Dilated Cardiomyopathy in a Pedigree With an Intragenic CTNNA3 Copy Number Variation.
Article in Clinical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
CTNNA3 encodes αT-catenin, which contributes to the integrity of the myocardium. Single nucleotide variants are occasionally associated with arrhythmogenic right ventricular cardiomyopathy, and structural variations are apparently enriched in neurodevelopmental disorders. We report a multiplex family in which a ~60 kb microdeletion of CTNNA3 co-segregates with a variable, heart-restricted phenotype including non-dilated left ventricle cardiomyopathy (NDLVC) in one individual and dilated cardiomyopathy in two, with or without apex hypertrabeculation. The intragenic deletion was identified by XONarray and, subsequently, characterized by long-read sequencing after nonconclusive multigene panel testing. This deletion selectively involved exon 9 and was predicted in-frame by removing 153 amino acids and, thus, disrupting the α-catenin/vinculin-like domain, which is critical for proper conformational homodimerization of the encoded αT-catenin. This intragenic deletion co-segregating with NDLVC and dilated cardiomyopathy confirms that CTNNA3 is a candidate gene for hereditary cardiomyopathies.
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