Arrhythmogenic cardiomyopathy with wooly hair and keratoderma: genes and variants

Arrhythmogenic cardiomyopathy with wooly hair and keratoderma is linked to 1 analyzed protein (DSP). 6 DNA variants are known to cause it; 1,833 more are uncertain, and 0 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Genes linked to Arrhythmogenic cardiomyopathy with wooly hair and keratoderma

Where Arrhythmogenic cardiomyopathy with wooly hair and keratoderma variants cluster

Known disease-causing variants in Arrhythmogenic cardiomyopathy with wooly hair and keratoderma

VariantPositionProtein partClinical label
DSP S299R299Spectrin 2Disease-causing (★★)
DSP R451G451Interaction with JUP and PKP2Disease-causing (★★)
DSP S597P597Spectrin 4Disease-causing (★)
DSP H618P618Spectrin 4Disease-causing (★)
DSP L622P622Spectrin 4Disease-causing (★)
DSP T638I638Interaction with MAPRE1Disease-causing (★)

Diseases related to Arrhythmogenic cardiomyopathy with wooly hair and keratoderma

Frequently asked questions

Which genes are linked to Arrhythmogenic cardiomyopathy with wooly hair and keratoderma?

In CATVariant, Arrhythmogenic cardiomyopathy with wooly hair and keratoderma is linked to 1 analyzed protein: DSP (Desmoplakin).

How many genetic variants are linked to Arrhythmogenic cardiomyopathy with wooly hair and keratoderma?

1,968 variants: 6 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 1,833 are of uncertain significance or have conflicting reports.

Which uncertain variants in Arrhythmogenic cardiomyopathy with wooly hair and keratoderma look disease-causing?

None of the uncertain variants currently reaches the likely-pathogenic range on computable evidence alone.

About this data

Variant–disease links come from ClinVar, Open Targets and UniProt, pooled from the latest public CATVariant analysis of each human protein. Evidence scores use the ACMG/AMP Bayesian points scale with computable criteria only (position among known disease variants, rarity in gnomAD, calibrated predictors, deep mutational scanning); there is no family or patient data, so they prioritise variants for expert review and never classify them.

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