Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1: genes and variants

Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1 is linked to 1 analyzed protein (FKRP). 1 DNA variants are known to cause it; 20 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 Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1

Known disease-causing variants in Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1

VariantPositionProtein partClinical label
FKRP P316R316Zinc finger loopDisease-causing (★★)

Same protein, different disease

Diseases related to Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1

Frequently asked questions

Which genes are linked to Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1?

In CATVariant, Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1 is linked to 1 analyzed protein: FKRP (Ribitol 5-phosphate transferase FKRP).

How many genetic variants are linked to Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1?

25 variants: 1 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 20 are of uncertain significance or have conflicting reports.

Which uncertain variants in Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A1 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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