Hypomagnesemia, seizures, and intellectual disability 2: genes and variants

Hypomagnesemia, seizures, and intellectual disability 2 is linked to 1 analyzed protein (ATP1A1). 6 DNA variants are known to cause it; 11 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 Hypomagnesemia, seizures, and intellectual disability 2

Where Hypomagnesemia, seizures, and intellectual disability 2 variants cluster

Known disease-causing variants in Hypomagnesemia, seizures, and intellectual disability 2

VariantPositionProtein partClinical label
ATP1A1 L302R302TransmembraneDisease-causing (★)
ATP1A1 M859R859TransmembraneDisease-causing (★)
ATP1A1 A274G274CytoplasmicDisease-causing (★)
ATP1A1 L302P302TransmembraneDisease-causing
ATP1A1 G303R303TransmembraneDisease-causing
ATP1A1 W931R931TransmembraneDisease-causing

Same protein, different disease

Diseases related to Hypomagnesemia, seizures, and intellectual disability 2

Frequently asked questions

Which genes are linked to Hypomagnesemia, seizures, and intellectual disability 2?

In CATVariant, Hypomagnesemia, seizures, and intellectual disability 2 is linked to 1 analyzed protein: ATP1A1 (Sodium/potassium-transporting ATPase subunit alpha-1).

How many genetic variants are linked to Hypomagnesemia, seizures, and intellectual disability 2?

19 variants: 6 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 11 are of uncertain significance or have conflicting reports.

Which uncertain variants in Hypomagnesemia, seizures, and intellectual disability 2 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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