Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures: genes and variants

Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures is linked to 2 analyzed proteins (CACNA1C and CACNA1A). 4 DNA variants are known to cause it; 2 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 Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures

Known disease-causing variants in Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures

VariantPositionProtein partClinical label
CACNA1C G406R406IDisease-causing (★★)
CACNA1A S1372L1372IIIDisease-causing (★)
CACNA1C L657F657IIDisease-causing
CACNA1C L1408V1408IVDisease-causing

Same protein, different disease

Diseases related to Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures

Frequently asked questions

Which genes are linked to Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures?

In CATVariant, Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures is linked to 2 analyzed proteins: CACNA1C (Voltage-dependent L-type calcium channel subunit alpha-1C) and CACNA1A (Voltage-dependent P/Q-type calcium channel subunit alpha-1A).

How many genetic variants are linked to Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures?

6 variants: 4 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 2 are of uncertain significance or have conflicting reports.

Which uncertain variants in Neurodevelopmental disorder with hypotonia, language delay, and skeletal defects with or without seizures 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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