Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome: genes and variants

Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome is linked to 1 analyzed protein (COL3A1). 6 DNA variants are known to cause it; 69 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 Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome

Known disease-causing variants in Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome

VariantPositionProtein partClinical label
COL3A1 G405R405Triple-helical regionDisease-causing (★★)
COL3A1 G666S666Triple-helical regionDisease-causing (★★)
COL3A1 G195R195Triple-helical regionDisease-causing (★★)
COL3A1 G855C855Triple-helical regionDisease-causing (★★)
COL3A1 P49A49VWFCDisease-causing (★★)
COL3A1 G489W489Triple-helical regionDisease-causing (★)

Same protein, different disease

Diseases related to Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome

Frequently asked questions

Which genes are linked to Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome?

In CATVariant, Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome is linked to 1 analyzed protein: COL3A1 (Collagen alpha-1(III) chain).

How many genetic variants are linked to Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome?

86 variants: 6 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 69 are of uncertain significance or have conflicting reports.

Which uncertain variants in Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome 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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