Congenital disorder of glycosylation, type IIw: genes and variants

Congenital disorder of glycosylation, type IIw is linked to 3 analyzed proteins (SLC37A4, SLC35A2 and CACNA1D). 8 DNA variants are known to cause it; 38 more are uncertain, and 0 of those already look disease-causing on computable evidence.

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

Also known as: congenital disorder of glycosylation; Congenital disorder of glycosylation, type Iw, autosomal dominant

Genes linked to Congenital disorder of glycosylation, type IIw

Known disease-causing variants in Congenital disorder of glycosylation, type IIw

VariantPositionProtein partClinical label
SLC37A4 C183R183TransmembraneDisease-causing (★★)
SLC37A4 R300H300CytoplasmicDisease-causing (★★)
SLC37A4 G339D339TransmembraneDisease-causing (★★)
SLC37A4 G20D20TransmembraneDisease-causing (★★)
SLC37A4 R28H28TransmembraneDisease-causing (★★)
SLC37A4 G150R150TransmembraneDisease-causing (★★)
SLC35A2 E103V103TransmembraneDisease-causing (★)
CACNA1D F747L747IIDisease-causing

Same protein, different disease

Diseases related to Congenital disorder of glycosylation, type IIw

Frequently asked questions

Which genes are linked to Congenital disorder of glycosylation, type IIw?

In CATVariant, Congenital disorder of glycosylation, type IIw is linked to 3 analyzed proteins: SLC37A4 (Glucose-6-phosphate exchanger SLC37A4), SLC35A2 (UDP-galactose translocator) and CACNA1D (Voltage-dependent L-type calcium channel subunit alpha-1D).

How many genetic variants are linked to Congenital disorder of glycosylation, type IIw?

50 variants: 8 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 38 are of uncertain significance or have conflicting reports.

Which uncertain variants in Congenital disorder of glycosylation, type IIw 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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