Chronic infantile neurological, cutaneous and articular syndrome: genes and variants

Chronic infantile neurological, cutaneous and articular syndrome is linked to 1 analyzed protein (NLRP3). 5 DNA variants are known to cause it; 0 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 Chronic infantile neurological, cutaneous and articular syndrome

Where Chronic infantile neurological, cutaneous and articular syndrome variants cluster

Known disease-causing variants in Chronic infantile neurological, cutaneous and articular syndrome

VariantPositionProtein partClinical label
NLRP3 T350M350NACHTDisease-causing (★★)
NLRP3 L355P355NACHTDisease-causing (★★)
NLRP3 Y861C861LRR 5Disease-causing (★★)
NLRP3 F311S311NACHTDisease-causing
NLRP3 F575S575Disease-causing

Same protein, different disease

Diseases related to Chronic infantile neurological, cutaneous and articular syndrome

Frequently asked questions

Which genes are linked to Chronic infantile neurological, cutaneous and articular syndrome?

In CATVariant, Chronic infantile neurological, cutaneous and articular syndrome is linked to 1 analyzed protein: NLRP3 (NACHT, LRR and PYD domains-containing protein 3).

How many genetic variants are linked to Chronic infantile neurological, cutaneous and articular syndrome?

5 variants: 5 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 0 are of uncertain significance or have conflicting reports.

Which uncertain variants in Chronic infantile neurological, cutaneous and articular 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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