Insulin-resistant diabetes mellitus AND acanthosis nigricans: genes and variants

Insulin-resistant diabetes mellitus AND acanthosis nigricans is linked to 1 analyzed protein (INSR). 7 DNA variants are known to cause it; 30 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 Insulin-resistant diabetes mellitus AND acanthosis nigricans

Where Insulin-resistant diabetes mellitus AND acanthosis nigricans variants cluster

Known disease-causing variants in Insulin-resistant diabetes mellitus AND acanthosis nigricans

VariantPositionProtein partClinical label
INSR V1054M1054Protein kinaseDisease-causing
INSR N489D489ExtracellularDisease-causing
INSR R762S762Fibronectin type-III 2Disease-causing
INSR G1035V1035Protein kinaseDisease-causing
INSR A1161T1161Protein kinaseDisease-causing
INSR A1162E1162Protein kinaseDisease-causing
INSR W1227S1227Protein kinaseDisease-causing

Same protein, different disease

Diseases related to Insulin-resistant diabetes mellitus AND acanthosis nigricans

Frequently asked questions

Which genes are linked to Insulin-resistant diabetes mellitus AND acanthosis nigricans?

In CATVariant, Insulin-resistant diabetes mellitus AND acanthosis nigricans is linked to 1 analyzed protein: INSR (Insulin receptor).

How many genetic variants are linked to Insulin-resistant diabetes mellitus AND acanthosis nigricans?

40 variants: 7 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 30 are of uncertain significance or have conflicting reports.

Which uncertain variants in Insulin-resistant diabetes mellitus AND acanthosis nigricans 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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