Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3: genes and variants

Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3 is linked to 1 analyzed protein (HNRNPA1). 1 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 Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3

Known disease-causing variants in Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3

VariantPositionProtein partClinical label
HNRNPA1 P340A340Nuclear targeting sequence (M9)Disease-causing (★)

Same protein, different disease

Diseases related to Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3

Frequently asked questions

Which genes are linked to Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3?

In CATVariant, Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3 is linked to 1 analyzed protein: HNRNPA1 (Heterogeneous nuclear ribonucleoprotein A1).

How many genetic variants are linked to Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3?

6 variants: 1 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 Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 3 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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