Radioulnar synostosis with amegakaryocytic thrombocytopenia 2: genes and variants

Radioulnar synostosis with amegakaryocytic thrombocytopenia 2 is linked to 1 analyzed protein (MECOM). 5 DNA variants are known to cause it; 18 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: Radioulnar synostosis with amegakaryocytic thrombocytopenia 1

Genes linked to Radioulnar synostosis with amegakaryocytic thrombocytopenia 2

Known disease-causing variants in Radioulnar synostosis with amegakaryocytic thrombocytopenia 2

VariantPositionProtein partClinical label
MECOM R929W929C2H2-type 8Disease-causing (★★)
MECOM T821A821Disease-causing
MECOM H930R930C2H2-type 8Disease-causing
MECOM T935A935Disease-causing
MECOM R941T941C2H2-type 9Disease-causing

Same protein, different disease

Diseases related to Radioulnar synostosis with amegakaryocytic thrombocytopenia 2

Frequently asked questions

Which genes are linked to Radioulnar synostosis with amegakaryocytic thrombocytopenia 2?

In CATVariant, Radioulnar synostosis with amegakaryocytic thrombocytopenia 2 is linked to 1 analyzed protein: MECOM (Histone-lysine N-methyltransferase MECOM).

How many genetic variants are linked to Radioulnar synostosis with amegakaryocytic thrombocytopenia 2?

29 variants: 5 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 18 are of uncertain significance or have conflicting reports.

Which uncertain variants in Radioulnar synostosis with amegakaryocytic thrombocytopenia 2 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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