Obesity due to melanocortin 4 receptor deficiency: genes and variants

Obesity due to melanocortin 4 receptor deficiency is linked to 2 analyzed proteins (MC4R and PCSK1). 6 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 Obesity due to melanocortin 4 receptor deficiency

Where Obesity due to melanocortin 4 receptor deficiency variants cluster

Known disease-causing variants in Obesity due to melanocortin 4 receptor deficiency

VariantPositionProtein partClinical label
MC4R R165Q165CytoplasmicDisease-causing (★★★★)
MC4R R165G165CytoplasmicDisease-causing (★★★★)
MC4R R165W165CytoplasmicDisease-causing (★★★★)
MC4R C271Y271ExtracellularDisease-causing (★★★★)
MC4R I316S316CytoplasmicDisease-causing (★★)
MC4R N62S62TransmembraneDisease-causing (★)

Same protein, different disease

Diseases related to Obesity due to melanocortin 4 receptor deficiency

Frequently asked questions

Which genes are linked to Obesity due to melanocortin 4 receptor deficiency?

In CATVariant, Obesity due to melanocortin 4 receptor deficiency is linked to 2 analyzed proteins: MC4R (Melanocortin receptor 4) and PCSK1 (Neuroendocrine convertase 1).

How many genetic variants are linked to Obesity due to melanocortin 4 receptor deficiency?

46 variants: 6 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 Obesity due to melanocortin 4 receptor deficiency 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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