3-methylcrotonyl-CoA carboxylase 1 deficiency: genes and variants

3-methylcrotonyl-CoA carboxylase 1 deficiency is linked to 1 analyzed protein (MCCC1). 21 DNA variants are known to cause it; 210 more are uncertain, and 4 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Genes linked to 3-methylcrotonyl-CoA carboxylase 1 deficiency

Known disease-causing variants in 3-methylcrotonyl-CoA carboxylase 1 deficiency

VariantPositionProtein partClinical label
MCCC1 G180V180ATP-graspDisease-causing (★★)
MCCC1 A289V289ATP-graspDisease-causing (★★)
MCCC1 T465I465Biotin carboxylationDisease-causing (★★)
MCCC1 R66C66Biotin carboxylationDisease-causing (★★)
MCCC1 E288G288ATP-graspDisease-causing (★★)
MCCC1 I434M434Biotin carboxylationDisease-causing (★★)
MCCC1 R444H444Biotin carboxylationDisease-causing (★★)
MCCC1 M1V1Disease-causing (★★)
MCCC1 R421W421Biotin carboxylationDisease-causing (★★)
MCCC1 C276R276ATP-graspDisease-causing (★)
MCCC1 R385G385Biotin carboxylationDisease-causing (★)
MCCC1 A435T435Biotin carboxylationDisease-causing (★)
MCCC1 L437P437Biotin carboxylationDisease-causing (★)
MCCC1 M1T1Disease-causing (★)
MCCC1 E366K366Biotin carboxylationDisease-causing (★)
MCCC1 E59G59Biotin carboxylationDisease-causing (★)
MCCC1 P152L152Biotin carboxylationDisease-causing (★)
MCCC1 Y430C430Biotin carboxylationDisease-causing (★)
MCCC1 S535F535Disease-causing (★)
MCCC1 I460M460Biotin carboxylationDisease-causing
MCCC1 D532H532Disease-causing

Uncertain variants in 3-methylcrotonyl-CoA carboxylase 1 deficiency that look disease-causing

VariantPositionProtein partClinical labelEvidence
MCCC1 R444C444Biotin carboxylationConflicting reports (★)+7: in a 3D region that tolerates change poorly (3R); R444H at the same position is pathogenic; seen in 8.2e-06 of gnomAD DNA copies; REVEL 0.904
MCCC1 C276G276ATP-graspUncertain (★)+7: in a 3D region that tolerates change poorly (3R); C276R at the same position is pathogenic; seen in 1.4e-06 of gnomAD DNA copies; REVEL 0.982
MCCC1 R66H66Biotin carboxylationUncertain (★)+7: in a 3D region that tolerates change poorly (1R); R66C at the same position is pathogenic; seen in 6.8e-06 of gnomAD DNA copies; REVEL 0.827
MCCC1 A435V435Biotin carboxylationUncertain (★)+6: 3 other pathogenic changes within 3 positions; A435T at the same position is pathogenic; REVEL 0.918

Which prediction tools work for 3-methylcrotonyl-CoA carboxylase 1 deficiency

How often each tool ranks a disease-causing variant above a harmless one (AUROC × 100).

Diseases related to 3-methylcrotonyl-CoA carboxylase 1 deficiency

Frequently asked questions

Which genes are linked to 3-methylcrotonyl-CoA carboxylase 1 deficiency?

In CATVariant, 3-methylcrotonyl-CoA carboxylase 1 deficiency is linked to 1 analyzed protein: MCCC1 (Methylcrotonoyl-CoA carboxylase subunit alpha, mitochondrial).

How many genetic variants are linked to 3-methylcrotonyl-CoA carboxylase 1 deficiency?

240 variants: 21 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 210 are of uncertain significance or have conflicting reports.

Which uncertain variants in 3-methylcrotonyl-CoA carboxylase 1 deficiency look disease-causing?

4 uncertain variants reach the likely-pathogenic range of the ACMG/AMP points scale on computable evidence, for example MCCC1 R444C, MCCC1 C276G, MCCC1 R66H and MCCC1 A435V. These are leads for expert review, not diagnoses.

Which variant effect predictor works best for 3-methylcrotonyl-CoA carboxylase 1 deficiency?

Among tools not trained on clinical labels, SIFT separates this disease's known disease-causing variants from harmless ones best (AUROC 0.95, based on 19 disease-causing and 16 harmless variants).

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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