TH (Tyrosine 3-monooxygenase) variants and mutations

TH (also known as Tyrosine 3-monooxygenase) is a human protein-coding gene encoding a tyrosine 3-monooxygenase protein. It catalyzes the rate-limiting conversion of tyrosine to L-DOPA before dopamine, norepinephrine, and epinephrine synthesis. Biallelic pathogenic variants cause tyrosine-hydroxylase deficiency, ranging from dopa-responsive dystonia to severe infantile parkinsonism. This analysis covers 465 TH variants and mutations. Of these, 78% have computational variant effect predictions. Disease context includes Autosomal recessive dopa-responsive dystonia, TH-deficient dopa-responsive dystonia, and dopa-responsive dystonia. Example TH variants include M1?, M1T, and P4L.

Variant analysis overview

Variant and mutation evidence

Clinical, disease, and population context

Protein structure and variant hotspots

Data sources

Evidence in this analysis draws on EBI Proteins Variation, UniProt, gnomAD v4, EuropePMC, 3D Hotspot Analysis, Interaction Network Analysis, Protein Data Bank, AlphaFold DB, gnomAD constraint, Open Targets, MaveDB, LitVar.

Notable TH variants

Examples include M1?, M1T, P4L, D5T, F14L, R16G, S19C, E20Q. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.