LYST (Lysosomal-trafficking regulator) variants and mutations

LYST (also known as Lysosomal-trafficking regulator) is a human protein-coding gene encoding a lysosomal-trafficking regulator protein. It controls size, trafficking, and exocytosis of lysosome-related organelles in immune cells, melanocytes, and other tissues. Biallelic loss-of-function variants cause Chediak-Higashi syndrome with partial albinism, recurrent infection, bleeding, and risk of hemophagocytic lymphohistiocytosis. This analysis covers 4,472 LYST variants and mutations. Of these, 72% have computational variant effect predictions. Disease context includes Chediak-Higashi syndrome, Chédiak-Higashi syndrome, and Parkinson disease. Example LYST variants include M1?, T3I, and T3N.

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, AlphaFold DB, gnomAD constraint, Open Targets, ClinGen, MaveDB, LitVar.

Notable LYST variants

Examples include M1?, T3I, T3N, D4E, D4N, S5N, N6D, N6K. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.