INS (Insulin) variants and mutations

INS (also known as Insulin) is a human protein-coding gene encoding an insulin protein. After processing to insulin, it lowers blood glucose by promoting cellular glucose uptake, glycogen and lipid synthesis, and suppression of hepatic glucose production. Pathogenic variants can cause neonatal diabetes, maturity-onset diabetes of the young, or hyperproinsulinemia depending on their effect on folding and secretion. This analysis covers 344 INS variants and mutations. Of these, 75% have computational variant effect predictions. Disease context includes diabetes mellitus, permanent neonatal 4, hyperproinsulinemia, and MODY. Example INS variants include M1?, M1I, and M1V.

Variant analysis overview

Variant and mutation evidence

Clinical, disease, and population context

Data sources

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

Notable INS variants

Examples include M1?, M1I, M1V, A2G, A2T, A2A, A2D, A2V. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.