Trpc1, encoding the TRPC1 ion channel, is the first cloned mammalian TRP channel. It functions as a cation-nonselective channel within pathways controlling Ca(2+) entry in response to cell-surface receptor activation, affecting basic cell functions like proliferation, survival, differentiation, secretion, and cell migration, as well as cell-type specific functions [1].

Genetically engineered mice with Trpc1 gene ablation have been used to study its biological role. These mice, though reaching adulthood, show defects in multiple organs and tissues including the cardiovascular, central nervous, skeletal and muscular, and immune systems. Genetic and functional studies suggest its implication in diseases such as diabetic nephropathy, Parkinson's disease, Huntington's disease, Duchenne muscular dystrophy, cancer, seizures, and Darier-White skin disease [1]. In colon cancer cells, inhibiting the expression of TRPC1 channels by DFMO eliminates their contribution to store-operated Ca2+ entry (SOCE), which abolishes cancer hallmarks [2].

In conclusion, Trpc1 is crucial for various cell functions through its role in Ca(2+) signaling pathways. Studies using Trpc1 knockout mouse models have revealed its significance in multiple disease areas, including neurodegenerative diseases, muscular dystrophy, and cancer, providing insights into disease mechanisms and potential therapeutic targets.