Calpain-15 (CAPN15)

Calpain-15 (CAPN15) is an intracellular, calcium-dependent cysteine protease that belongs to the non-classical small optic lobes (SOL) family of calpains[1][2][3]. In mammals, CAPN15 is predominantly expressed during embryonic brain and eye development. Its loss in mice leads to neurodevelopmental defects, reduced brain size, congenital eye abnormalities (such as microphthalmia, anophthalmia, coloboma, and cataracts), and growth delays—phenotypes that mirror clinical findings in humans with biallelic CAPN15 variants[1][2]. Unlike the classical calpains (Calpain-1 and -2), CAPN15 possesses a unique N-terminal zinc finger and a C-terminal SOL homology domain, the latter of which is evolutionarily conserved but functionally still unclear[1][2]. CAPN15 has been implicated in proteolytic regulation of developmentally important proteins, regulatory transcription factors (e.g. Pax2, Pax5), and has roles in neuronal plasticity, but its direct protein substrates in vivo remain largely unidentified[1]. There are currently no drugs or validated biomarkers targeting CAPN15, but its crucial function in development makes it a candidate gene in diagnostic panels for congenital eye and neurodevelopmental disorders[2].

Other names

CAPN15Calpain-15SOLHSmall optic lobes homologOGINzmp:0000001110