Binds to the C-terminal PTS1-type tripeptide peroxisomal targeting signal (SKL-type) and plays an essential role in peroxisomal protein import. Interacts with PEX7, PEX12, PEX13 and PEX14. Interacts (Cys-linked ubiquitinated) with ZFAND6 (By similarity). Interacts with VWA8 in a PEX7-dependent manner (By similarity). Its distribution appears to be dynamic. It is probably a cycling receptor found mainly in the cytoplasm and as well associated to the peroxisomal membrane through a docking factor (PEX13). Monoubiquitination at Cys-11 is required for proper export from peroxisomes and recycling. Liver-specific knockout mice display a growth retardation from the third postnatal week resulting in a 30% to 40% lower body weight than control mice at the age of 7 weeks. Thereafter, mice tend to catch up in growth, and by 3 months their weight is not different from control mice. Throughout this period, the mice look healthy, are fertile and liver function is unaffected. However, 10-week-old mutant mice display a severe hepatomegaly due to hypertrophic and hyperplastic hepatocytes. Mutant mice survive but develope extensive liver tumors from 12 months on (PubMed:15732085). Peroxisomes are absent in mutant hepatocytes and multiple ultrastructural alterations are noticed, smooth endoplasmic reticulum proliferation, and accumulation of lipid droplets and lysosomes. Most prominent is the abnormal structure of the inner mitochondrial membrane. This is accompanied by severely reduced activities of complex I, III, and V and a collapse of the mitochondrial inner membrane potential (PubMed:15732085). Liver-specific knockout mice display severely impaired oxidation of 2-methylhexadecanoic acid, the bile acid intermediate trihydroxycholestanoic acid (THCA), and tetradecanedioic acid. In contrast, mitochondrial beta-oxidation rates of palmitate are doubled (PubMed:17442273). Belongs to the peroxisomal targeting signal receptor family.