Reelin is a large extracellular glycoprotein of 420-450 kDa that controls cortical development and secreted by several neurons, such as cortical Cajal-Retzius cells. Defective Reelin is the cause of the reeler malformation in mouse and the Norman-Roberts type lissencephaly in human. Reelin is thought to deliver a signal to migrating neurons, instructing them to assume their correct position. Their response requires binding of Reelin to at least one of two lipoprotein receptors, very-low-density lipoprotein receptor (VLDLR) and apolipoprotein-E receptor type 2 (ApoER2), thereby inducing phosphorylation of the Dab1 (Disabled 1) adapter that interacts with the cytoplasmic tail of receptors. Anti-Reelin monoclonal antibody CR-50 interferes with Reelin homopolymerization and with Dab1 phosphorylation. Intraventricular injection of CR-50 disrupts the organized development of the hippocampus, resulting in a pattern similar to that found in reeler.