Receptor for SEMA5A that plays a role in axon guidance, invasive growth and cell migration. Stimulates neurite outgrowth and mediates Ca(2+)/Mg(2+)-dependent cell aggregation. In glioma cells, SEMA5A stimulation of PLXNB3 results in the disassembly of F-actin stress fibers, disruption of focal adhesions and cellular collapse as well as inhibition of cell migration and invasion through ARHGDIA-mediated inactivation of RAC1 (By similarity). Seem to be non-essential for normal development and function of the central nervous system. Binds MET and MST1R. Interacts with RIT2/RIN. May form homodimers (via Sema domain) (By similarity). Interacts (via cytoplasmic domain) with FSCN1, ARHGDIA and RAC1. Colocalizes with RIT2/RIN at the plasma membrane. Expressed in brain (at protein level). In cerebellum, strongest expression detected in Purkinje and granular cells. Detected at very low levels in several fetal tissues, including dorsal root ganglia (DRG), heart, lung, optic bulb, brain and liver. In brain, detected first perinatally, with expression reaching maximal levels at postnatal day 9 (P9). In the developing nervous system, barely detectable until birth, and postnatally expressed in white matter tracks including the corpus callosum, external capsule, fimbria hippocampi and corticospinal tracts. In spinal cord, not detected until birth, and postnatally expressed in spinal white matter. In cerebellum, expressed only in cerebellar white matter cells, with expression detected first shortly after birth in the cerebellar peduncle and increasing progressively in the white matter tracts of the cerebellar lobes until P10. Mutant mice are viable and fertile and display no obvious morphological abnormalities in the brain or spinal cord. Belongs to the plexin family. Contains intronic sequences.