Bifunctional axonal guidance cue regulated by sulfated proteoglycans; attractive effects result from interactions with heparan sulfate proteoglycans (HSPGs), while the inhibitory effects depend on interactions with chondroitin sulfate proteoglycans (CSPGs). Ligand for receptor PLXNB3. 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). May promote angiogenesis by increasing endothelial cell proliferation and migration and inhibiting apoptosis. Binds PLXNB3. In adult, detected in liver, brain, kidney, heart, lung and spleen. Differentially expressed in embryonic and adult tissues. Its abundance decreases from 10 dpc to birth. At 10.5 dpc, detected in the atrial septum and endocardial cushions, and at lower levels in the atrial and ventricular endocardium. Strong expression detected in embryonic and postnatal retina. At P0 and P3, expression detected in the outer neuroblastic layer. After P7, the expression becomes more restricted and is observed in the middle to outer part of inner nuclear layer, and is not detectable at P21 when retinal development is almost complete. Mutant mice die between 11.5 and 12.5 dpc. At this stage, no defects are detected in the development of extraembryonic tissues, cardiovascular system, axonal trajectories and peripheral nervous system. Mutants display decreased complexity of the hierarchically organized branches of the cranial blood vessels (PubMed:15743826). Mutant mice are viable and fertile (PubMed:21835343). Belongs to the semaphorin family.