Plexin A4 binds to neuropilin 1 (Nrp1) and neuropilin 2 (Nrp2) and transduces signals from Sema3A, Sema6A, and Sema6B.[6] These Nrp-plexin and semaphorin complexes initiate cascades that regulate diverse processes such as axon pruning and repulsion, dendritic attraction and branching, regulation of cell migration, vascular remodeling, and growth cone collapse.[7][8] Both upregulation and downregulation of Plexin A4 has been observed following neural injury suggesting a dynamic role for Sema3A and Plexin A4 in neural maintenance and regeneration.[7][9] Additionally, Sema3A and therefore its receptor, Plexin A4, have been implicated as possible components of fast-fatigable muscle fiber denervation in ALS.[10]
^Spinelli ED, McPhail LT, Oschipok LW, Teh J, Tetzlaff W (February 2007). "Class A plexin expression in axotomized rubrospinal and facial motoneurons". Neuroscience. 144 (4): 1266–77. doi:10.1016/j.neuroscience.2006.10.057. PMID17197097. S2CID30980461.
^De Winter F, Vo T, Stam FJ, Wisman LA, Bär PR, Niclou SP, van Muiswinkel FL, Verhaagen J (2006). "The expression of the chemorepellent Semaphorin 3A is selectively induced in terminal Schwann cells of a subset of neuromuscular synapses that display limited anatomical plasticity and enhanced vulnerability in motor neuron disease". Mol. Cell. Neurosci. 32 (1–2): 102–17. doi:10.1016/j.mcn.2006.03.002. PMID16677822. S2CID466902.