sema3a การใช้

• The absence of SGC in the axon causes the repulsion from Sema3a.
• In addition, SEMA3a is known to repel Schwann cells.
• SGC generates cGMP, leading to a sequence of chemical activations that result in the attraction towards Sema3a.
• Class 3 semaphorins are one of the most versatile semaphorin classes, in which Sema3a is the most studied.
• Increased expression of Sema3A is associated with schizophrenia and is seen in a variety of human tumor cell lines.
• Guidance cues, such as Sema3A, induce the collapse and paralysis of neuronal growth cones during development of the nervous system.
• Additionally, the terminal Schwann cells of ALS mice ( SOD1 mutant ) express Sema3A at synaptic weakening and denervation that precedes motor neuron apoptosis in ALS.
• The SEMA3A gene is a member of the semaphorin family and encodes a protein with an Ig-like chemoattractive agent, stimulating the growth of apical dendrites.
• For instance, Sema3a repels axons from the dorsal root ganglia, facial nerves, vagal nerves, olfactory-sensory, cortical nerves, hippocampal nerves and cerebellar nerves.
• Studies have suggested that Sema3A / Neuropilin 2 ( Npn2 ) interactions mediate synapse elimination and axonal pruning, as demonstrated by Sema3A / Npn2 loss-of-function studies in mice.
• Studies have suggested that Sema3A / Neuropilin 2 ( Npn2 ) interactions mediate synapse elimination and axonal pruning, as demonstrated by Sema3A / Npn2 loss-of-function studies in mice.
• NRP1 is a membrane-bound coreceptor to a tyrosine kinase receptor for both vascular endothelial growth factor ( VEGF; MIM 192240 ) and semaphorin ( see SEMA3A; MIM 603961 ) family members.
• In addition, soluble Sema3A binds to Neuropilin-1, which lacks an intracellular domain and thus co-signals with Plexin A . Sema4A in its membrane form binds to Plexin B1 for its signaling pathway.
• In DRG neurons, CRMP-2 is phosphorylated by Rho kinase in LPA signaling but not in Sema3A signaling, revealing the presence of both Rho kinase-dependent and Rho kinase-independent pathways for the growth cone collapse.
• Semaphorins also play a critical role in cranial nerve development; studies using mice deficient in Sema3A and Sema3F have resulted in abnormal cranial nerve extension and defasciculation, while Sema3F has been suggested to be required in order to establish projections of cranial nerves.