|Other Names||Semaphorin-6A, Semaphorin VIA, Sema VIA, Semaphorin-6A-1, SEMA6A-1, SEMA6A, KIAA1368, SEMAQ|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Cell surface receptor for PLXNA2 that plays an important role in cell-cell signaling. Required for normal granule cell migration in the developing cerebellum. Promotes reorganization of the actin cytoskeleton and plays an important role in axon guidance in the developing central nervous system. Can act as repulsive axon guidance cue. Has repulsive action towards migrating granular neurons. May play a role in channeling sympathetic axons into the sympathetic chains and controlling the temporal sequence of sympathetic target innervation (By similarity).|
|Cellular Location||Cell membrane; Single-pass type I membrane protein|
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Provided below are standard protocols that you may find useful for product applications.
SEMA6A belongs to a subfamily characterized by an extracellular semaphorin domain, a transmembrane domain, and a long cytoplasmic tail. Members of this class can repel sympathetic and dorsal root ganglion axons in vitro, consistent with a traditional role as guidance signals. However, the length of the cytoplasmic tail, which includes an EVL-binding site in SEMA6A and an Src-binding site in SEMA6B, suggests that these semaphorins may also function as receptors. SEMA6A is expressed in developing neural tissue and is required for proper development of the thalamocortical projection. SEMA6A directly links the Ena/VASP and the semaphorin protein families since the SEMA6A protein is capable of selective binding to the protein EVL (Ena/VASP-like protein).
Johnson, M.P., et al. Hum. Genet. 126(5):655-666(2009)Landers, J.E., et al. Proc. Natl. Acad. Sci. U.S.A. 106(22):9004-9009(2009)Prislei, S., et al. Mol. Cancer Ther. 7(1):233-241(2008)
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