Recombinant Human Semaphorin 4A Fc Chimera Protein, CF Summary
Details of Functionality
Measured by its ability to cause collapse of chick embryonic dorsal root ganglia (DRG) neuron growth cones. 2.5-5.0 µg/mL of Recombinant Human Semaphorin 4A Fc Chimera causes >50% growth cone collapse in the presence of 10 ng/mL of Recombinant Human beta ‑NGF (Catalog # 256-GF). Optimal dilutions should be determined by each laboratory for each application.
Mouse myeloma cell line, NS0-derived human Semaphorin 4A protein
Human Semaphorin 4A (Gly32-His 683) Accession # Q9H3S1
>85%, by SDS-PAGE under reducing conditions and visualized by silver stain
<0.1 EU per 1 μg of the protein by the LAL method.
98.5 kDa (monomer). Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
Semaphorin 4A (Sema4A, previously semB) is a Class 4 transmembrane Semaphorin with activity in the immune and nervous systems (1). The 761 amino acid (aa) human Sema4A precursor contains a 32 aa signal sequence, a 651 aa extracellular domain (ECD) containing sema, PSI and C2-type immunoglobulin domains, a 21 aa transmembrane domain, and a 57 aa cytoplasmic domain with two Ser/Thr phosphorylation sites (2). Human Sema4A ECD shares 87%, 87%, 86% and 85% aa identity with mouse, rat, bovine and canine Sema4A, respectively, and shares 32-37% aa identity with other human Sema4 family members. Of six reported splice variants with 723, 629, 370, 321, 236 and 220 aa, five lack the N-terminus and/or portions of the sema domain, and three lack the transmembrane and cytoplasmic domains in the C-terminus (3). Sema4A was first described as a molecule that enhances T cell activation and interacts with TIM-2 (T cell immunoglobulin and mucin domain-2 (4). Mice with targeted disruption of Sema4A show defects in dendritic cell-mediated T cell priming and Th1 responses (5). Roles for Sema4A have also been identified in the brain, the endothelium and the eye. It mediates hippocampal neuron growth cone collapse in vitro through interaction of the sema domain with plexin-B1 (6). Interaction of Sema4A with endothelial cell plexin-D1 causes opposition to the angiogenic, proliferative, chemotactic and integrin-mediated adhesive actions of VEGF (7). The retina of Sema4A-/- mice shows severe degeneration, and mutations of Sema4A are associated with retinitis pigmentosa and cone rod dystrophy in humans (8, 9).
Kumanogoh, A. et al. (2003) J. Cell Sci. 116:3463.
Swissprot Accession # Q9H3S1.
Entrez Accession # CAI15528, CAI15529, CAI15531, CAI15532, CAI15533 and EAW52993.
Kumanogoh, A. et al. (2002) Nature 419:629.
Kumanogoh, A. et al. (2005) Immunity 22:305.
Yukawa, K. et al. (2005) Int. J. Mol. Med. 16:115.
Toyofuku, T. et al. (2007) EMBO J. 26:1373.
Rice, D.S. et al. (2004) Invest. Ophthalmol. Vis. Sci. 45:2767.
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