Recombinant Human Semaphorin 3F Fc Chimera Protein, CF

Recombinant Human Semaphorin 3F Fc Chimera Protein, CF Summary

Product Specifications

Product Datasheets

Carrier Free

CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.

In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.

Background: Semaphorin 3F

Semaphorin 3F (Sema 3F; previously Sema IV) is one of six Class 3 (secreted) semaphorins. Class 3 semaphorins are potent chemorepellents that function in axon guidance and/or vascular tip cell guidance during development (1). Sema 3F is expressed in the developing nervous system, especially in the dorsal spinal cord (2, 3). In adults, Sema 3F is expressed in the lung and most other tissues (2). Crystal structures of semaphorins reveal that the 500 amino acid (aa) N-terminal Sema domain forms a seven-blade beta-propeller similar to that found in integrin molecules. Fourteen conserved cysteine residues and one or more N-glycosylation sites are thought to be critical for forming the secondary structure (4). Isoform 2 is missing aa 153-183 within the Sema domain relative to the long form (Isoform 1) but appears to have similar activity. C-terminal to the Sema domain, Sema 3F has a basic domain, a cysteine-knot plexin/semaphorin/integrin (PSI) domain, an Ig-like domain, a cysteine for dimerization and another basic domain at the C-terminus. Dimerization and cleavage at the C-terminus are required for repulsing activity of class 3 semaphorins (5). Human Sema 3F shares 96% aa identity with mouse and rat Sema 3F. Sema 3F signaling is transduced by type-A plexins, especially Plexin-A3, via interaction with neuropilin-2 (3, 6). Sema 3F-Npn-2-Plexin-A3 signaling regulates AMPA-type glutamate receptor (AMPAR) homeostatic downscaling in response to increased neuronal activity of cortical neurons (7). Genetic disruption of either Sema 3F or neuropilin-2 alters motor axon trajectory to the ventral forelimb (3). Sema 3F is deleted or down-regulated in many metastatic tumors such as colorectal cancer, oral squamous carcinoma, lung cancer, and many others (8-10). Restoration of Sema 3F decreases tumorigenicity, vascularization and adhesiveness, most likely through repulsive interactions, VEGF antagonism and downstream integrin regulation (11).

Related Research Areas

• Axon Guidance and Neuron Migration
• Proteoglycans
• Semaphorins, Plexin Receptors, and Related Molecules