SCN3B Protein

Sodium channel, voltage-gated, type III, beta Protein Datasheet

SCN3B Protein Product Information

• Synonym: HSA243396, SCNB3
• Protein Construction: A DNA sequence encoding the human SCN3B (Q9NY72) extracellular domain (Met 1- Glu 159) was fused with the Fc region of human IgG₁ at the C-terminus.
• Source: Human
• Expression Host: Human Cells

SCN3B Protein QC Testing

• Purity: > 96 % as determined by SDS-PAGE
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method
• Stability: Samples are stable for up to twelve months from date of receipt at -70℃
• Predicted N terminal: Phe 23
• Molecular Mass: The recombinant human SCN3B/Fc is a disulfide-linked homodimeric protein. The reduced monomer consists of 378 amino acids and has a predicted molecular mass of 42.5 kDa. The apparent molecular mass of the reduced monomer is approximately 50-55 kDa in SDS-PAGE under reducing conditions due to glycosylation.
• Formulation: Lyophilized from sterile PBS, pH7.4
  1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
  2. Please contact us for any concerns or special requirements.
• SDS-PAGE: SCN3B protein

SCN3B Protein Usage Guide

• Storage: Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Reconstitution: A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

SCN3B Protein Description

SCN3B (sodium channel, voltage-gated, type III, beta ,human IgG1-Fc chimera) belongs to the sodium channel auxiliary subunit SCN3B (TC 8.A.17) family. It contains 1 Ig-like C2-type (immunoglobulin-like) domain. SCN3B modulates channel gating kinetics; causes unique persistent sodium currents; inactivates the sodium channel opening more slowly than the subunit beta-1. Its association with neurofascin may target the sodium channels to the nodes of ranvier of developing axons and retain these channels at the nodes in mature myelinated axons. Defects in SCN3B are the cause of Brugada syndrome type 7. A tachyarrhythmia characterized by right bundle branch block and ST segment elevation on an electrocardiogram. It can cause the ventricles to beat so fast that the blood is prevented from circulating efficiently in the body. When this situation occurs (called ventricular fibrillation), the individual will faint and may die in a few minutes if the heart is not reset.

References

1. Morgan K. et al., 2000, Proc Natl Acad Sci. 97 (5): 2308-13.
2. Hartley JL. et al. Genome Res. 10 (11): 1788-95.
3. Hirosawa M. et al., 2000, DNA Res. 6 (5): 329-36.