Recombinant Human IFITM3 Protein (Fc Tag) | PKSH030843

Recombinant Human IFITM3 Protein (Fc Tag) | PKSH030843 | Gentaur US, UK & Europe Disrtribition

Synonyms: 1-8U;DSPA2b;IP15

Active Protein: N/A

Activity: A DNA sequence encoding the human IFITM3 (NP_066362.2) (Met1-His57) was expressed, fused with the Fc region of mouse IgG1 at the N-terminus.

Protein Construction: A DNA sequence encoding the human IFITM3 (NP_066362.2) (Met1-His57) was expressed, fused with the Fc region of mouse IgG1 at the N-terminus.

Fusion Tag: N-Fc

Species: Human

Expressed Host: HEK293 Cells

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Purity: > 99 % as determined by reducing SDS-PAGE.

Endotoxin: < 1.0 EU per µg as determined by the LAL method.

Stability and Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.

Molecular Mass: 32.9 kDa

Formulation: Lyophilized from sterile PBS, pH 7.4

Reconstitution: Please refer to the printed manual for detailed information.

Background: Interferon-induced transmembrane protein 3 (IFITM3) belongs to the CD225 family. To replicate, viruses must gain access to the host cell's resources. Interferon (IFN) regulates the actions of a large complement of interferon effector genes (IEGs) that prevent viral replication. The interferon inducible transmembrane protein family members, IFITM1, 2 and 3, are IEGs required for inhibition of influenza A virus, dengue virus, and West Nile virus replication in vitro. IFITM3 is an IFN-induced antiviral protein that mediates cellular innate immunity to at least three major human pathogens, namely influenza A H1N1 virus, West Nile virus (WNV), and dengue virus (WNV), by inhibiting the early step(s) of replication. It is both necessary and sufficient for preventing the emergence of viral genomes from the endosomal pathway. Viral pseudoparticles were inhibited from transferring their contents into the host cell cytosol by IFN, and IFITM3 was required and sufficient for this action. IFITM3 overexpression is sufficient for this phenotype. Moreover, IFITM3 partially resides in late endosomal and lysosomal structures, placing it in the path of invading viruses.

Research Area: Developmental Biology, Stem cells