Viperin Antibody (MaP.VIP) Summary
| Immunogen |
Recombinant mouse viperin fragment (residues 92-362)
|
| Specificity |
Mouse Viperin
|
| Isotype |
IgG2a
|
| Clonality |
Monoclonal
|
| Host |
Mouse
|
| Gene |
RSAD2
|
| Purity |
Protein A or G purified
|
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|
Applications/Dilutions
| Dilutions |
|
| Application Notes |
For flow cytometry and Western blotting, dilutions to be used depend on detection system applied. It is recommended that users test the reagent and determine their own optimal dilutions. The typical starting working dilution is 1:50.
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. |
| Theoretical MW |
42 kDa.
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. |
Reactivity Notes
Human.
Packaging, Storage & Formulations
| Storage |
Store at 4C. Do not freeze.
|
| Buffer |
0.2 um filtered solution in PBS and 0.1% BSA
|
| Preservative |
0.02% Sodium Azide
|
| Concentration |
0.1 mg/ml
|
| Purity |
Protein A or G purified
|
Alternate Names for Viperin Antibody (MaP.VIP)
- 2510004L01Rik
- cig33
- cig5
- Cytomegalovirus-induced gene 5 protein
- interferon-inducible
- radical S-adenosyl methionine domain containing 2
- radical S-adenosyl methionine domain-containing protein 2
- vig1
- viperin
- Virus inhibitory protein, endoplasmic reticulum-associated
Background
The monoclonal antibody MaP.VIP recognizes mouse Viperin, a 42 kDa protein belonging to the RSAD2 family. Viperin is the abbreviation of Virus inhibitory protein endoplasmic reticulum-associated interferon-inducible. It is an evolutionary conserved protein that is highly inducible by both type I and type II interferons. However, little or no induction by interferon gamma is observed in monocytic cell lines. Infection by many viruses, including human cytomegalovirus (hCMV), hepatitis C virus, yellow fever virus and Sendai virus, strongly induces viperin expression, suggesting a role in the host antiviral response. Viperin has also been shown to be important for the host anti-HIV responses. Furthermore, expression of viperin inhibits influenza replication by perturbing its release from the plasma membrane. Viperin expression alters plasma membrane fluidity by affecting formation of lipid rafts which are detergent-resistant membrane microdomains known to be the sites of influenza virus budding. HCMV infection induces the redistribution of viperin from the endoplasmic reticulum to the Golgi complex and ultimately to cytoplasmic vacuoles, suggesting that viperin may function at a distinct level in the viral lifecycle, at the point of glycosylated viral protein transport.
