RSAD2 antibody

Catalog No. ABIN2191757

Product Details anti-RSAD2 Antibody

Target: RSAD2 (Radical S-Adenosyl Methionine Domain Containing 2 (RSAD2))

Reactivity: Mouse

Host: Human

Clonality: Monoclonal

Conjugate: This RSAD2 antibody is un-conjugated

Application: Western Blotting (WB), Immunofluorescence (IF), Immunoprecipitation (IP), Flow Cytometry (FACS)

Sterility: 0.2 μm filtered

Clone: MaP-VIP

Application Details

Application Notes: recommended that users test the reagent and determine their own optimal dilutions. The typical starting working dilution is 1:50. Product should be stored at 4 °C. Under recommended storage conditions, product is stable for one

Restrictions: For Research Use only

Handling

Buffer: PBS, containing 0.1 % bovine serum albumin and 0.02 % sodium azide.

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Storage: 4 °C

Storage Comment: Product should be stored at 4 °C. Under recommended storage conditions, product is stable for one year.

Expiry Date: 12 months

References for anti-RSAD2 antibody (ABIN2191757)

Lackman, Jamieson, Griffith, Geuze, Cresswell: "Innate immune recognition triggers secretion of lysosomal enzymes by macrophages." in: Traffic (Copenhagen, Denmark), Vol. 8, Issue 9, pp. 1179-89, (2007) (PubMed).

Target Details for RSAD2

Target: RSAD2 (Radical S-Adenosyl Methionine Domain Containing 2 (RSAD2))

Alternative Name: Viperin (RSAD2 Products)

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. Radical S-adenosine methionine domain-containing protein 2, Virus inhibitory protein endoplasmic Aliases reticulum-associated interferon-inducible, Cytomegalovirus-induced gene 5 protein, Cig5 Recombinant mouse viperin fragment (residues 92-362) Immunogen Mouse IgG2a

Pathways: Regulation of Leukocyte Mediated Immunity, Positive Regulation of Immune Effector Process, Production of Molecular Mediator of Immune Response