RSAD2 Antikörper

Produktnummer ABIN2191757

Produktdetails anti-RSAD2 Antikörper

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

Reaktivität: Maus

Wirt: Human

Klonalität: Monoklonal

Konjugat: Dieser RSAD2 Antikörper ist unkonjugiert

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

Sterilität: 0.2 μm filtered

Klon: MaP-VIP

Anwendungsinformationen

Applikationshinweise: 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

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

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

Konservierungsmittel: Sodium azide

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

Lagerung: 4 °C

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

Haltbarkeit: 12 months

Referenzen für anti-RSAD2 Antikörper (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).

Details zu RSAD2

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

Andere Bezeichnung: Viperin (RSAD2 Produkte)

Hintergrund: 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