Influenza A Virus H1N1 Antikörper (FITC)

Produktnummer ABIN648061

Produktdetails

Target: Influenza A Virus H1N1

Reaktivität: Influenza A Virus H1N1

Wirt: Ziege

Konjugat: FITC

Applikation: Bitte anfragen

Spezifität: Purified virions. Specific to H1N1 by IHA. Does not react with Influenza B, RSV, Para 1-3 or Adeno. Does not react with HEp-2 cells. May react with chicken cellular proteins.

Produktmerkmale: Goat Anti-Influenza A H1N1 (virions)

Immunogen: Influenza A Strain USSR (H1N1)

Anwendungsinformationen

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 4-5 mg/ml (OD280nm, E^0.1% = 1.4)

Buffer: 0.01M PBS, pH 7.2 containing 10mg/ml BSA

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

Antigendetails

Target: Influenza A Virus H1N1

Substanzklasse: Influenza Virus

Hintergrund: Actin polymerization is required for a variety of cell functions. Cells trigger Actin polymerization through either the de novo nucleation of filaments from monomeric Actin, the severing of existing filaments to create uncapped barbed ends, or the uncapping existing barbed ends. The nucleation of Actin is a rate-limiting and unfavorable reaction in Actin polymerization and therefore requires the involvement of the Arp2/3 complex, which helps create new filaments and promotes the end-to-side cross-linking of Actin filaments into the branching meshwork. The Arp2/3 complex consists of the Actinrelated proteins Arp2 and Arp3, as well as p41-ARC, p34-ARC, p21-ARC, p20-ARC and p16-ARC. The Arp2/3 complex promotes Actin nucleation by binding the pointed end of Actin filaments, or by associating with the side of an existing filament, and nucleates growth in the barbed direction. In addition, the Arp2/3 complex mediates Actin cytoskeletal outgrowths that are regulated by the Rho family of small GTPases. In response to GTPbinding Cdc42, the Arp2/3 complex binds the Cdc42 substrates, namely the WASP proteins, and initiates the formation of lamellipodia and filopodia.