Fx1a Antikörper

Produktnummer ABIN675159

Zitiert in 1 Publikation. Der Kaninchen Polyklonal anti-Fx1a Antikörper (ABIN675159) detektiert spezifisch Fx1a in IF (cc), IF (p), ELISA, IHC (fro) und IHC (p). Dieser Antikörper reagiert spezifisch mit Proben aus Human, Maus und Ratte.

Kurzübersicht für Fx1a Antikörper (ABIN675159)

Target: Fx1a

Reaktivität: Human, Maus, Ratte

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Unkonjugiert

Applikation: Immunofluorescence (Cultured Cells) (IF (cc)), Immunofluorescence (Paraffin-embedded Sections) (IF (p)), ELISA, Immunohistochemistry (Frozen Sections) (IHC (fro)), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Produktdetails

Kreuzreaktivität: Human, Maus, Ratte

Aufreinigung: Purified by Protein A.

Immunogen: Fx1A protein

Isotyp: IgG

Anwendungsinformationen

Applikationshinweise: ELISA 1:500-1000
IHC-P 1:200-400
IHC-F 1:100-500
IF(IHC-P) 1:50-200
IF(IHC-F) 1:50-200
IF(ICC) 1:50-200

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 1 μg/μL

Buffer: 0.01M TBS( pH 7.4) with 1 % BSA, 0.02 % Proclin300 and 50 % Glycerol.

Konservierungsmittel: ProClin

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

Lagerung: 4 °C,-20 °C

Informationen zur Lagerung: Shipped at 4°C. Store at -20°C for one year. Avoid repeated freeze/thaw cycles.

Haltbarkeit: 12 months

Referenzen

Wu, Feng, Cui, Hou, Tang, Zhou, Cai, Xie, Hong, Fu, Chen: "Rapamycin upregulates autophagy by inhibiting the mTOR-ULK1 pathway, resulting in reduced podocyte injury." in: PLoS ONE, Vol. 8, Issue 5, pp. e63799, (2013) (PubMed).

Antigendetails

Target: Fx1a

Hintergrund: Optional[synonyms]: Binding of anti-Fx1A to Heymann nephritis antigens (HA) on rat glomerular epithelial cells (GECs) in culture leads to capping and disappearance of antigens from the cell surface. This process may contribute to the formation of glomerular subepithelial immune deposits in vivo. The authors differentially extracted GECs to determine whether HA redistribution is mediated by cytoskeletal components. Observations were made by phase-contrast and immunofluorescence microscopy on primary and passaged GECs in monolayer culture and by spectrofluorimetry on GECs in suspension.