MOUSE ANTI HUMAN CD243 from MyBioSource.com

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MOUSE ANTI HUMAN CD243

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MyBioSource.com's MOUSE ANTI HUMAN CD243 is a Mouse monoclonal antibody. The MOUSE ANTI HUMAN CD243 Antibody was generated using ABCB1, Abcb1a, Abcb1b, ATP-binding cassette, sub-family B (MDR/TAP), member 1A, CD243, and MDR as the antigen. It reacts with Human, and Non-Human Primate. This antibody has been shown to work in applications such as: Flow Cytometry, Immunofluorescence, Immunohistochemistry, and Immunoprecipitation.

Description

Mouse anti Human CD243, clone UIC2 recognizes an extracellular conformational epitope of CD243, also known as MDR1 (multi-drug resistance protein 1) and Pgp (P-glycoprotein), a multi pass transmembrane protein and member of the ABC transporter (ATP-binding cassette) family, containing two ABC transporter type 1 domains and two ABC transporter domains. CD243 acts as an active efflux pump for a diverse range of lipophillic compounds. CD243 is expressed at low levels in the cell membrane of peripheral blood leucocytes, and constitutively expressed on the apical plasma membrane of excretory epithelial cells of the kidney, liver, brain and small intestine. CD243 mediates resistance to many chemotherapeutic agents used for tumour suppression and is therefore of special interest to oncologists. Clone UIC2 is a strong inhibitor of CD243-mediated efflux and of the resistance of MDR cells to CD243 transported cytotoxic drugs. Clone UIC2 can be used in a shift assay to selectively demonstrate the expression and functional activity of CD243 in a target cell (Park et al. 2003). Clone UIC2 does not cross-react with mitochondrial pyruvate carboxylase. Exposure of monocytes, which do not constitutively express CD243 leads to an increase in surface expression and a significant enhancement of its substrate efflux activity. This increase in cell surface expression and efflux activity has implications for the drug resistance actions of CD243, not allowing concentrations of therapeutic agents such as cyclosporine (ritonavir) to reach beneficial levels in cells (Tempestilli et al. 2014)