CST, 78335S, CFTR (D6W6L) Rabbit Monoclonal Antibody

Monoclonal Antibody for studying CFTR. Validated for Western Blotting,Immunoprecipitation,Immunofluorescence (Immunocytochemistry). Available in 2 sizes. Highly specific and rigorously validated in-house, CFTR (D6W6L) Rabbit Monoclonal Antibody (CST #78335) is ready to ship. Product Usage Information Western Blotting: 1:1000 Immunoprecipitation: 1:50 Immunofluorescence (Immunocytochemistry): 1:400 - 1:1600 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody. For a carrier free (BSA and azide free) version of this product see product # 30167 . Protocol Available protocols: Western Blotting, Immunoprecipitation, Immunofluorescence (Immunocytochemistry) Specificity / Sensitivity CFTR (D6W6L) Rabbit Monoclonal Antibody recognizes endogenous levels of total CFTR protein. This antibody also detects a 60 kDa band of unknown origin in some cell lines. Species Reactivity: Human Source / Purification Monoclonal antibody is produced by immunizing animals with recombinant protein fragment of human CFTR protein. The epitope corresponds to a region surrounding Arg735 of human CFTR. Background CFTR (ABC35, ABCC7, CBAVD, CF, dj760C5.1, MRP7, TNR-CFTR) is a member of the ATP-binding cassette (ABC) transporter superfamily. Mutations in ABC genes have been linked to many diseases. CFTR is a plasma membrane cyclic AMP activated chloride channel that is expressed in the epithelial cells of the lung and several other organs (1,2). It mediates the secretion of Cl- and also regulates several channels including the epithelial sodium channel (ENaC), K+ channels , ATP release mechanisms, anion exchangers, sodium bicarbonate transporters and aquaporin water channels (3,4,5,6,7,8 9,10). Mutations in the CFTR gene cause cystic fibrosis, a disease that is characterized by exocrine pancreatic insufficiency, increase in sweat gland NaCl, male infertility and airway disease (1,2,11). Intracellular trafficking regulates the number of CFTR molecules at the cell surface, which in part regulates Cl- secretion. Deletion of phenylalanine 508 (deltaF508) is the most common mutation in CF patients. This mutation results in retention in the ER, where ER quality control mechanisms target the deltaF508 mutant to the proteosome for degradation (12-14). Therefore, disruption of CFTR trafficking leads to disregulation of Cl- secretion at the plasma membrane of epithelial cells. Alternate Names ABC35; ABCC7; ATP-binding cassette sub-family C member 7; ATP-binding cassette transporter sub-family C member 7; cAMP-dependent chloride channel; CF; CF transmembrane conductance regulator; CFTR; CFTR/MRP; Channel conductance-controlling ATPase; cystic fibrosis transmembrane conductance regulating; Cystic fibrosis transmembrane conductance regulator; cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7); dJ760C5.1; MRP7; TNR-CFTR Specification REACTIVITY: H SENSITIVITY: Endogenous MW (kDa): 150-220 Source/Isotype: Rabbit IgG