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GeneBio Systems

CFTR (Phospho-Ser737) rabbit pAb

CFTR (Phospho-Ser737) rabbit pAb

SKU:ES17503

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Size: 100μL

Source:Rabbit

Applications:IHC;IF;WB

Reactivity:Human; Mouse; Rat

Dilution:IHC-p 1:50-200, WB 1:500-2000

Immunogen:Synthesized peptide derived from human CFTR (Phospho-Ser737)

Storage_stability:-20°C/1 year

Clonality:Polyclonal

Isotype:IgG

Concentration:1 mg/ml

Observed_band(KD):166kD

Human_gene_id:1080

Human_swiss_prot_no:P13569

Subcellular_location:Apical cell membrane ; Multi-pass membrane protein . Early endosome membrane ; Multi-pass membrane protein . Cell membrane ; Multi-pass membrane protein . Recycling endosome membrane ; Multi-pass membrane protein . Endoplasmic reticulum membrane ; Multi-pass membrane protein . Nucleus . The channel is internalized from the cell surface into an endosomal recycling compartment, from where it is recycled to the cell membrane (PubMed:17462998, PubMed:19398555, PubMed:20008117). In the oviduct and bronchus, detected on the apical side of epithelial cells, but not associated with cilia (PubMed:22207244). In Sertoli cells, a processed product is detected in the nucleus (By similarity). ER stress induces GORASP2-mediated unconventional (ER/Golgi-independent) trafficking of core-glycosylated CFTR t

Other_name:Cystic fibrosis transmembrane conductance regulator (CFTR;ATP-binding cassette sub-family C member 7;Channel conductance-controlling ATPase;EC 3.6.3.49;cAMP-dependent chloride channel)

Background:This gene encodes a member of the ATP-binding cassette (ABC) transporter superfamily. ABC proteins transport various molecules across extra- and intra-cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). This protein is a member of the MRP subfamily that is involved in multi-drug resistance. The encoded protein functions as a chloride channel and controls the regulation of other transport pathways. Mutations in this gene are associated with the autosomal recessive disorders cystic fibrosis and congenital bilateral aplasia of the vas deferens. Alternatively spliced transcript variants have been described, many of which result from mutations in this gene. [provided by RefSeq, Jul 2008],

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