Rabbit anti-Rat CFTR Polyclonal Antibody | anti-CFTR antibody

Anti-CFTR Antibody

Cat. Num. AAA4159166

• Gene Names: CFTR; CF; MRP7; ABC35; ABCC7; CFTR/MRP; TNR-CFTR; dJ760C5.1
• Reactivity: Rat
• Applications: Western Blot, Immunohistochemistry
• Purity: Affinity Purified On Immobilized Antigen.
• Synonyms: CFTR; Polyclonal Antibody; Anti-CFTR Antibody; anti-CFTR antibody

• Host: Rabbit
• Reactivity: Rat
• Clonality: Polyclonal
• Specificity: Mouse, rat, pig-13/14 residues identical.
• Purity/Purification: Affinity Purified On Immobilized Antigen.
• Form/Format: Liquid; PBS, pH 7.4 with 0.05% sodium azide.
• Concentration: 1ug/ul (varies by lot)
• Sequence Length: 17

• Applicable Applications for anti-CFTR antibody: Western Blot (WB), Immunohistochemistry (IHC)
• Application Notes: WB: Rat lung membranes (1:200); IHC: Rat lung sections
• Immunogen: Peptide (C)KEETEEEVQDTRL, corresponding to amino acid residues 1468-1480 of human CFTR (Accession # P13569).
• Preparation and Storage: This product is stable for several weeks at 4 degree C as an undiluted liquid. Dilute only prior to immediate use.; For extended storage, aliquot contents and freeze at-20 degree C or below. Avoid cycles of freezing and thawing. Expiration date is one (1) year from date of receipt.

Testing Data

Testing Data

Related Product Information for anti-CFTR antibody

The cystic fibrosis transmembrane conductance regulator (CFTR) is the most dominant Cl-channel in several epithelial tissues, especially in lung and colon. Remarkably, CFTR is a member of the ATP-binding cassette (ABC) transporter superfamily that uses ATP hydrolyzation as the driving force for the translocation of a wide variety of substrates including sugars, amino acids, proteins and hydrophobic compounds, across cellular membranes. The CFTR is unique among ABC transporters in that it is a cAMP-regulated Cl-channel. It shares the superfamily topology of 12 transmembrane domains with two nucleotide-binding domains (NBDs) and a regulatory (R) domain in the large third intracytoplasmic loop that is phosphorylated in multiple sites by PKA. Mutations in the CFTR gene cause channel dysfunction in several ways, ranging from complete loss of surface expression to diminished Cl-secretion. Defects in the CFTR gene cause cystic fibrosis (CF), the most common genetic disease among Caucasians, as well as a form of male sterility. Regulation of the CFTR channel is accomplished through the activation of surface receptors that couple to adenyl cyclase, raise cAMP cellular levels and thus activate PKA. This has been demonstrated for the adenosine and b2 adrenergic receptor and the vasopressin hormone among others. Besides enhanced Cl-conductance, activation of CFTR also leads to the regulation of other ion channels. The best-studied case is its interaction with the epithelial Na+ channels (ENaC), although it can probably regulate other ion channels as well (Kir1.1 for example). The mechanism by which CFTR regulates other ion channels is not clear, but it may involve protein-protein interactions via molecules that interact with its C-terminal PDZ binding motif, such as the NHERF adaptor protein.

NCBI and Uniprot Product Information

• NCBI GI #: 1041521608
• NCBI GeneID: 1080
• NCBI Official Full Name: CFTR, partial
• NCBI Official Synonym Full Names: CF transmembrane conductance regulator
• NCBI Official Symbol: CFTR
• NCBI Official Synonym Symbols: CF; MRP7; ABC35; ABCC7; CFTR/MRP; TNR-CFTR; dJ760C5.1
• NCBI Protein Information: cystic fibrosis transmembrane conductance regulator
• Protein Family: Cystic fibrosis transmembrane conductance regulator

NCBI Description

This gene encodes a member of the ATP-binding cassette (ABC) transporter superfamily. The encoded protein functions as a chloride channel, making it unique among members of this protein family, and controls ion and water secretion and absorption in epithelial tissues. Channel activation is mediated by cycles of regulatory domain phosphorylation, ATP-binding by the nucleotide-binding domains, and ATP hydrolysis. Mutations in this gene cause cystic fibrosis, the most common lethal genetic disorder in populations of Northern European descent. The most frequently occurring mutation in cystic fibrosis, DeltaF508, results in impaired folding and trafficking of the encoded protein. Multiple pseudogenes have been identified in the human genome. [provided by RefSeq, Aug 2017]