SAB4501942
Anti-CFTR antibody produced in rabbit
affinity isolated antibody
Synonym(s):
ABCC7, Cystic fibrosis transmembrane conductance regulator, cAMP- dependent chloride channel
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About This Item
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 168 kDa
species reactivity
rat, mouse, human
concentration
~1 mg/mL
technique(s)
ELISA: 1:1000
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000
NCBI accession no.
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... CFTR(1080)
General description
Anti-CFTR Antibody detects endogenous levels of total CFTR protein.
CFTR (Cystic fibrosis transmembrane conductance regulator, ATP-binding cassette sub-family C, member 7) is a membrane-associated, N-linked glycoprotein.
Immunogen
The antiserum was produced against synthesized peptide derived from human CFTR.
Immunogen Range: 711-760
Immunogen Range: 711-760
Application
Anti-CFTR antibody produced in rabbit is suitable for immunohistochemistry and western blot applications.
Biochem/physiol Actions
CFTR (Cystic fibrosis transmembrane conductance regulator, ATP-binding cassette sub-family C, member 7) is mainly involved in the regulation of Na+ and Cl- transport by acting as a linear, cAMP activated, chloride channel. In addition, it is also associated with different transport signaling pathways. It has been reported that CFTR controls functionality of outwardly rectifying Cl- channels (ORCCs) by facilitating the transport and delivery of potent autacoid agonist and ORCC regulator ATP. It has also been suggested that CFTR can interact with Na+-reabsorptive pathway. CFTR is associated with congenital bilateral absence of the vas deferens (CBAVD) and causes the genital form of cystic fibrosis (CF). The CFTR gene may also responsible for male infertility. It may be useful for assisting reproduction technology.
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Certificates of Analysis (COA)
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Karen Sánchez et al.
Investigacion clinica, 55(1), 44-54 (2014-04-25)
Mutations in the CFTR gene in Cystic Fibrosis (CF) patients have geographic differences and there is scant data on their prevalence in Venezuelan patients. This study determined the frequency of common CFTR gene mutations in these patients. We amplified and
S H Cheng et al.
Cell, 63(4), 827-834 (1990-11-16)
The gene associated with cystic fibrosis (CF) encodes a membrane-associated, N-linked glycoprotein called CFTR. Mutations were introduced into CFTR at residues known to be altered in CF chromosomes and in residues believed to play a role in its function. Examination
Himanshu Sharma et al.
Gene, 548(1), 43-47 (2014-07-11)
High incidence of mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is associated with congenital bilateral absence of the vas deferens (CBAVD) and is considered as the genital form of cystic fibrosis (CF). The CFTR gene may also
E M Schwiebert et al.
Cell, 81(7), 1063-1073 (1995-06-30)
The cystic fibrosis transmembrane conductance regulator (CFTR) functions to regulate both Cl- and Na+ conductive pathways; however, the cellular mechanisms whereby CFTR acts as a conductance regulator are unknown. CFTR and outwardly rectifying Cl- channels (ORCCs) are distinct channels but
C Norez et al.
British journal of pharmacology, 171(21), 4831-4849 (2014-07-30)
The most common mutation in cystic fibrosis (CF), F508del, causes defects in trafficking, channel gating and endocytosis of the CF transmembrane conductance regulator (CFTR) protein. Because CF is an orphan disease, therapeutic strategies aimed at improving mutant CFTR functions are
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