MAB3482
Anti-Cystic Fibrosis Transmembrane Conductance Regulator Antibody, clone MM13-4
clone MM13-4, Chemicon®, from mouse
Synonym(s):
CFTR
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
MM13-4, monoclonal
species reactivity
human
should not react with
mouse, shark
manufacturer/tradename
Chemicon®
technique(s)
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable
isotype
IgG1
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... CFTR(1080)
Specificity
Human cystic fibrosis transmembrane conductance regulator (CFTR). Recognizes an epitope at the N-terminal between residues 24 and 35.
Immunogen
Synthetic peptide (RKGYRQRLELSD) corresponding to residues 25-36 of human cystic fibrosis transmembrane conductance regulator (CFTR).
Application
Detect Cystic Fibrosis Transmembrane Conductance Regulator using this Anti-Cystic Fibrosis Transmembrane Conductance Regulator Antibody, clone MM13-4 validated for use in IC, IP & WB.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Ion Channels & Transporters
Ion Channels & Transporters
Western blot: 10 μg/mL, recognizes CFTR (150-170kDa) and two additional proteins at 52kDa and 38kDa
Immunoprecipitation
Immunofluorescence
Note: Does not work on paraffin embedded tissue.
Optimal working dilutions must be determined by the end user.
Immunoprecipitation
Immunofluorescence
Note: Does not work on paraffin embedded tissue.
Optimal working dilutions must be determined by the end user.
Physical form
Format: Purified
Purified immunoglobulin. Liquid in 0.02 M Phosphate buffer, 0.25 M NaCl, pH 7.6 with 0.1% sodium azide.
Storage and Stability
Maintain at 2-8°C in undiluted aliquots up to 6 months.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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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Description
Pricing
Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Jie Ting Zhang et al.
Scientific reports, 7(1), 5233-5233 (2017-07-14)
Cystic fibrosis transmembrane conductance regulator (CFTR), known as a cAMP-activated Cl- channel, is widely expressed at the apical membrane of epithelial cells in a wide variety of tissues. Of note, despite the abundant expression of CFTR in mammalian kidney, the
Yukiko Sato et al.
Scientific reports, 11(1), 23256-23256 (2021-12-03)
There is evidence that the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel is highly expressed at the apical pole of ciliated cells in human bronchial epithelium (HBE), however recent studies have detected little CFTR mRNA in those cells. To
Onofrio Laselva et al.
Frontiers in pharmacology, 9, 719-719 (2018-07-20)
The psoralen-related compound, 4,6,4'-trimethylangelicin (TMA) potentiates the cAMP/PKA-dependent activation of WT-CFTR and rescues F508del-CFTR-dependent chloride secretion in both primary and secondary airway cells homozygous for the F508del mutation. We recently demonstrated that TMA, like lumacaftor (VX-809), stabilizes the first membrane-spanning
Alexandre Hinzpeter et al.
PLoS genetics, 6(10) (2010-10-16)
Approximately 30% of alleles causing genetic disorders generate premature termination codons (PTCs), which are usually associated with severe phenotypes. However, bypassing the deleterious stop codon can lead to a mild disease outcome. Splicing at NAGNAG tandem splice sites has been
Iwona Pranke et al.
ERJ open research, 4(1) (2018-03-03)
Premature termination codons (PTCs) are generally associated with severe forms of genetic diseases. Readthrough of in-frame PTCs using small molecules is a promising therapeutic approach. Nonetheless, the outcome of preclinical studies has been low and variable. Treatment efficacy depends on:
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