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Key Documents

05-583

Sigma-Aldrich

Anti-CFTR Antibody, clone M3A7

clone M3A7, Upstate®, from mouse

Synonyme(s) :

ATP-binding cassette sub-family C, member 7, ATP-binding cassette transporter sub-family C member 7, cAMP-dependent chloride channel, cystic fibrosis transmembrane conductance regulator, cystic fibrosis transmembrane conductance regulator (ATP-binding ca

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

M3A7, monoclonal

Espèces réactives

human

Fabricant/nom de marque

Upstate®

Technique(s)

immunohistochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable

Isotype

IgG1

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... CFTR(1080)

Description générale

CFTR (Cystic Fibrosis Transmembrane Regulator) is an integral membrane protein shown to be involved in the transport of chloride ions. It is found on the surface of the epithelial cells lining the lungs and other organs. CFTR defects are the cause of cystic fibrosis. Cystic Fibrosis (CF) is a common lethal genetic disease caused by mutations of the gene coding for the cystic fibrosis transmembrane conductance factor, a cAMP regulated chloride channel. Approximately 70% of all CF cases share the deletion of a phenylalanine at position 508 (delta F508), which results in abnormal chloride transport. Since the CF mutation is lethal, most often by lung and liver disease, it raises the question of why this genetic disease remains as common as it is.

Spécificité

Other species not tested.
This antibody recognizes CFTR, Mr 170 kDa.

Immunogène

Epitope: a.a. 1365-1395
GST-fusion protein corresponding to residues 1197-1480 of human cystic fibrosis transmembrane conductance regulator (CFTR). The epitope maps within amino acids 1365-1395. Clone M3A7.

Application

Detect CFTR using this Anti-CFTR Antibody, clone M3A7 validated for use in IH, IP & WB.
Immunoprecipitation:
This antibody has been reported to immunoprecipitate CFTR. (Kartner, N., 1998.)

Immunohistochemistry:
This antibody has been reported to immunostain CFTR in human pancreatic tissue sections. (Kartner, N., 1998.)
Research Category
Neuroscience
Research Sub Category
Ion Channels & Transporters

Qualité

Routinely evaluated by western blot on human T84 colon carcinoma epithelial RIPA cell lysates or from CFTR-transfected BHK2.

Western Blot Analysis:
0.5-2 µg/mL of this lot detected CFTR from 20-50 µg of human T84 colon carcinoma epithelial RIPA cell lysates. 0.5-2 µg/mL of a previous lot detected CFTR from CFTR-transfected BHK (Haardt, M., 1999).
Note: Do not boil the lysate. Instead incubate at 37°C for 30 minutes. CFTR can run as a diffuse protein on SDS-PAGE.

Description de la cible

170 kDa

Forme physique

Format: Purified
Protein G Purified
Purified mouse monoclonal IgG1 in buffer containing 0.1 M Tris-glycine, pH 7.4, 0.15 M NaCl, 0.05% sodium azide and 30% glycerol.

Stockage et stabilité

Stable for 1 year at -20°C from date of receipt.

Handling Recommendations:
Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerol-containing solutions to become frozen during storage.

Remarque sur l'analyse

Control
T84 cell lysate.

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Informations légales

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 1


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Mark R Silvis et al.
The Journal of biological chemistry, 278(13), 11554-11560 (2003-01-17)
Cystic fibrosis is a common lethal genetic disease among Caucasians. The cystic fibrosis gene encodes a cyclic adenosine monophosphate-activated chloride channel (cystic fibrosis transmembrane conductance regulator (CFTR)) that mediates electrolyte transport across the luminal surfaces of a variety of epithelial
M Haardt et al.
The Journal of biological chemistry, 274(31), 21873-21877 (1999-07-27)
Defective cAMP-stimulated chloride conductance of the plasma membrane of epithelial cell is the hallmark of cystic fibrosis (CF) and results from mutations in the cystic fibrosis transmembrane conductance regulator, CFTR. In the majority of CF patients, mutations in the CFTR
Marybeth Howard et al.
The Journal of biological chemistry, 278(37), 35159-35167 (2003-07-03)
In cystic fibrosis, the absence of functional CFTR results in thick mucous secretions in the lung and intestines, as well as pancreatic deficiency. Although expressed at high levels in the kidney, mutations in CFTR result in little or no apparent
Nicoletta Pedemonte et al.
American journal of physiology. Cell physiology, 298(4), C866-C874 (2010-01-08)
Cystic fibrosis (CF) is caused by mutations in the CFTR chloride channel. Deletion of phenylalanine 508 (F508del), the most frequent CF mutation, impairs the maturation and gating of the CFTR protein. Such defects may be corrected in vitro by pharmacological
Miquéias Lopes-Pacheco et al.
Chembiochem : a European journal of chemical biology, 17(6), 493-505 (2016-02-13)
We evaluated whether small molecule correctors could rescue four nucleotide-binding domain 1 (NBD1) mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene (A455E, S492F, ΔI507, and R560T). We first transfected Cos-7 cells (green monkey kidney cells) with A455E, S492F, ΔI507

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