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Key Documents

SAB4501175

Sigma-Aldrich

Anti-Connexin 43 antibody produced in rabbit

affinity isolated antibody

Synonyme(s) :

CX43, CXA1, CXN-43, Connexin 43, Gap junction 43 kDa heart protein

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 43 kDa

Espèces réactives

mouse, human, rat

Concentration

~1 mg/mL

Technique(s)

ELISA: 1:10000
immunofluorescence: 1:100-1:500
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000

Numéro d'accès NCBI

P17302

Numéro d'accès UniProt

P17302

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... GJA1(2697)

Catégories apparentées

Description générale

Anti-Connexin 43 Antibody detects endogenous levels of total Connexin 43 protein.
Connexin 43 (Cx43) is also known as GJA1 (gap junction protein α 1) and belongs to a large family of homologous connexin proteins. It has an intracellular N-terminus, four transmembrane domains, two extracellular loops, one cytoplasmic loop and an intracellular C-terminus. It is located on human chromosome 6q22-q23.

Immunogène

The antiserum was produced against synthesized peptide derived from human Connexin 43.

Immunogen Range: 333-382

Actions biochimiques/physiologiques

Mutations in Connexin 43 (Cx43) gene result in pleiotropic phenotype of oculodentodigital dysplasia. Connexin 43 participates in the multiplication and differentiation of mature T cells. It also participates in the secretion and manufacturing of cytokines. It helps to release lactate from glycolytic pancreatic ductal adenocarcinoma cells.

Caractéristiques et avantages

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Forme physique

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

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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Up-regulation of gap junction in peripheral blood T lymphocytes contributes to the inflammatory response in essential hypertension
Ni X, et al.
PLoS ONE, 12 (2017)
Connexin-43 channels are a pathway for discharging lactate from glycolytic pancreatic ductal adenocarcinoma cells
Dovmark TH, et al.
Oncogene, 36, 4538-4550 (2017)
Connexin 43 (GJA1) mutations cause the pleiotropic phenotype of oculodentodigital dysplasia
Paznekas WA, et al.
American Journal of Human Genetics, 72, 408-418 (2003)
Layal El-Hajjar et al.
International journal of molecular sciences, 24(3) (2023-02-12)
Gap-junction-forming connexins are exquisitely regulated by post-translational modifications (PTMs). In particular, the PTM of connexin 43 (Cx43), a tumor suppressor protein, regulates its turnover and activity. Here, we investigated the interaction of Cx43 with the ubiquitin-related modifier 1 (URM-1) protein
Camilla Schinner et al.
JCI insight, 5(9) (2020-05-08)
Arrhythmogenic cardiomyopathy (AC) is a genetic disease causing arrhythmia and sudden cardiac death with only symptomatic therapy available at present. Mutations of desmosomal proteins, including desmoglein-2 (Dsg2) and plakoglobin (Pg), are the major cause of AC and have been shown
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