Key features and details
- Goat polyclonal to Connexin 43 / GJA1
- Suitable for: WB
- Reacts with: Rat, Human
- Isotype: IgG
Product nameAnti-Connexin 43 / GJA1 antibody
See all Connexin 43 / GJA1 primary antibodies
DescriptionGoat polyclonal to Connexin 43 / GJA1
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Rat, Human
Predicted to work with: Rabbit, Guinea pig, Dog, Pig, Cynomolgus monkey
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Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Storage bufferpH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 0.5% BSA, Tris buffered saline
Concentration information loading...
PurityImmunogen affinity purified
Purification notesab87645 is purified from goat serum by ammonium sulphate precipitation followed by antigen affinity chromatography using the immunizing peptide.
Our Abpromise guarantee covers the use of ab87645 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.3 - 1 µg/ml. Predicted molecular weight: 43 kDa.
1 hour primary incubation is recommended for this product.
FunctionOne gap junction consists of a cluster of closely packed pairs of transmembrane channels, the connexons, through which materials of low MW diffuse from one cell to a neighboring cell. May play a critical role in the physiology of hearing by participating in the recycling of potassium to the cochlear endolymph.
Tissue specificityExpressed in the heart and fetal cochlea.
Involvement in diseaseDefects in GJA1 are the cause of autosomal dominant oculodentodigital dysplasia (ODDD) [MIM:164200]; also known as oculodentoosseous dysplasia. ODDD is a highly penetrant syndrome presenting with craniofacial (ocular, nasal, dental) and limb dysmorphisms, spastic paraplegia, and neurodegeneration. Craniofacial anomalies tipically include a thin nose with hypoplastic alae nasi, small anteverted nares, prominent columnella, and microcephaly. Brittle nails and hair abnormalities of hypotrichosis and slow growth are present. Ocular defects include microphthalmia, microcornea, cataracts, glaucoma, and optic atrophy. Syndactyly type 3 and conductive deafness can occur in some cases. Cardiac abnormalities are observed in rare instances.
Defects in GJA1 are the cause of autosomal recessive oculodentodigital dysplasia (ODDD autosomal recessive) [MIM:257850].
Defects in GJA1 may be the cause of syndactyly type 3 (SDTY3) [MIM:186100]. Syndactyly is an autosomal dominant trait and is the most common congenital anomaly of the hand or foot. It is marked by persistence of the webbing between adjacent digits, so they are more or less completely attached. In this type there is usually complete and bilateral syndactyly between the fourth and fifth fingers. Usually it is soft tissue syndactyly but occasionally the distal phalanges are fused. The fifth finger is short with absent or rudimentary middle phalanx. The feet are not affected.
Defects in GJA1 are a cause of hypoplastic left heart syndrome (HLHS) [MIM:241550]. HLHS refers to the abnormal development of the left-sided cardiac structures, resulting in obstruction to blood flow from the left ventricular outflow tract. In addition, the syndrome includes underdevelopment of the left ventricle, aorta, and aortic arch, as well as mitral atresia or stenosis.
Defects in GJA1 are a cause of Hallermann-Streiff syndrome (HSS) [MIM:234100]. HSS is a disorder characterized by a typical skull shape (brachycephaly with frontal bossing), hypotrichosis, microphthalmia, cataracts, beaked nose, micrognathia, skin atrophy, dental anomalies and proportionate short stature. Mental retardation is present in a minority of cases.
Sequence similaritiesBelongs to the connexin family. Alpha-type (group II) subfamily.
Cellular localizationCell membrane. Cell junction > gap junction.
- Information by UniProt
- Connexin 43 antibody
- Connexin-43 antibody
- Cx 43 antibody
ab87645 has been referenced in 4 publications.
- Zheng L et al. Phosphorylation of Cx43 residue Y313 by Src contributes to blocking the interaction with Drebrin and disassembling gap junctions. J Mol Cell Cardiol 126:36-49 (2019). PubMed: 30448479
- Uribe P et al. Study on site-specific expression of bone formation and resorption factors in human dental follicles. Eur J Oral Sci 126:439-448 (2018). PubMed: 30216610
- Shen Y et al. Connexin 43 SUMOylation improves gap junction functions between liver cancer stem cells and enhances their sensitivity to HSVtk/GCV. Int J Oncol 52:872-880 (2018). PubMed: 29393359
- Shibata M et al. Involvement of glial cells in the autoregulation of optic nerve head blood flow in rabbits. Invest Ophthalmol Vis Sci 53:3726-32 (2012). PubMed: 22589427