Key features and details
- Goat polyclonal to Connexin 43 / GJA1 - C-terminal
- Suitable for: WB, ICC/IF, IHC-P
- Reacts with: Human, Monkey
- Isotype: IgG
Product nameAnti-Connexin 43 / GJA1 antibody - C-terminal
See all Connexin 43 / GJA1 primary antibodies
DescriptionGoat polyclonal to Connexin 43 / GJA1 - C-terminal
SpecificityThis antibody detects endogenous levels of total Connexin 43 / GJA1
Tested applicationsSuitable for: WB, ICC/IF, IHC-Pmore details
Species reactivityReacts with: Human, Monkey
Predicted to work with: Mouse, Rat, Dog
Recombinant fragment within Rat Connexin 43/ GJA1 aa 230-382 (C terminal). The exact sequence is proprietary. Produced in E.coli.
Database link: P08050
- WB - COS7 cell lysate ICC/IF - Primary RPE cells IHCP - Human uterus, endometrium tissue
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In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.05% Sodium azide
Constituents: 79% PBS, 20% Glycerol
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab219493 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/2000. Predicted molecular weight: 43 kDa.|
|ICC/IF||1/50 - 1/250.|
|IHC-P||Use a concentration of 10 µg/ml. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.|
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
Anti-Connexin 43 / GJA1 antibody - C-terminal (ab219493) at 1/1000 dilution + COS7 cell lysate at 100 µg
Rabbit polyclonal to Goat IgG (HRP) at 1/10000 dilution
Predicted band size: 43 kDa
Immunohistochemical analysis of formalin fixed, paraffin embedded Human uterus endometrium tissue labeling Connexin 43 / GJA1 with ab219493 at 10 µg/ml.
Immunofluorescent analysis of primary RPE cells labeling Connexin 43 / GJA1 with ab219493 at 1/100 dilution.
ab219493 has been referenced in 1 publication.
- Li K et al. Hypoxic Preconditioning Maintains GLT-1 Against Transient Global Cerebral Ischemia Through Upregulating Cx43 and Inhibiting c-Src. Front Mol Neurosci 11:344 (2018). PubMed: 30323740