Key features and details
- Rabbit polyclonal to Connexin 43 / GJA1 (phospho S368)
- Suitable for: IHC-P, WB
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
Product nameAnti-Connexin 43 / GJA1 (phospho S368) antibody
See all Connexin 43 / GJA1 primary antibodies
DescriptionRabbit polyclonal to Connexin 43 / GJA1 (phospho S368)
Tested applicationsSuitable for: IHC-P, WBmore details
Species reactivityReacts with: Mouse, Rat, Human
Synthetic peptide within Human Connexin 43/ GJA1 (phospho S368). The exact sequence is proprietary.
Database link: P17302
- PMA treated 293 cell lysate, human breast carcinoma tissue
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 bufferpH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 49% PBS, 50% Glycerol
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab194928 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/50 - 1/100.|
|WB||1/500 - 1/2000. Predicted molecular weight: 43 kDa.|
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
ab194928 has not yet been referenced specifically in any publications.