Anti-Connexin 43 / GJA1 (phospho S368) antibody (ab194928)
Key features and details
- Rabbit polyclonal to Connexin 43 / GJA1 (phospho S368)
- Suitable for: WB
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
Overview
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Product name
Anti-Connexin 43 / GJA1 (phospho S368) antibody
See all Connexin 43 / GJA1 primary antibodies -
Description
Rabbit polyclonal to Connexin 43 / GJA1 (phospho S368) -
Host species
Rabbit -
Tested applications
Suitable for: WBmore details -
Species reactivity
Reacts with: Mouse, Rat, Human -
Immunogen
Synthetic peptide within Human Connexin 43/ GJA1 (phospho S368). The exact sequence is proprietary.
Database link: P17302 -
General notes
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
Properties
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Form
Liquid -
Storage instructions
Shipped 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 buffer
pH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 49% PBS, 50% Glycerol -
Concentration information loading...
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Purity
Immunogen affinity purified -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
Applications
The Abpromise guarantee
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.
Application | Abreviews | Notes |
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WB |
1/500 - 1/2000. Predicted molecular weight: 43 kDa.
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Notes |
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WB
1/500 - 1/2000. Predicted molecular weight: 43 kDa. |
Target
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Function
One 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 specificity
Expressed in the heart and fetal cochlea. -
Involvement in disease
Defects 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 similarities
Belongs to the connexin family. Alpha-type (group II) subfamily. -
Cellular localization
Cell membrane. Cell junction > gap junction. - Information by UniProt
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Database links
- Entrez Gene: 2697 Human
- Entrez Gene: 14609 Mouse
- Entrez Gene: 24392 Rat
- Omim: 121014 Human
- SwissProt: P17302 Human
- SwissProt: P23242 Mouse
- SwissProt: P08050 Rat
- Unigene: 74471 Human
see all -
Alternative names
- Connexin 43 antibody
- Connexin-43 antibody
- Cx 43 antibody
see all
Images
Datasheets and documents
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SDS download
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Datasheet download
References (1)
ab194928 has been referenced in 1 publication.
- Huang Y et al. Glycated serum albumin decreases connexin 43 phosphorylation in the corpus cavernosum. Transl Androl Urol 11:1486-1494 (2022). PubMed: 36507487