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AB3841 | Anti-Connexin 43 Antibody, phospho-specific (Ser368)

100 µL  
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      Replacement Information

      Key Specifications Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      H, Ht, M, Mk, R WB Rb Affinity Purified Polyclonal Antibody
      Catalogue NumberAB3841
      Brand Family Chemicon®
      Trade Name
      • Chemicon
      DescriptionAnti-Connexin 43 Antibody, phospho-specific (Ser368)
      Product Information
      FormatAffinity Purified
      PresentationProtein A and peptide affinity purified immunoglobulin. Liquid in 10 mM sodium HEPES, pH 7.5, 150 mM NaCl, 100 μg/mL BSA, with 50% glycerol.
      ApplicationThis Anti-Connexin 43 Antibody, phospho-specific (Ser368) is validated for use in WB for the detection of Connexin 43.
      Key Applications
      • Western Blotting
      Application NotesWestern blotting 1:1,000 (for best results, incubate membrane with diluted antibody in 5% BSA, 1X TBS, 0.1% Tween-20 at 4°C with gentle shaking, overnight)

      Optimal working dilutions must be determined by the end user.
      Biological Information
      ImmunogenKLH-conjugated, synthetic phospho-peptide corresponding to residues surrounding Ser368 of human Connexin 43.
      Epitopephospho-specific (Ser368)
      SpecificityRecognizes Ser368 phosphorylated Connexin 43. Connexin 43 (Cx43) is a member of the large family of gap junction proteins. Connexins assemble as a hexamer and are transported to the plasma membrane to create a hemichannel that can associate with hemichannels on nearby cells to create cell-to-cell channels. Clusters of these channels assemble to make gap junctions. Gap-junction communication is important in development and regulation of cell growth.
      Species Reactivity
      • Human
      • Hamster
      • Mouse
      • Monkey
      • Rat
      Antibody TypePolyclonal Antibody
      Entrez Gene Number
      Entrez Gene SummaryThis gene is a member of the connexin gene family. The encoded protein is a component of gap junctions, which are composed of arrays of intercellular channels that provide a route for the diffusion of low molecular weight materials from cell to cell. The encoded protein is the major protein of gap junctions in the heart that are thought to have a crucial role in the synchronized contraction of the heart and in embryonic development. A related intronless pseudogene has been mapped to chromosome 5. Mutations in this gene have been associated with oculodentodigital dysplasia and heart malformations.
      Gene Symbol
      • GJA1
      • GJAL
      • Cx43
      • DFNB38
      • SDTY3
      • CX43
      • ODD
      • ODDD
      • ODOD
      • Connexin-43
      • Phosphorylation
      UniProt Number
      UniProt SummaryFUNCTION: SwissProt: P17302 # 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.
      SIZE: 382 amino acids; 43008 Da
      SUBUNIT: A connexon is composed of a hexamer of connexins. Interacts with SGSM3.
      SUBCELLULAR LOCATION: Cell membrane; Multi-pass membrane protein. Cell junction, gap junction.
      TISSUE SPECIFICITY: Expressed in the heart and fetal cochlea.
      DISEASE: SwissProt: P17302 # 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 III and conductive deafness can occur in some cases. Cardiac abnormalities are observed in rare instances. & Defects in GJA1 may be the cause of syndactyly type III (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 a the 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.
      SIMILARITY: SwissProt: P17302 ## Belongs to the connexin family. Alpha-type (group II) subfamily.
      Physicochemical Information
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Usage Statement
      • 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.
      Storage and Shipping Information
      Storage ConditionsMaintain at -20ºC for 12 months after date of receipt. Do not aliquot.
      Packaging Information
      Material Size100 µL
      Transport Information
      Supplemental Information




      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number


      Reference overviewPub Med ID
      Ischemia induces closure of gap junctional channels and opening of hemichannels in heart-derived cells and tissue.
      Johansen, D; Cruciani, V; Sundset, R; Ytrehus, K; Mikalsen, SO
      Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 28 103-14 2011

      Show Abstract
      21865853 21865853
      Calcium-induced permeability transition in rat brain mitochondria is promoted by carbenoxolone through targeting connexin43.
      Azarashvili, T; Baburina, Y; Grachev, D; Krestinina, O; Evtodienko, Y; Stricker, R; Reiser, G
      American journal of physiology. Cell physiology 300 C707-20 2011

      Show Abstract
      21148408 21148408
      An angiotensin II- and NF-kappaB-dependent mechanism increases connexin 43 in murine arteries targeted by renin-dependent hypertension.
      Alonso, F; Krattinger, N; Mazzolai, L; Simon, A; Waeber, G; Meda, P; Haefliger, JA
      Cardiovascular research 87 166-76 2010

      Show Abstract Full Text Article
      20110337 20110337
      Mechanisms of unpinning and termination of ventricular tachycardia.
      Ripplinger, CM; Krinsky, VI; Nikolski, VP; Efimov, IR
      American journal of physiology. Heart and circulatory physiology 291 H184-92 2006

      Show Abstract
      16501014 16501014

      Data Sheet


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