Overview

Description

  • Nature
    Synthetic

Specifications

Our Abpromise guarantee covers the use of ab92658 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

  • Applications

    Blocking - Blocking peptide for Anti-Connexin 43 / GJA1 antibody - Intercellular Junction Marker (ab63851)

  • Purity
    70 - 90% by HPLC.

  • Form
    Liquid
  • Additional notes

    - First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions.
    - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer.
    - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent.
    - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised.
    - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.

  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.

    Information available upon request.

General Info

  • Alternative names
    • Connexin 43
    • Connexin-43
    • Cx 43
    • Cx43
    • CXA1_HUMAN
    • DFNB38
    • Gap junction 43 kDa heart protein
    • Gap junction alpha-1 protein
    • Gap junction protein alpha 1 43kDa
    • Gap junction protein alpha 1 43kDa (connexin 43)
    • Gap junction protein alpha like
    • GJA 1
    • Gja1
    • GJAL
    • ODD
    • ODDD
    • ODOD
    • SDTY3
    see all
  • 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

References

ab92658 has not yet been referenced specifically in any publications.

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Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"

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