Connexin 26, ELISA Kit

CX26/Connexin 26/GJB2/Connexin-26/DFNB1/DFNA3A/Gap junction beta 2 protein

For Research Use Only. Not for use in diagnostic procedures.

Store at 4 degree C if kit is to be used within 1 week. Stable for 6 months (if micro ELISA Plate, Lyophilized Standard and Concentrated Biotinylated Detection Protein stored at-20 degree C. Other components at 2-8 degree C). Stable for 12 months (if the entire kit is stored at-20 degree C).

Manufactured in an ISO 13485:2003 and EN ISO 13485:2012 Certified Laboratory.

Select online data sheet information is drawn from bioinformatics databases, occasionally resulting in ambiguous or non-relevant product information. It is the responsibility of the customer to review, verify, and evaluate the information to make sure it matches their requirements before purchasing the kit. Our ELISA Kit assays are dynamic research tools and sometimes they may be updated and improved. If the format of this assay is important to you then please request the current manual or contact our technical support team with a presales inquiry before placing an order. We will confirm the current details of the assay. We cannot guarantee the sample manual posted online is the most current manual.

Small volumes of CX26 elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS763657 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Connexin 26 (CX26) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing CX26. The ELISA analytical biochemical technique of the MBS763657 kit is based on CX26 antibody-CX26 antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect CX26 antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, CX26. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

Principle of the Assay||This kit was based on sandwich enzyme-linked immune-sorbent assay technology anti-Human CX26 antibody was pre-coated onto 96-well plates. And the biotin conjugated anti-Human CX26 antibody was used as detection antibodies. The standards, test samples and biotin conjugated detection antibody were added to the wells subsequently, and wash with wash buffer. HRP-Streptavidin was added and unbound conjugates were washed away with wash buffer. TMB substrates were used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the Human CX26 amount of sample captured in plate. Read the O.D. absorbance at 450nm in a microplate reader, and then the concentration of Human CX26 can be calculated.

26,215 Da

gap junction protein beta 2

gap junction beta-2 protein

Gap junction beta-2 protein

Cx26  [Similar Products]

CXB2_HUMAN

This gene encodes a member of the gap junction protein family. The gap junctions were first characterized by electron microscopy as regionally specialized structures on plasma membranes of contacting adherent cells. These structures were shown to consist of cell-to-cell channels that facilitate the transfer of ions and small molecules between cells. The gap junction proteins, also known as connexins, purified from fractions of enriched gap junctions from different tissues differ. According to sequence similarities at the nucleotide and amino acid levels, the gap junction proteins are divided into two categories, alpha and beta. Mutations in this gene are responsible for as much as 50% of pre-lingual, recessive deafness. [provided by RefSeq, Oct 2008]

GJB2: 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. Defects in GJB2 are the cause of deafness autosomal recessive type 1A (DFNB1A). DFNB1A is a form of sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. Defects in GJB2 are the cause of deafness autosomal dominant type 3A (DFNA3A). Defects in GJB2 are a cause of Vohwinkel syndrome (VS). VS is an autosomal dominant disease characterized by hyperkeratosis, constriction on finger and toes and congenital deafness. Defects in GJB2 are a cause of palmoplantar keratoderma with deafness (PPKDFN). PPKDFN is an autosomal dominant disorder characterized by the association of palmoplantar hyperkeratosis with progressive, bilateral, high-frequency, sensorineural deafness. Defects in GJB2 are a cause of keratitis-ichthyosis- deafness syndrome (KID syndrome); an autosomal dominant form of ectodermal dysplasia. Ectodermal dysplasias (EDs) constitute a heterogeneous group of developmental disorders affecting tissues of ectodermal origin. EDs are characterized by abnormal development of two or more ectodermal structures such as hair, teeth, nails and sweat glands, with or without any additional clinical sign. Each combination of clinical features represents a different type of ectodermal dysplasia. KID syndrome is characterized by the association of hyperkeratotic skin lesions with vascularizing keratitis and profound sensorineural hearing loss. Clinical features include deafness, ichthyosis, photobia, absent or decreased eyebrows, sparse or absent scalp hair, decreased sweating and dysplastic finger and toenails. Defects in GJB2 are the cause of Bart-Pumphrey syndrome (BPS). BPS is an autosomal dominant disorder characterized by sensorineural hearing loss, palmoplantar keratoderma, knuckle pads, and leukonychia, It shows considerable phenotypic variability. Defects in GJB2 are the cause of ichthyosis hystrix-like with deafness syndrome (HID syndrome). HID syndrome is an autosomal-dominant inherited keratinizing disorder characterized by sensorineural deafness and spiky hyperkeratosis affecting the entire skin. HID syndrome is considered to differ from the similar KID syndrome in the extent and time of occurrence of skin symptoms and the severity of the associated keratitis. Belongs to the connexin family. Beta-type (group I) subfamily.

Protein type: Motility/polarity/chemotaxis; Membrane protein, integral; Membrane protein, multi-pass; Cell adhesion

Chromosomal Location of Human Ortholog: 13q11-q12

Cellular Component: connexon complex; ER-Golgi intermediate compartment; integral to membrane; lateral plasma membrane; plasma membrane

Molecular Function: gap junction channel activity

Biological Process: cell-cell signaling; decidualization; gap junction assembly; male genitalia development; response to estradiol stimulus; response to progesterone stimulus; sensory perception of sound; transmembrane transport; transport

Disease: Deafness, Autosomal Dominant 3a; Deafness, Autosomal Recessive 1a; Deafness, Congenital, With Keratopachydermia And Constrictions Of Fingers And Toes; Deafness, X-linked 2; Ichthyosis, Hystrix-like, With Deafness; Keratitis-ichthyosis-deafness Syndrome, Autosomal Dominant; Keratoderma, Palmoplantar, With Deafness; Knuckle Pads, Leukonychia, And Sensorineural Deafness

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