Analytical Data
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Gene name
CX26
- Application
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Alternative Names
KID; DFNA3; DFNB1; HID; NSRD1; PPK; GJB2; Gap Junction Protein Beta 2
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Species
Human
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Source
E. coli
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Tag
N-His
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Purity
Greater than 90% as determined by SDS-PAGE.
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Uniprot
P29033
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Expression Region
Val95~Thr135
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Molecular Weight
12kDa
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Endotoxin
< 1.0 EU per μg protein as determined by the LAL method.
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Form
Freeze-dried powder
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Buffer formulation
PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300.
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Reconstitution
Reconstitute in ddH2O to a concentration of 0.1-0.5 mg/mL. Do not vortex.
- Customization
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Stability Test
The thermal stability is described by the loss rate. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37℃ for 48h, and no obvious degradation and precipitation were observed. The loss rate isless than 8% within the expiration date under appropriate storage condition.
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Storage & Shelf Life
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
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Shipping
In general, recombinant proteins are supplied as lyophilized powder and shipped at ambient temperature. For bulk packages, the proteins are provided as frozen liquid and shipped with blue ice, unless otherwise requested by the customer.
Quality inspection process
Related Products
Protein Description
CX26, or Connexin 26, is a protein that forms gap junctions, which are essential for cell-to-cell communication in various tissues, particularly in the cochlea of the inner ear, where it plays a crucial role in auditory function. Mutations in the GJB2 gene, which encodes the CX26 protein, are among the most common genetic causes of non-syndromic hearing loss worldwide. Research into CX26 recombinant proteins has gained significant attention as scientists seek to understand the mechanisms by which these mutations disrupt cellular communication and contribute to hearing impairment. By creating and studying recombinant forms of CX26, researchers can analyze how specific mutations affect the protein's structure, function, and interaction with other cellular components. This research holds the potential to uncover therapeutic targets for gene therapy and other interventions aimed at restoring or mitigating hearing loss associated with CX26 mutations. Furthermore, understanding the functional properties of CX26 can provide insights into broader cellular processes and the role of gap junctions in various physiological and pathological conditions. Consequently, the study of CX26 recombinant proteins not only advances our understanding of hearing loss mechanisms but also contributes to the development of innovative therapeutic strategies.
