Gap Junction Alpha-4 Protein / CX55 (GJA4) Antibody

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Description
Gap junctions permit direct cell-to-cell passage of small cytoplasmic molecules, including ions, metabolic intermediates, and second messengers, and thereby mediate intercellular communication. Gap junction channels consist of connexin protein subunits encoded by a multigene family. Erythrokeratodermia variabilis (EKV) is an autosomal dominant disorder of keratinization characterized by migratory erythematous lesions and fixed keratotic plaques. Mutations in the GJB3 gene have been reported in some but not all families, although it has been postulated that the absence of connexin 30.3 can be compensated by other connexins.
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Product specifications
Category | Primary Antibodies |
Immunogen Target | Gap Junction Alpha-4 Protein / CX55 (GJA4) |
Host | Rabbit |
Reactivity | Mouse |
Recommended Dilution | WB: 1/1000, IHC-P: 1/10 - 1/50. Not tested in IHC-F. Optimal dilutions/concentrations should be determined by the end user. |
Clonality | Polyclonal |
Conjugation | Unconjugated |
Isotype | IgG |
Purification | Purified through a protein G column, eluted with high and low pH buffers and neutralized immediately, followed by dialysis against PBS. |
Size 1 | 80 µl |
Size 2 | 400 µl |
Form | Liquid |
Tested Applications | ELISA, WB, IHC |
Buffer | PBS containing 0.09% sodium azide. |
Availability | Shipped within 5-10 working days. |
Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
UniProt ID | P35212 |
Background | Antibody anti-GJA4 |
Status | RUO |
Descripción
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Gap junctions permit direct cell-to-cell passage of small cytoplasmic molecules, including ions, metabolic intermediates, and second messengers, and thereby mediate intercellular communication. Gap junction channels consist of connexin protein subunits encoded by a multigene family. Erythrokeratodermia variabilis (EKV) is an autosomal dominant disorder of keratinization characterized by migratory erythematous lesions and fixed keratotic plaques. Mutations in the GJB3 gene have been reported in some but not all families, although it has been postulated that the absence of connexin 30.3 can be compensated by other connexins.
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