|Application ||WB, IHC-P, E|
|Calculated MW||37414 Da|
|Antigen Region||303-333 aa|
|Other Names||Gap junction alpha-4 protein, Connexin-37, Cx37, GJA4|
|Target/Specificity||This Connexin 37 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 303-333 amino acids from the C-terminal region of human Connexin 37.|
|Format||Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Connexin 37 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|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.|
|Cellular Location||Cell membrane; Multi-pass membrane protein. Cell junction, gap junction|
|Tissue Location||Expressed in multiple organs and tissues, including heart, uterus, ovary, and blood vessel endothelium|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
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.
Strausberg, R.L., et al., Proc. Natl. Acad. Sci. U.S.A. 99(26):16899-16903 (2002).
Saito, T., et al., Int. J. Cancer 86(1):67-70 (2000).
Boerma, M., et al., J. Intern. Med. 246(2):211-218 (1999).
Krutovskikh, V., et al., Carcinogenesis 17(8):1761-1763 (1996).
Reed, K.E., et al., J. Clin. Invest. 91(3):997-1004 (1993).
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