|Other Names||Claudin-16, Paracellin-1, PCLN-1, CLDN16, PCLN1|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Plays a major role in tight junction-specific obliteration of the intercellular space, through calcium- independent cell-adhesion activity. Involved in paracellular magnesium reabsorption. Required for a selective paracellular conductance. May form, alone or in partnership with other constituents, an intercellular pore permitting paracellular passage of magnesium and calcium ions down their electrochemical gradients. Alternatively, it could be a sensor of magnesium concentration that could alter paracellular permeability mediated by other factors.|
|Cellular Location||Cell junction, tight junction. Cell membrane; Multi-pass membrane protein|
|Tissue Location||Kidney-specific, including the thick ascending limb of Henle (TAL)|
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Provided below are standard protocols that you may find useful for product applications.
Tight junctions represent one mode of cell-to-celladhesion in epithelial or endothelial cell sheets, formingcontinuous seals around cells and serving as a physical barrier toprevent solutes and water from passing freely through theparacellular space. These junctions are comprised of sets ofcontinuous networking strands in the outwardly facing cytoplasmicleaflet, with complementary grooves in the inwardly facingextracytoplasmic leaflet. The protein encoded by this gene, amember of the claudin family, is an integral membrane protein and acomponent of tight junction strands. It is found primarily in thekidneys, specifically in the thick ascending limb of Henle, whereit acts as either an intercellular pore or ion concentration sensorto regulate the paracellular resorption of magnesium ions. Defectsin this gene are a cause of primary hypomagnesemia, which ischaracterized by massive renal magnesium wasting withhypomagnesemia and hypercalciuria, resulting in nephrocalcinosisand renal failure. This gene and the CLDN1 gene are clustered onchromosome 3q28.
Kuo, S.J., et al. Oncol. Rep. 24(3):759-766(2010)Efrati, E., et al. Cell. Physiol. Biochem. 25(6):705-714(2010)Shuen, A.Y., et al. Clin. Chim. Acta 409 (1-2), 28-32 (2009) :Al-Haggar, M., et al. Clin. Exp. Nephrol. 13(4):288-294(2009)Lal-Nag, M., et al. Genome Biol. 10 (8), 235 (2009) :
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