CLDN16 Antibody | 27-910

CLDN16 Antibody | 27-910 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

Immunogen: Antibody produced in rabbits immunized with a synthetic peptide corresponding a region of human CLDN16.

Research Area: Membrane, Cancer

Tested Application: E, WB

Application: CLDN16 antibody can be used for detection of CLDN16 by ELISA at 1:312500. CLDN16 antibody can be used for detection of CLDN16 by western blot at 1.25 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50, 000 - 100, 000.

Specificiy: N/A

Positive Control 1: Cat. No. 1211 - HepG2 Cell Lysate

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 34 kDa

Validation: N/A

Isoform: N/A

Purification: Antibody is purified by protein A chromatography method.

Clonality: Polyclonal

Clone: N/A

Isotype: N/A

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

Concentration: batch dependent

Storage Condition: For short periods of storage (days) store at 4˚C. For longer periods of storage, store CLDN16 antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles.

Alternate Name: CLDN16, HOMG3, PCLN1

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. These junctions are comprised of sets of continuous networking strands in the outwardly facing cytoplasmic leaflet, with complementary grooves in the inwardly facing extracytoplasmic leaflet. The protein encoded by this gene, a member of the claudin family, is an integral membrane protein and a component of tight junction strands. It is found primarily in the kidneys, specifically in the thick ascending limb of Henle, where it acts as either an intercellular pore or ion concentration sensor to regulate the paracellular resorption of magnesium ions. Defects in this gene are a cause of primary hypomagnesemia, which is characterized by massive renal magnesium wasting with hypomagnesemia and hypercalciuria, resulting in nephrocalcinosis and renal failure.