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Mouse Anti-CLDN16 Recombinant Antibody (CBXC-2223) (CBMAB-C5913-CQ)

This product is a mouse antibody that recognizes CLDN16. The antibody CBXC-2223 can be used for immunoassay techniques such as: IF.
See all CLDN16 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBXC-2223
Antibody Isotype
IgG
Application
IF

Basic Information

Immunogen
Full length for Claudin-16 protein
Specificity
Human
Antibody Isotype
IgG
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Concentration
LYOPH
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
claudin 16
Introduction
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. This gene and the CLDN1 gene are clustered on chromosome 3q28.
Entrez Gene ID
10686
UniProt ID
Q9Y5I7
Alternative Names
Claudin 16; Paracellin-1; Hypomagnesemia 3, With Hypercalciuria And Nephrocalcinosis; PCLN-1; PCLN1; Claudin-16; HOMG3;
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.
Biological Process
Bicellular tight junction assembly Source: GO_Central
Calcium-independent cell-cell adhesion via plasma membrane cell-adhesion molecules Source: UniProtKB
Cell adhesion Source: GO_Central
Cellular metal ion homeostasis Source: ProtInc
Excretion Source: ProtInc
Cellular Location
Cell membrane; Tight junction
Involvement in disease
Hypomagnesemia 3 (HOMG3):
A progressive renal disease characterized by primary renal magnesium wasting with hypomagnesemia, hypercalciuria and nephrocalcinosis. Recurrent urinary tract infections and kidney stones are often observed. In spite of hypercalciuria, patients do not show hypocalcemia.
Topology
Cytoplasmic: 1-73
Helical: 74-94
Extracellular: 95-150
Helical: 151-171
Cytoplasmic: 172-185
Helical: 186-206
Extracellular: 207-239
Helical: 240-260
Cytoplasmic: 261-305

Prot-Bertoye, C., Griveau, C., Skjødt, K., Cheval, L., Brideau, G., Lievre, L., ... & Dimke, H. (2021). Differential localization patterns of Claudin 10, 16 and 19 in human, mouse, and rat renal tubular epithelia. American Journal of Physiology-Renal Physiology.

García‐Castaño, A., Perdomo‐Ramirez, A., Vall‐Palomar, M., Ramos‐Trujillo, E., Madariaga, L., Ariceta, G., & Claverie‐Martin, F. (2020). Novel compound heterozygous mutations of CLDN16 in a patient with familial hypomagnesemia with hypercalciuria and nephrocalcinosis. Molecular Genetics & Genomic Medicine, 8(11), e1475.

Hou, J., Renigunta, V., Nie, M., Sunq, A., Himmerkus, N., Quintanova, C., ... & Wolf, M. T. F. (2019). Phosphorylated claudin-16 interacts with Trpv5 and regulates transcellular calcium transport in the kidney. Proceedings of the National Academy of Sciences, 116(38), 19176-19186.

Vianna, J. G. P., Simor, T. G., Senna, P., De Bortoli, M. R., Costalonga, E. F., Seguro, A. C., & Luchi, W. M. (2019). Atypical presentation of familial hypomagnesemia with hypercalciuria and nephrocalcinosis in a patient with a new claudin-16 gene mutation. Clinical nephrology. Case studies, 7, 27.

Perdomo-Ramirez, A., Aguirre, M., Davitaia, T., Ariceta, G., Ramos-Trujillo, E., Group, R., & Claverie-Martin, F. (2019). Characterization of two novel mutations in the claudin-16 and claudin-19 genes that cause familial hypomagnesemia with hypercalciuria and nephrocalcinosis. Gene, 689, 227-234.

Marunaka, K., Fujii, N., Kimura, T., Furuta, T., Hasegawa, H., Matsunaga, T., ... & Ikari, A. (2019). Rescue of tight junctional localization of a claudin-16 mutant D97S by antimalarial medicine primaquine in Madin-Darby canine kidney cells. Scientific reports, 9(1), 1-14.

Breiderhoff, T., Himmerkus, N., Drewell, H., Plain, A., Günzel, D., Mutig, K., ... & Bleich, M. (2018). Deletion of claudin-10 rescues claudin-16–deficient mice from hypomagnesemia and hypercalciuria. Kidney international, 93(3), 580-588.

Marunaka, K., Furukawa, C., Fujii, N., Kimura, T., Furuta, T., Matsunaga, T., ... & Ikari, A. (2017). The RING finger-and PDZ domain-containing protein PDZRN3 controls localization of the Mg2+ regulator claudin-16 in renal tube epithelial cells. Journal of Biological Chemistry, 292(31), 13034-13044.

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For research use only. Not intended for any clinical use.

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