Human CLDN19 ELISA Kit (V2LY-0626-LY2804)

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Tested Data
Request for COA
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Basic Information

Sensitivity
0.0086 ng/mL
Detection Range
0.02-6 ng/mL
Sample Type
Serum, Plasma, cell culture supernates
Specificity
Human
Assay Type
Sandwich
Reactivity
Human
Assay Time
1.5 h
Molecule Mass
23.2 kDa
Components
  • Pre-coated ELISA plate: 12 wells * 8 detachable strips
  • Standard solution: 0.5ml x1
  • Standard diluent: 3ml x1
  • Streptavidin-HRP: 6ml x1
  • Stop solution: 6ml x1
  • Substrate solution A: 6ml x1
  • Substrate solution B: 6ml x1
  • Wash buffer concentrate (25x): 20ml x1
  • Biotinylated antibody: 1ml x1

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

Storage
Store at 2-8°C
More Infomation

Target

Full Name
Claudin 19
Function
Plays a major role in tight junction-specific obliteration of the intercellular space, through calcium-independent cell-adhesion activity.
Biological Process
Actin cytoskeleton reorganization Source: ARUK-UCL
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
Negative regulation of cell migration Source: ARUK-UCL
Negative regulation of cell population proliferation Source: ARUK-UCL
Negative regulation of gene expression Source: ARUK-UCL
Negative regulation of wound healing Source: ARUK-UCL
Neuronal action potential propagation Source: Ensembl
Positive regulation of cell junction assembly Source: ARUK-UCL
Positive regulation of gene expression Source: ARUK-UCL
Positive regulation of protein phosphorylation Source: ARUK-UCL
Regulation of transepithelial transport Source: ARUK-UCL
Response to stimulus Source: UniProtKB-KW
Visual perception Source: UniProtKB-KW
Cellular Location
Cell membrane; Tight junction
Involvement in disease
Hypomagnesemia 5, renal, with or without ocular involvement (HOMG5):
A progressive renal disease characterized by primary renal magnesium wasting with hypomagnesemia, hypercalciuria and nephrocalcinosis associated with severe ocular abnormalities such as bilateral chorioretinal scars, macular colobomata, significant myopia and nystagmus. The renal phenotype is virtually undistinguishable from that of patients with HOMG3.
Topology
Cytoplasmic: 1-7
Helical: 8-28
Extracellular: 29-81
Helical: 82-102
Cytoplasmic: 103-117
Helical: 118-138
Extracellular: 139-160
Helical: 161-181
Cytoplasmic: 182-224

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.

Liu, F., Peng, S., Adelman, R. A., & Rizzolo, L. J. (2021). Knockdown of Claudin-19 in the Retinal Pigment Epithelium Is Accompanied by Slowed Phagocytosis and Increased Expression of SQSTM1. Investigative ophthalmology & visual science, 62(2), 14-14.

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.

Wang, S. B., Xu, T., Peng, S., Singh, D., Ghiassi-Nejad, M., Adelman, R. A., & Rizzolo, L. J. (2019). Disease-associated mutations of claudin-19 disrupt retinal neurogenesis and visual function. Communications biology, 2(1), 1-13.

Khan, A. O., Patel, N., Ghazi, N. G., Alzahrani, S. S., Arold, S. T., & Alkuraya, F. S. (2018). Familial non-syndromic macular pseudocoloboma secondary to homozygous CLDN19 mutation. Ophthalmic genetics, 39(5), 577-583.

Yamaguti, P. M., Neves, F. D. A. R., Hotton, D., Bardet, C., de La Dure-Molla, M., Castro, L. C., ... & Acevedo, A. C. (2017). Amelogenesis imperfecta in familial hypomagnesaemia and hypercalciuria with nephrocalcinosis caused by CLDN19 gene mutations. Journal of Medical Genetics, 54(1), 26-37.

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

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