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Mouse Anti-CLDN19 Recombinant Antibody (693202) (CBMAB-C7969-LY)

This product is antibody recognizes CLDN19. The antibody 693202 immunoassay techniques such as: IHC-P.
See all CLDN19 antibodies
Published Data

Summary

Host Animal
Mouse
Specificity
Human
Clone
693202
Antibody Isotype
IgG1
Application
IHC-P

Basic Information

Immunogen
NS0 mouse myeloma cell line transfected with human Claudin-19
Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal
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!]

Format
Liquid
Buffer
5% trehalose
Concentration
0.5 mg/ml
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Claudin 19
Introduction
The product of this gene belongs to the claudin family. It plays a major role in tight junction-specific obliteration of the intercellular space, through calcium-independent cell-adhesion activity. Defects in this gene are the cause of hypomagnesemia renal with ocular involvement (HOMGO). HOMGO is 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. Alternatively spliced transcript variants encoding distinct isoforms have been identified for this gene. [provided by RefSeq, Jun 2010]
Entrez Gene ID
UniProt ID
Alternative Names
Claudin 19; Claudin-19; HOMG5;
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.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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