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Mouse Anti-CLDN19 Recombinant Antibody (EG720) (V2LY-1206-LY22)

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Published Data

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
EG720
Antibody Isotype
IgG1, κ
Application
ELISA, IF, IP, WB

Basic Information

Immunogen
Amino acids 160-224 mapping at the C-terminus of claudin-19 of human.
Host Species
Mouse
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal Antibody
Application Notes
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500
ELISA1:100-1:1,000
IHC-P1:50-1:500

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

Format
Liquid
Buffer
0.1% gelatin
Preservative
<0.1% sodium azide
Concentration
0.2 mg/ml
Purity
>95% as determined by analysis by SDS-PAGE
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
Entrez Gene ID
UniProt ID
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
More Infomation

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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