Mouse Anti-CLDN19 Recombinant Antibody (C5071) (V2LY-1206-LY20)

Name: Mouse Anti-CLDN19 Recombinant Antibody (C5071)
SKU: V2LY-1206-LY20
Rating: 5 (1 reviews)

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Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

C5071

Application

ELISA, IF, IP, WB

Immunogen

Amino acids 185-219 within a C-terminal cytoplasmic domain of claudin-19 of mouse.

Host Species

Mouse

Specificity

Human, Mouse, Rat

Antibody Isotype

IgG1, κ

Clonality

Monoclonal Antibody

Application Notes

Application	Note
WB	1:100-1:1,000
IP	1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)	1:50-1:500
ELISA	1:100-1:1,000

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.

More Infomation

Target

Full Name

Claudin 19

Entrez Gene ID

Human	149461
Mouse	242653
Rat	298487

UniProt ID

Human	Q8N6F1
Mouse	Q9ET38
Rat	Q5QT56

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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Isotype control

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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