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Merck

SAB4200462

Sigma-Aldrich

Anti-Claudin-1 antibody produced in rabbit

~1.0 mg/mL, affinity isolated antibody

Sinónimos:

Anti-CLD1, Anti-CLDN1, Anti-ILVASC, Anti-SEMP1

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~23 kDa

species reactivity

human, rat

concentration

~1.0 mg/mL

technique(s)

immunohistochemistry: 20 μg/mL using formalin-fixed, paraffin-embedded rat kidney.
western blot: 1.5-3.0 μg/mL using extracts of rat kidney (S1 fraction).

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... CLDN1(9076)
rat ... Cldn1(65129)

General description

Anti-Claudin-1 is produced in rabbit using as immunogen a synthetic peptide corresponding to a sequence located at the C-terminal region of human claudin-1, conjugated to KLH. Claudin-1 (also known as CLDN1, senescence-associated epithelial membrane protein (SEMP1) and ILVASC) is a 22 kDa protein. It is expressed at high levels in kidney and liver and at lower levels in spleen, heart, brain, lung and testis. Claudins are located in both epithelial and endothelial cells in tissues. Claudins consist of four transmembrane domains and two extracellular loops, required to form tight junction strands. CLDN1 gene is located on human chromosome 3q28.

Immunogen

synthetic peptide corresponding to a sequence located at the C-terminal region of human claudin-1, conjugated to KLH. The corresponding sequence is identical in rat claudin-1 and highly conserved (single amino acid substitution) in mouse claudin-1.

Application

Anti-Claudin-1 antibody produced in rabbit has been used in immunohistochemistry and immunoblotting,

Biochem/physiol Actions

Claudin-1 is frequently up-regulated in colorectal carcinomas (CRCs), resulting in tumor differentiation and progression. Defects in the gene encoding claudin-1 are the cause of an autosomal recessive syndrome named ichthyosis-sclerosing cholangitis neonatal (NISCH). It participates in the barrier formation of tight junction. It modulates the tight junctions in human airway epithelium. CLDN1 acts as a receptor for the hepatitis C virus entry.

Physical form

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Referencia del producto
Descripción
Precios

Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Taurine supplementation alleviates puromycin aminonucleoside damage by modulating endoplasmic reticulum stress and mitochondrial-related apoptosis in rat kidney
Stacchiotti A, et al.
Nutrients, 10(6), 689-689 (2018)
Claudin association with CD81 defines hepatitis C virus entry
Harris HJ, et al.
The Journal of biological chemistry, jbc-M110 (2010)
Tracking the fate of glomerular epithelial cells in vivo using serial multiphoton imaging in new mouse models with fluorescent lineage tags
Hackl MJ, et al.
Nature Medicine, 19(12), 1661-1661 (2013)
Contribution of tight junction proteins to ion, macromolecule, and water barrier in keratinocytes
Kirschner N, et al.
The Journal of Investigative Dermatology, 133(5), 1161-1169 (2013)
Claudin-1 regulates cellular transformation and metastatic behavior in colon cancer
Dhawan P, et al.
The Journal of Clinical Investigation, 115(7), 1765-1776 (2005)

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