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Key Documents

SAB5200104

Sigma-Aldrich

Anti-SLC12A3 antibody produced in rabbit

1 mg/mL, affinity isolated antibody

Synonyme(s) :

Anti-NCC, Anti-Slc12a3

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous glycerol solution

Poids mol.

antigen predicted mol wt 160 kDa

Espèces réactives

human, rat, mouse

Concentration

1 mg/mL

Technique(s)

western blot: suitable

Numéro d'accès NCBI

NP_000330
NP_062218

Numéro d'accès UniProt

P55017

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... SLC12A3(6559)
rat ... Slc12a3(54300)

Description générale

Solute carrier family 12 member 3 (SLC12A3) is also known as thiazide-sensitive Na+-Cl- cotransporter (NCCT). It is expressed in the apical cells of the distal convoluted tubule. The gene encoding this 1021 amino acid protein is localized on human chromosome 16q13. The gene ID for the protein is 6559.

Spécificité

Detects ~160 kDa.

Immunogène

AA74-95 (rat), 76-97 (hum)

Actions biochimiques/physiologiques

Solute carrier family 12 member 3 (SLC12A3) is one of the major components of the sodium chloride reabsorption pathway. It controls the Cl- concentration and is also involved in the transepithelial ion absorption and secretion. Mutations in the gene encoding SLC12A3 have been associated with Gitelman syndrome.
This Na-Cl cotransporter is associated with maintaining blood pressure.

Caractéristiques et avantages

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Forme physique

PBS, 50% glycerol, and 0.09% sodium azide

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Genetic variants of SLC12A3 modulate serum lipid profiles in a group of Mongolian pedigree population
An C, et al.
Lipids in Health and Disease, 17(1), 83-83 (2018)
Jiewei Luo et al.
Endocrine journal, 62(1), 29-36 (2014-10-03)
Gitelman syndrome (GS) is a salt-wasting tubulointerstitial disease of autosomal recessive inheritance (OMIM613395) caused by genic mutation of SLC12A3, which codes thiazide-sensitive Na-Cl cotransporter (NCCT) gene. The gene mutation of the majority of GS patients is compound heterozygous. This study
Linghong Wang et al.
Acta biochimica et biophysica Sinica, 47(5), 325-334 (2015-04-07)
The thiazide-sensitive Na(+)-Cl(-) cotransporter (TSC) is responsible for the major sodium chloride reabsorption pathway, which is located in the apical membrane of the epithelial cells of the distal convoluted tubule. TSC is involved in several physiological activities including transepithelial ion
Koichiro Susa et al.
Human molecular genetics, 23(19), 5052-5060 (2014-05-14)
Pseudohypoaldosteronism type II (PHAII) is a hereditary disease characterized by salt-sensitive hypertension, hyperkalemia and metabolic acidosis, and genes encoding with-no-lysine kinase 1 (WNK1) and WNK4 kinases are known to be responsible. Recently, Kelch-like 3 (KLHL3) and Cullin3, components of KLHL3-Cullin3
P Gailly et al.
Pflugers Archiv : European journal of physiology, 466(11), 2035-2047 (2014-01-28)
Luminal nucleotide stimulation is known to reduce Na(+) transport in the distal nephron. Previous studies suggest that this mechanism may involve the thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC), which plays an essential role in NaCl reabsorption in the cells lining the distal

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