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Key Documents

SAB4300781

Sigma-Aldrich

Anti-SLCO1B1 antibody produced in rabbit

affinity isolated antibody

Synonyme(s) :

LST-1, Liver-specific organic anion transporter 1, OATP 2, Sodium-independent organic anion-transporting polypeptide 2, Solute carrier family 21 member 6

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.43

Source biologique

rabbit

Niveau de qualité

100

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

76 kDa

Espèces réactives

human

Concentration

1.0 mg/mL

Technique(s)

western blot: 1:500-1:3000 (Cell Lysate)

Isotype

IgG

Numéro d'accès

NP_006437.3

Numéro d'accès UniProt

Q9Y6L6

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... SLCO1B1(10599)

Description générale

Solute carrier organic anion transporter family member 1B1 (SLCO1B1) or liver-specific organic anion transporter 1 (LST-1) and sodium-independent organic anion-transporting polypeptide 2 (OATP-2), is formerly known as solute carrier family 21 (organic anion transporter), member 6 (SLC21A6). SLCO1B1 is predominantly expressed in liver. It is expressed in the basolateral membrane. It has 12 transmembrane domains. In human chromosome, the gene SLCO1B1 is localized on 12p12.1

Spécificité

The antibody detects endogenous levels of total SLCO1B1 protein.

Immunogène

Synthesized peptide derived from internal of human SLCO1B1.

Actions biochimiques/physiologiques

Solute carrier organic anion transporter family member 1B1 (SLCO1B1) transports taurocholate, conjugated steroids, eicosanoids, and thyroid hormones, in a sodium independent manner. SLCO1B1 is the key transporter of bile for the clearance of human liver. Polymorphism in SLCO1B1 might lead to life threatening drug toxicities. Mutations in SLCO1B1 and SLCO1B3 leads to rotor syndrome in human, affecting conjugated bilirubin reuptake in liver. Genetic variability in SLCO1B1 affects the plasma concentration of statins.

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

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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

Integrative genomics strategies to elucidate the complexity of drug response
Kasarskis A, et al.
Pharmacogenomics, 12(12), 1695-1715 (2011)
A novel human organic anion transporting polypeptide localized to the basolateral hepatocyte membrane
Ko?nig J, et al.
American Journal of Physiology: Gastrointestinal and Liver Physiology, 278(1), G156-G164 (2000)
Identification of a novel gene family encoding human liver-specific organic anion transporter LST-1
Abe T, et al.
The Journal of Biological Chemistry, 274(24), 17159-17163 (1999)
The clinical pharmacogenomics implementation consortium: CPIC guideline for SLCO1B1 and simvastatin-induced myopathy
Wilke RA, et al.
Clinical Pharmacology and Therapeutics, 92(1), 112-117 (2012)
Evita van de Steeg et al.
The Journal of clinical investigation, 122(2), 519-528 (2012-01-11)
Bilirubin, a breakdown product of heme, is normally glucuronidated and excreted by the liver into bile. Failure of this system can lead to a buildup of conjugated bilirubin in the blood, resulting in jaundice. The mechanistic basis of bilirubin excretion
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