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Merck

HPA014967

Anti-SLC12A1 antibody produced in rabbit

enhanced validation

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

Sinonimo/i:

Anti-Bumetanide-sensitive sodium-(potassium)-chloride cotransporter 2, Anti-Kidney-specific Na-K-Cl symporter, Anti-Solute carrier family 12 member 1


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100 μL

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Informazioni su questo articolo

Codice UNSPSC:
12352203
Numero Human Protein Atlas:
NACRES:
NA.41

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Origine biologica

rabbit

Coniugato

unconjugated

Forma dell’anticorpo

affinity isolated antibody

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Nome Commerciale

Prestige Antibodies® Powered by Atlas Antibodies

Stato

buffered aqueous glycerol solution

Reattività contro le specie

human

Convalida avanzata

independent
orthogonal RNAseq
Learn more about Antibody Enhanced Validation

tecniche

immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:200-1:500

Sequenza immunogenica

MSLNNSSNVFLDSVPSNTNRFQVSVINENHESSAAADDNTDPPHYEETSFGDEAQKRLRISFRPGNQECYDNFLQSGETAKTDASFHAYDSHTNTYYLQTFGHNTMDAVPKIEYYRNTGSI

N° accesso UniProt

Condizioni di spedizione

wet ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

human ... SLC12A1(6557)

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Questo articolo
AV41388SAB5200103HPA013742
Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

biological source

rabbit

biological source

rabbit

biological source

rabbit

biological source

rabbit

product line

Prestige Antibodies® Powered by Atlas Antibodies

product line

-

product line

-

product line

Prestige Antibodies® Powered by Atlas Antibodies

UniProt accession no.

Q13621

UniProt accession no.

Q8IUN5

UniProt accession no.

Q13621

UniProt accession no.

Q92959

Descrizione generale

SLC12A1 (solute carrier family 12, member 1) is a member of SLC12A family of electrically neutral cation-chloride cotransporters, which contains both NaCl and KCl co-transporters. It is a bumetanide-sensitive Na-K-2Cl cotransporter and is also called NKCC2. This gene is localized to human chromosome 15 (NKCC2). This transporter resides predominantly in the plasma membrane, and has three different isoforms namely, NKCC2B, NKCC2A and NKCC2F. It has twelve transmembrane helices, with its N-terminal facing the cytoplasm. Its transport domain is made of two structurally homologous domains, made of 5-helices each. It has a large C-terminal, present intracellularly, which is responsible for dimerization of the protein.

Immunogeno

Solute carrier family 12 member 1 recombinant protein epitope signature tag (PrEST)

Applicazioni

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

Azioni biochim/fisiol

SLC12A1 (solute carrier family 12, member 1) plays a key role in blood pressure homeostasis, and has a predominant role in the transport of salt in the thick ascending limb of Henle′s loop. It is responsible for the simultaneous movement of Na+, 1 K+, and 2 Cl- across the plasma membrane. Elevated activity of this transporter leads to inherited hypertension. Mutations in this gene are linked to type I Bartter syndrome (BS), which is characterized by hypokalaemia, excess volume depletion, and metabolic alkalosis usually leading to prenatal fatality. Mutations in this gene are also linked to atypical type I Bartter syndrome, which also includes focal segmental glomerulosclerosis. Rare mutations in this gene lead to decreased salt reabsorption in kidney, which results in hypotension.

Caratteristiche e vantaggi

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Stato fisico

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

Altre note

Corresponding Antigen APREST73255

Note legali

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

Esclusione di responsabilità

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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Codice della classe di stoccaggio

10 - Combustible liquids

Classe di pericolosità dell'acqua (WGK)

WGK 1

Dispositivi di protezione individuale

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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Justin J Lee et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 35(11), e21982-e21982 (2021-10-26)
Activation of the basolateral calcium sensing receptor (CaSR) in the renal tubular thick ascending limb (TAL) increases claudin-14 expression, which reduces paracellular calcium (Ca2+ ) permeability, thus increasing urinary Ca2+ excretion. However, the upstream signaling pathway contributing to altered CLDN14
Hajime Yamazaki et al.
Pediatric nephrology (Berlin, Germany), 24(2), 415-418 (2008-10-03)
Type I Bartter syndrome (BS) is caused by mutations of the Na-K-2Cl cotransporter (NKCC2)-encoding SLC12A1 gene. The clinical phenotype of this severe form of BS is characterized by polyhydramnios, premature delivery, failure to thrive, and nephrocalcinosis, and the diagnosis is
Sebastian Frische et al.
American journal of physiology. Renal physiology, 320(1), F74-F86 (2020-12-08)
Variations in the claudin-14 (CLDN14) gene have been linked to increased risk of hypercalciuria and kidney stone formation. However, the exact cellular localization of CLDN14 and its regulation remain to be fully delineated. To this end, we generated a novel
Masanori Adachi et al.
Endocrine journal, 54(6), 1003-1007 (2007-11-14)
Bartter syndrome (BS) type 1, also referred to antenatal BS, is a genetic tubulopathy with hypokalemic metabolic alkalosis and prenatal onset of polyuria leading to polyhydramnios. It has been shown that BS type 1 is caused by mutations in the
Patrick G J F Starremans et al.
Journal of the American Society of Nephrology : JASN, 14(6), 1419-1426 (2003-05-23)
Bartter syndrome (BS) is a heterogeneous renal tubular disorder affecting Na-K-Cl reabsorption in the thick ascending limb of Henle's loop. BS type I patients typically present with profound hypokalemia and metabolic alkalosis. The main goal of the present study was

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