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Key Documents

HPA006360

Sigma-Aldrich

Anti-HPRT1 antibody produced in rabbit

enhanced validation

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

Sinônimo(s):

Anti-HGPRT antibody produced in rabbit, Anti-HGPRTase antibody produced in rabbit, Anti-Hypoxanthine-guanine phosphoribosyltransferase antibody produced in rabbit

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About This Item

Código UNSPSC:
12352203
Número do Atlas de Proteínas Humanas:
HPA006360

fonte biológica

rabbit

Nível de qualidade

100

conjugado

unconjugated

forma do anticorpo

affinity isolated antibody

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

linha de produto

Prestige Antibodies® Powered by Atlas Antibodies

forma

buffered aqueous glycerol solution

reatividade de espécies

human

validação aprimorada

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

técnica(s)

immunoblotting: 0.04-0.4 μg/mL
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:200-1:500

sequência de imunogênio

SDDEPGYDLDLFCIPNHYAEDLERVFIPHGLIMDRTERLARDVMKEMGGHHIVALCVLKGGYKFFADLLDYIKALNRNSDRSIPMTVDFIRLKSYCNDQSTGDIKVIGGDDLSTLTGKNVLIVEDIIDTGKTMQTLLSLVRQYNPKMV

nº de adesão UniProt

P00492

Condições de expedição

wet ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... HPRT1(3251)

Categorias relacionadas

Descrição geral

HPRT1 (hypoxanthine phosphoribosyltransferase 1) enzyme is an essential part of the purine salvage pathway. The corresponding gene is localized to human chromosome Xq26-27, which is composed of nine exons. The encoded protein is composed of 218 amino acids.

Imunogênio

Hypoxanthine-guanine phosphoribosyltransferase recombinant protein epitope signature tag (PrEST)

Aplicação

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)

Ações bioquímicas/fisiológicas

HPRT1 (hypoxanthine phosphoribosyltransferase 1) functions in the purine salvage pathway, where it recycles guanine and hypoxanthine into available nucleotides. Degree of enzyme inactivity determines the severity of the related disorder. Incomplete inactivation results in Kelley-Seegmiller syndrome, which is characterized by uric acid nephrolithiasis, hyperuricemia, hyperuricaciduria, and gout arthritis. Severest disorder caused by inactivation of this gene is called Lesch-Nyhan disease (LND).

Características e benefícios

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.

Ligação

Corresponding Antigen APREST71132

forma física

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

Informações legais

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

Exoneração de responsabilidade

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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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Equipamento de proteção individual

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

Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.

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Yasukazu Yamada et al.
Nucleosides, nucleotides & nucleic acids, 33(4-6), 218-222 (2014-06-19)
Mutation of hypoxanthine guanine phosphoribosyltransferase (HPRT) gives rise to Lesch-Nyhan syndrome, which is characterized by hyperuricemia, severe motor disability, and self-injurious behavior, or HPRT-related gout with hyperuricemia. Four mutations were detected in two Lesch-Nyhan families and two families with partial
Lina Mastrangelo et al.
Proceedings of the National Academy of Sciences of the United States of America, 109(9), 3377-3382 (2012-02-15)
Lesch-Nyhan disease (LND) is an X-linked genetic disorder caused by mutations of the hypoxanthine guanine phosphoribosyltransferase (HPRT) purine biosynthesis gene and characterized by aberrant purine metabolism, deficient basal ganglia dopamine levels, dystonia, and severe neurobehavioral manifestations, including compulsive self-injurious behavior.
Gitte H Bruun et al.
Nucleic acids research, 46(15), 7938-7952 (2018-05-16)
Familial dysautonomia (FD) is a severe genetic disorder causing sensory and autonomic dysfunction. It is predominantly caused by a c.2204+6T>C mutation in the IKBKAP gene. This mutation decreases the 5' splice site strength of IKBKAP exon 20 leading to exon
Khue Vu Nguyen et al.
Nucleosides, nucleotides & nucleic acids, 32(3), 155-160 (2013-03-12)
Inherited mutation of the purine salvage enzyme, hypoxanthine guanine phosphoribosyltransferase (HPRT) gives rise to Lesch-Nyhan syndrome (LNS) or Lesch-Nyhan variants (LNVs). We report three novel independent mutations in the coding region of HPRT gene: exon 3: c.141delA, p.D47fs53X; exon 5:
Gitte H Bruun et al.
BMC biology, 14, 54-54 (2016-07-07)
Many pathogenic genetic variants have been shown to disrupt mRNA splicing. Besides splice mutations in the well-conserved splice sites, mutations in splicing regulatory elements (SREs) may deregulate splicing and cause disease. A promising therapeutic approach is to compensate for this
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