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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

Synonim(y):

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

Kod UNSPSC:
12352203
Numer w atlasie ludzkich białek:
HPA006360

pochodzenie biologiczne

rabbit

Poziom jakości

100

białko sprzężone

unconjugated

forma przeciwciała

affinity isolated antibody

rodzaj przeciwciała

primary antibodies

klon

polyclonal

linia produktu

Prestige Antibodies® Powered by Atlas Antibodies

Postać

buffered aqueous glycerol solution

reaktywność gatunkowa

human

rozszerzona walidacja

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

metody

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

sekwencja immunogenna

SDDEPGYDLDLFCIPNHYAEDLERVFIPHGLIMDRTERLARDVMKEMGGHHIVALCVLKGGYKFFADLLDYIKALNRNSDRSIPMTVDFIRLKSYCNDQSTGDIKVIGGDDLSTLTGKNVLIVEDIIDTGKTMQTLLSLVRQYNPKMV

numer dostępu UniProt

P00492

Warunki transportu

wet ice

temp. przechowywania

−20°C

docelowa modyfikacja potranslacyjna

unmodified

informacje o genach

human ... HPRT1(3251)

Powiązane kategorie

Opis ogólny

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.

Immunogen

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

Zastosowanie

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

Działania biochem./fizjol.

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).

Cechy i korzyści

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.

Powiązanie

Corresponding Antigen APREST71132

Postać fizyczna

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

Informacje prawne

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

Oświadczenie o zrzeczeniu się odpowiedzialności

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.
This page may contain text that has been machine translated.

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Kod klasy składowania

10 - Combustible liquids

Klasa zagrożenia wodnego (WGK)

WGK 1

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable

Środki ochrony indywidualnej

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

Certyfikaty analizy (CoA)

Poszukaj Certyfikaty analizy (CoA), wpisując numer partii/serii produktów. Numery serii i partii można znaleźć na etykiecie produktu po słowach „seria” lub „partia”.

Masz już ten produkt?

Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

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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