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Merck

H7540

Sigma-Aldrich

Anti-Huntingtin Disease (HD/HTT) Antibody

enhanced validation

rabbit polyclonal

Synonym(e):

Anti-HD, Anti-HTT, Anti-Huntington Disease, Anti-IT15

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About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

Produktbezeichnung

Anti-Huntingtin (N-terminal) antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution

Biologische Quelle

rabbit

Qualitätsniveau

Konjugat

unconjugated

Antikörperform

affinity isolated antibody

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Form

buffered aqueous solution

Mol-Gew.

antigen ~110 kDa

Speziesreaktivität

mouse, human, rat

Erweiterte Validierung

recombinant expression
Learn more about Antibody Enhanced Validation

Konzentration

~1.5 mg/mL

Methode(n)

western blot: 0.5-1.0 μg/mL using a HEK-293T cell lysate expressing a N-terminal fragment of human huntingtin

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... HTT(3064)
mouse ... Htt(15194)
rat ... Htt(29424)

Allgemeine Beschreibung

Anti-Huntingtin (N-terminal) is produced in rabbit using as immunogen a synthetic peptide corresponding to human huntingtin, conjugated to KLH.

Anwendung

Anti-Huntingtin (N-terminal) antibody has been used:
  • in magnetic bead-assisted immunopurification
  • in western blotting
  • in immunofluorescent staining
  • in immunoblotting

Biochem./physiol. Wirkung

Huntingtin (Htt) is essential for embryonic development and neurogenesis. Htt associates with various cell organelles like the nucleus, endoplasmic reticulum and Golgi complex. It is also found in neurites and synapses where it associates with vesicular structures and microtubules, suggesting that it may play a role in intracellular vesicular trafficking, calcium homeostasis, neuronal survival, morphogenesis and transcriptional regulation. Aberrant expansion of glutamine repeats (polyQ) in the N-terminal region of huntingtin (htt) causes Huntington′s disease (HD) which is an autosomal dominant neurodegenerative disorder.

Physikalische Form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Haftungsausschluss

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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Empfehlung

Lagerklassenschlüssel

10 - Combustible liquids

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Persönliche Schutzausrüstung

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


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In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

Introducing an expanded CAG tract into the huntingtin gene causes a wide spectrum of ultrastructural defects in cultured human cells
Morozova K N, et al.
PLoS ONE, 13(10), e0204735-e0204735 (2018)
I Alexandra Amaro et al.
Journal of neurodegenerative diseases, 2016, 7120753-7120753 (2016-09-07)
Huntington's disease (HD) is a fatal progressive disease linked to expansion of glutamine repeats in the huntingtin protein and characterized by the progressive loss of cognitive and motor function. We show that expression of a mutant human huntingtin exon-1-GFP fusion
Prefibrillar huntingtin oligomers isolated from HD brain potently seed amyloid formation
Morozova O A, et al.
Febs Letters, 589(15), 1897-1903 (2015)
Luisa Massai et al.
BMC biochemistry, 14, 34-34 (2013-11-28)
Huntington's disease (HD) is a monogenic disorder caused by an aberrant expansion of CAG repeats in the huntingtin gene (HTT). Pathogenesis is associated with expression of the mutant (mHTT) protein in the CNS, with its levels most likely related to
Huntingtin-protein interactions and the pathogenesis of Huntington's disease
Li SH and Li XJ
Trends in Genetics, 20(3), 146-154 (2004)

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