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H7540

Sigma-Aldrich

Anti-Huntingtin Disease (HD/HTT) Antibody

enhanced validation

rabbit polyclonal

Synonyma:

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

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

Název produktu

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

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~110 kDa

species reactivity

mouse, human, rat

enhanced validation

recombinant expression
Learn more about Antibody Enhanced Validation

concentration

~1.5 mg/mL

technique(s)

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

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

General description

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

Application

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

Biochem/physiol Actions

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.

Physical form

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

Disclaimer

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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Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

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


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Dokumenty související s produkty, které jste v minulosti zakoupili, byly za účelem usnadnění shromážděny ve vaší Knihovně dokumentů.

Navštívit knihovnu dokumentů

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
A phenotypic screening assay for modulators of Huntingtin-induced transcriptional dysregulation
Lazzeroni G, et al.
Journal of Biomolecular Screening, 18(9), 984-996 (2013)
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)
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
Normal huntingtin function: an alternative approach to Huntington's disease
Cattaneo E, et al.
Nature Reviews. Neuroscience, 6(12), 919-919 (2005)

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