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MAB5492

Sigma-Aldrich

Anti-Huntingtin Antibody, a.a. 1-82

ascites fluid, clone 2B4, Chemicon®

Synonym(s):

Anti-Huntingtin, Anti-Huntingtin Antibody, Detection Antibody

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

ascites fluid

antibody product type

primary antibodies

clone

2B4, monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable

isotype

IgG1

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

Specificity

Reacts huntingtin protein, amino acids 1-82. The antibody recognizes wild type and mutant huntingtin.

Immunogen

Epitope: a.a. 1-82
Recombinant human huntingtin, amino acids 1-82.

Application

Anti-Huntingtin Antibody, a.a. 1-82 is an antibody against Huntingtin for use in ELISA, IC, IH & WB.
Research Category
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Western blot: 1:500-1:5,000

Immunocytochemistry (1): 1:500-1:5,000

Immunohistochemistry (1,2): 1:500-1:5,000

ELISA: 1:500-1:5,000

Optimal working dilutions must be determined by end user.

Target description

348 kDa

Physical form

Ascites fluid containing no preservatives.
Unpurified

Storage and Stability

Maintain for 1 year at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Analysis Note

Control
Normal human cerebral cortex lysate, Mouse brain cortex samples from HD or wild type mice

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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 Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Phosphorylation of mutant huntingtin at serine 116 modulates neuronal toxicity.
Watkin, EE; Arbez, N; Waldron-Roby, E; O'Meally, R; Ratovitski, T; Cole, RN; Ross, CA
Testing null
Sean M DeGuire et al.
The Journal of biological chemistry, 293(48), 18540-18558 (2018-09-07)
Huntington's disease is a fatal neurodegenerative disorder resulting from a CAG repeat expansion in the first exon of the gene encoding the Huntingtin protein (Htt). Phosphorylation of this protein region (Httex1) has been shown to play important roles in regulating
Sophie Vieweg et al.
The Journal of biological chemistry, 291(23), 12074-12086 (2016-03-24)
The first exon of the Huntingtin protein (Httex1) is one of the most actively studied Htt fragments because its overexpression in R6/2 transgenic mice has been shown to recapitulate several key features of Huntington disease. However, the majority of biophysical
Gennady Ermak et al.
The Journal of biological chemistry, 284(18), 11845-11853 (2009-03-10)
Our work suggests an important new link between the RCAN1 gene and Huntington disease. Huntington disease is caused by expansion of glutamine repeats in the huntingtin protein. How the huntingtin protein with expanded polyglutamines (mutant huntingtin) causes the disease is
S-nitrosylation of dynamin-related protein 1 mediates mutant huntingtin-induced mitochondrial fragmentation and neuronal injury in Huntington's disease.
Haun, F; Nakamura, T; Shiu, AD; Cho, DH; Tsunemi, T; Holland, EA; La Spada, AR; Lipton, SA
Antioxidants & Redox Signaling null

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