MAB5490
Anti-Huntingtin Antibody, a.a. 115-129
ascites fluid, Chemicon®
Sinônimo(s):
Anti-HD
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About This Item
Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Produtos recomendados
fonte biológica
mouse
forma do anticorpo
ascites fluid
tipo de produto de anticorpo
primary antibodies
clone
monoclonal
reatividade de espécies
human
fabricante/nome comercial
Chemicon®
técnica(s)
ELISA: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable
Isotipo
IgG1κ
nº de adesão NCBI
nº de adesão UniProt
Condições de expedição
dry ice
modificação pós-traducional do alvo
unmodified
Informações sobre genes
human ... HTT(3064) , SLC6A4(6532)
Especificidade
Reacts huntingtin protein, amino acids 115-129. The antibody recognizes wild type and mutant huntingtin.
Imunogênio
Epitope: a.a. 115-129
Recombinant human huntingtin, amino acids 115-129.
Aplicação
Anti-Huntingtin Antibody, a.a. 115-129 detects level of Huntingtin & has been published & validated for use in ELISA, WB, IC, IH.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurodegenerative Diseases
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.
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.
forma física
Ascites fluid. Liquid. Contains no preservative.
Armazenamento e estabilidade
Maintain at -20°C in undiluted aliquots for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.
Informações legais
CHEMICON 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
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”.
Já possui este produto?
Encontre a documentação dos produtos que você adquiriu recentemente na biblioteca de documentos.
Ser46 phosphorylation and prolyl-isomerase Pin1-mediated isomerization of p53 are key events in p53-dependent apoptosis induced by mutant huntingtin.
Grison, A; Mantovani, F; Comel, A; Agostoni, E; Gustincich, S; Persichetti, F; Del Sal, G
Proceedings of the National Academy of Sciences of the USA null
Katarina Trajkovic et al.
Bio-protocol, 8(1) (2018-01-13)
Quantitative analysis of proteins secreted from the cells poses a challenge due to their low abundance and the interfering presence of a large amount of bovine serum albumin (BSA) in the cell culture media. We established assays for detection of
Tamara Ratovitski et al.
Cell cycle (Georgetown, Tex.), 14(11), 1716-1729 (2015-05-01)
Abnormal protein interactions of mutant huntingtin (Htt) triggered by polyglutamine expansion are thought to mediate Huntington's disease (HD) pathogenesis. Here, we explored a functional interaction of Htt with protein arginine methyltransferase 5 (PRMT5), an enzyme mediating symmetrical dimethylation of arginine
IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome.
Thompson, LM; Aiken, CT; Kaltenbach, LS; Agrawal, N; Illes, K; Khoshnan et al.
The Journal of cell biology null
Jacqueline Gire O'Rourke et al.
Cell reports, 4(2), 362-375 (2013-07-23)
A key feature in Huntington disease (HD) is the accumulation of mutant Huntingtin (HTT) protein, which may be regulated by posttranslational modifications. Here, we define the primary sites of SUMO modification in the amino-terminal domain of HTT, show modification downstream of
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