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MAB1574

Sigma-Aldrich

Anti-Polyglutamine-Expansion Diseases Marker Antibody, clone 5TF1-1C2

ascites fluid, clone 5TF1-1C2, Chemicon®

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Synonym(s):
Poly-Glu, PolyQ
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

ascites fluid

antibody product type

primary antibodies

clone

5TF1-1C2, monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable (paraffin)
immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgG1κ

shipped in

dry ice

target post-translational modification

unmodified

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This Item
P1874MAB2166MABN2427
antibody form

ascites fluid

antibody form

purified from hybridoma cell culture

antibody form

ascites fluid

antibody form

purified immunoglobulin

clone

5TF1-1C2, monoclonal

clone

3B5H10, monoclonal

clone

1HU-4C8, monoclonal

clone

MW1, monoclonal

species reactivity

human

species reactivity

human

species reactivity

rat, rabbit

species reactivity

mouse, rat, human

manufacturer/tradename

Chemicon®

manufacturer/tradename

-

manufacturer/tradename

Chemicon®

manufacturer/tradename

-

technique(s)

ELISA: suitable, immunocytochemistry: suitable, immunohistochemistry: suitable (paraffin), immunoprecipitation (IP): suitable, western blot: suitable

technique(s)

immunocytochemistry: suitable, immunoprecipitation (IP): suitable, western blot: 1-2 μg/mL using extract of HEK-293T cells transfected with an N-terminal 171 amino acid fragment of human Huntingtin with a 68 glutamine stretch

technique(s)

ELISA: suitable, immunocytochemistry: suitable, immunohistochemistry: suitable (paraffin), immunoprecipitation (IP): suitable, western blot: suitable

technique(s)

immunocytochemistry: suitable, immunohistochemistry: suitable, western blot: suitable

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General description

Huntington’s disease (HD) belongs to a family of polyglutamine diseases, which includes dentatorubralpallidoluysian atrophy (DRPLA), spinobulbar muscular atrophy (SBMA) and spinocerebellar ataxia (SCA) types 1–3, 6, 7 and 17. In these diseases, the non-pathogenic alleles contain fewer than approximately 35 consecutive glutamine repeats and encode a normal polyglutamine domain. In contrast, the pathogenic alleles usually contain 39 or more consecutive glutamine repeats. Higher repeat numbers lead to lower ages of onset. Patients with 40-60 glutamine repeats normally develop disease as adults, whereas patients with more than 60 repeats develop a juvenile onset disease. Each polyglutamine expansion disorder displays characteristic pathology, with neuronal loss evident in specific regions of the brain. HD results from expansions of a glutamine tract in a large cystolic protein known as huntingtin.

Specificity

The epitope of MAB1574 was found to be a homopolymeric glutamine stretch. The original immunogen was the general transcription factor TATA Box-binding protein (TBP) which contains a 38-glns stretch (Lescure et al). Other polyglutamine-containing proteins are recognized by the MAB1574, notably those involved in several human neurodegenerative diseases caused by a CAG repeat expansion, like Huntington′s disease and spinocerebellar ataxia type 2, 3 and 7 (Trottier et al., 1995). Importantly, for proteins involved in these neurodegenerative disorders, MAB1574 showed remarkable property of detecting much better the pathological proteins that contain a polyglutamine expansion (37 glns) than the wild type proteins (Trottier et al., 1995). MAB1574 has been used to identify new neurodegenerative diseases caused by polyglutamine expansion and to help for cloning of the corresponding affected genes (Trottier 1995-1998; Imbert 1996; Stevanin 1996). MAB1574 is also able to detect intracellular inclusions, which is a hallmark of such diseases (Paulson, 1997).

Immunogen

N-terminal part of the human TATA Box Binding Protein (TBP).

Application

Anti-Polyglutamine-Expansion Diseases Marker Antibody, clone 5TF1-1C2 is an antibody against Polyglutamine-Expansion Diseases Marker for use in ELISA, IC, IH(P), IP & WB.
ELISA: 1:1,000-1:20,000

Western Blot: 1:1,000-1:20,000

Immunohistochemistry on frozen and paraffin sections (human tissue): 1:1,000-1:20,000

Immunocytochemistry on transfected cells: 1:1,000-1:20,000 Immunoprecipitation: 1:1,000-1:20,000

Optimal working dilutions must be determined by end user.
Research Category
Neuroscience
Research Sub Category
Neurodegenerative Diseases

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
Huntigton′s Disease brain

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.

Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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HYPK, a Huntingtin interacting protein, reduces aggregates and apoptosis induced by N-terminal Huntingtin with 40 glutamines in Neuro2a cells and exhibits chaperone-like activity.
Raychaudhuri, S; Sinha, M; Mukhopadhyay, D; Bhattacharyya, NP
Human Molecular Genetics null
Qiuli Liang et al.
Molecular neurodegeneration, 6, 37-37 (2011-06-03)
Huntington's disease is caused by aggregation of mutant huntingtin (mHtt) protein containing more than a 36 polyQ repeat. Upregulation of macroautophagy was suggested as a neuroprotective strategy to degrade mutant huntingtin. However, macroautophagy initiation has been shown to be highly
Ashish Kumar et al.
Human molecular genetics, 25(8), 1619-1636 (2016-02-26)
Identifying molecular drivers of pathology provides potential therapeutic targets. Differentiating between drivers and coincidental molecular alterations presents a major challenge. Variation unrelated to pathology further complicates transcriptomic, proteomic and metabolomic studies which measure large numbers of individual molecules. To overcome
Yan Hong et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 36(34), 8790-8801 (2016-08-26)
Brain-derived neurotrophic factor (BDNF) is essential for neuronal differentiation and survival. We know that BDNF levels decline in the brains of patients with Huntington's disease (HD), a neurodegenerative disease caused by the expression of mutant huntingtin protein (mHtt), and furthermore
Ian H Kratter et al.
The Journal of clinical investigation, 126(9), 3585-3597 (2016-08-16)
Huntington's disease (HD) is a progressive, adult-onset neurodegenerative disease caused by a polyglutamine (polyQ) expansion in the N-terminal region of the protein huntingtin (HTT). There are no cures or disease-modifying therapies for HD. HTT has a highly conserved Akt phosphorylation

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