MAB1574
Anti-Polyglutamine-Expansion Diseases Marker Antibody, clone 5TF1-1C2
ascites fluid, clone 5TF1-1C2, Chemicon®
Synonym(s):
Poly-Glu, PolyQ
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
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
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.
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
Neuroscience
Research Sub Category
Neurodegenerative Diseases
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
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.
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recommended
Storage Class Code
10 - 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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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
Reduction of mutant huntingtin accumulation and toxicity by lysosomal cathepsins D and B in neurons.
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
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
Suppression of neurodegeneration and increased neurotransmission caused by expanded full-length huntingtin accumulating in the cytoplasm.
Romero, E; Cha, GH; Verstreken, P; Ly, CV; Hughes, RE; Bellen, HJ; Botas, J
Neuron null
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
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