제품 이름
Anti-Amyloid β Antibody, clone W0-2, clone WO2, from mouse
biological source
mouse
antibody form
purified immunoglobulin
clone
WO2, monoclonal
species reactivity
mouse, human
technique(s)
ELISA: suitable
immunohistochemistry: suitable (paraffin)
western blot: suitable
isotype
IgG2aκ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Quality Level
Gene Information
human ... APP(351)
Analysis Note
Control
Human Alzheimer diseased brain tissue lysate
Human Alzheimer diseased brain tissue lysate
Evaluated by Western Blot in human Alzheimer disease brain tissue lysate.
Western Blot Analysis: 0.5 µg/ml of this antibody detected Amyloid β in 10 µg of human Alzheimer diseased brain tissue lysate.
Western Blot Analysis: 0.5 µg/ml of this antibody detected Amyloid β in 10 µg of human Alzheimer diseased brain tissue lysate.
Application
Detect Amyloid β using this Anti-Amyloid β Antibody, clone W0-2 validated for use in WB, IH, ELISA.
Immunohistochemistry Analysis: 1:500 dilution from a previous lot detected Amyloid β in Alzheimer’s diseased hippocampus.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Neurodegenerative Diseases
Biochem/physiol Actions
This antibody recognizes amino acid residues 4-10 of human Amyloid β.
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.
General description
The cerebral and vascular plaques associated with Alzheimer′s disease (AD) are mainly composed of amyloid beta peptides (Aβ). Aβ is derived from cleavage of the amyloid precursor protein (APP) and varies in length from 39 to 43 amino acids. Aβ [1-40], Aβ [1-42], and Aβ [1-43] peptides result from cleavage of APP after residues 40, 42, and 43, respectively. The cleavage takes place by gamma-secretase during the last APP processing step. Aβ [1-40], [1-42] and [1-43] peptides are major constituents of the plaques and tangles that occur in AD. These Amyloid beta antibodies and peptides have been developed as tools for elucidating the biology of AD.
Calculated MW is 4 kDa This antibody can also show 120 and 105 kDa APP proteins, and ~45 kDa oligomers of amyloid proteins on our western blot of human Alzheimer diseased brain lysate.
Immunogen
Epitope: Amino acid residues 4-10
Human Amyloid β peptide
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Replaces: MAB1561
Physical form
Format: Purified
Protein G Purified
Purified mouse monoclonal IgG2aκ in buffer containing 0.1 M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.05% sodium azide.
Preparation Note
Stable for 1 year at 2-8°C from date of receipt.
저장 등급
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
Yuhai Zhao et al.
Frontiers in aging neuroscience, 8, 140-140 (2016-07-06)
One prominent and distinguishing feature of progressive, age-related neurological diseases such as Alzheimer's disease (AD) and prion disease (PrD) is the gradual accumulation of amyloids into dense, insoluble end-stage protein aggregates. These polymorphic proteolipid lesions are known to contribute to
Luisa Diomede et al.
Neurobiology of disease, 62, 521-532 (2013-11-05)
Although Alzheimer's disease (AD) is usually sporadic, in a small proportion of cases it is familial and can be linked to mutations in β-amyloid precursor protein (APP). Unlike the other genetic defects, the mutation [alanine-673→valine-673] (A673V) causes the disease only
Deficits in the miRNA-34a-regulated endogenous TREM2 phagocytosis sensor-receptor in Alzheimer's disease (AD); an update.
Bhattacharjee, S; Zhao, Y; Lukiw, WJ
Frontiers in Aging Neuroscience null
Eitan Wong et al.
Proceedings of the National Academy of Sciences of the United States of America, 116(13), 6385-6390 (2019-03-10)
The mechanism by which γ-secretase activating protein (GSAP) regulates γ-secretase activity has not yet been elucidated. Here, we show that knockout of GSAP in cultured cells directly reduces γ-secretase activity for Aβ production, but not for Notch1 cleavage, suggesting that
Daniela A Gutierrez et al.
Frontiers in cellular neuroscience, 13, 526-526 (2019-12-19)
Spine pathology has been implicated in the early onset of Alzheimer's disease (AD), where Aβ-Oligomers (AβOs) cause synaptic dysfunction and loss. Previously, we described that pharmacological inhibition of c-Abl prevents AβOs-induced synaptic alterations. Hence, this kinase seems to be a
관련 콘텐츠
Alzheimer’s Disease: Amyloid Cascade and Beyond Product Focus
국제 무역 품목 번호
| SKU | GTIN |
|---|---|
| MABN10 | 04053252668081 |
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