Beta Amyloid antibody | DE2B4
Mouse anti Human beta amyloid antibody, clone DE2B4 (MCA2172) used for the evaluation of amyloid deposition in brain lysates by dot and western blotting.
Image caption:
Soluble and insoluble TPC6A aggregates are present in the hippocampi of nondemented human controls and AD samples (A) Frozen postmortem AD and control human hippocampal tissues were homogenized by sonication. After centrifugation, the insoluble pellets were further extracted and analyzed by filter retardation assay. Western blotting was then carried out using specific antibodies for TPC6A (pan-specific), TIAF1, Tyr33-phosphorylated WWOX (p-WWOX), NFT and Aβ. No significant difference was shown in TPC6A or TIAF1 aggregation for samples between younger nondemented controls (14 samples per group; total 3 groups; 42 to 76 years old) and older AD patients (24 samples per group; total 4 groups; 71 to 90 years old). C = control; A or AD = Alzheimer's disease. (B) The supernatants of the aforementioned samples were analyzed by 7% non-reducing SDS-PAGE. Western blotting analyses show the presence of soluble aggregates of TPC6A and Aβ in the representative protein preparations. Sample numbers are shown in each panel. Molecular weight markers: 170, 130, 95, 72 kDa. (C) Hippocampal tissue sections of APP/PS1-transgenic mice were stained with aliquots of TPC6A pan-specific antiserum and then with an Alexa Fluor 488-conjugated secondary antibody. Fluoro-Jade C was used for staining degenerative neurons, and nuclei stained with DAPI. TPC6A aggregates are localized in the degenerative neurons. A representative tissue section is shown. Scale bar: 50 μm. In negative controls, the sections were stained with the secondary antibody only, followed by staining with Fluoro-Jade C and DAPI. (D) Immuno-intensity was measured and normalized to negative controls (mean ± standard deviation, n = 5; **p <0.05, student's t test).
From: Chang JY, Lee MH, Lin SR, Yang LY, Sun HS, Sze CI, Hong Q, Lin YS, Chou YT, Hsu LJ, Jan MS, Gong CX, Chang NS.
Trafficking protein particle complex 6A delta (TRAPPC6AΔ) is an extracellular plaque-forming protein in the brain.
Oncotarget. 2015 Feb 28;6(6):3578-89.
This image is from an open access article distributed under the terms of the Creative Commons Attribution License.
Mouse anti Human beta amyloid antibody, clone DE2B4 used for the evaluation of amyloid deposition in brain immunofluorescence.
Image caption:
GF-β1 induces TPC6AΔ aggregation for leading to caspase activation (A) Neuroblastoma SK-N-SH cells were transiently expressed with ECFP or ECFP-TPC6AΔ and treated with TGF-β1 (5 ng/ml) for indicated times, followed by fixation, permeabilization and staining with Aβ antibody. The ratios of the expression of Aβ to TPC6AΔ are shown (n=5). (B) TPC6A aggregates (green) are present in the mitochondria of degenerative neurons in the AD hippocampus. Tissue sections were pre-stained with the Bielschowsky stain (brown to dark), and then stained with Fluoro-Jade C Red for degenerative neurons (red), specific COX4 antibody for mitochondria (cyan), DAPI for nuclei (blue) and pan-specific antibody for TPC6A (green). 600x magnification; Scale bar: 10μm. (C) In negative controls, no primary antibody was used in the immunostaining. (D) Transiently overexpressed EYFP-TPC6AΔ was aggregated in SK-N-SH cells, and caspase 3 became activated (Casp3*). (E) No caspase 3 activation was observed, if ectopic TPC6AΔ was not aggregated. (F) TGF-β1 increased TPC6AΔ aggregation and caspase 3 activation. (G–H) Wild type TPC6A (TPC6Awt), either in a native or an aggregated state, did not induce caspase 3 activation. (I–J) SK-N-SH cells were transiently overexpressed with the indicated expression constructs. The number of cells harboring protein aggregation was counted, and the extent of caspase 3 activation was measured (n=3; Student's t tests; ~50 cells counted per experiment). (K) Colocalization of S35-phosphorylated TPC6AΔ with activated caspase 3 in the AD hippocampal tissue sections. A representative data is shown.
From: Chang JY, Lee MH, Lin SR, Yang LY, Sun HS, Sze CI, Hong Q, Lin YS, Chou YT, Hsu LJ, Jan MS, Gong CX, Chang NS.
Trafficking protein particle complex 6A delta (TRAPPC6AΔ) is an extracellular plaque-forming protein in the brain.
Oncotarget. 2015 Feb 28;6(6):3578-89.
This image is from an open access article distributed under the terms of the Creative Commons Attribution License.
Mouse anti Human Beta Amyloid (aa1-17)
- Product Type
- Monoclonal Antibody
- Clone
- DE2B4
- Isotype
- IgG1
- Specificity
- Beta Amyloid
- Region
- (aa1-17)
Antibody Quality and Performance Guarantee
| Mouse anti Human beta amyloid antibody, clone DE2B4 recognizes the human beta amyloid peptide, the major protein component of amyloid cores in neuritic plaques. In immunohistology the antibody detects extracellular amyloid beta with senile plaques and vessel amyloid in Alzheimer's disease brain. |
- Target Species
- Human
- Product Form
- Purified IgG - liquid
- Preparation
- Purified IgG prepared by affinity chromatography on Protein A from tissue culture supernatant
- Buffer Solution
- Phosphate buffered saline
- Preservative Stabilisers
- 0.09% sodium azide (NaN3)
- Carrier Free
- Yes
- Immunogen
- Synthetic peptide consisting of residues 1 - 17 of the amyloid beta protein.
- Approx. Protein Concentrations
- IgG concentration 1.0 mg/ml
- Regulatory
- For research purposes only
- Guarantee
- 12 months from date of despatch
This product is shipped at ambient temperature. It is recommended to aliquot and store at -20°C on receipt. When thawed, aliquot the sample as needed. Keep aliquots at 2-8°C for short term use (up to 4 weeks) and store the remaining aliquots at -20°C.
Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended.
Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended.
This product has been reported to work in the following applications. This information is derived from testing within our laboratories, peer-reviewed publications or personal communications from the originators. Please refer to references indicated for further information. For general protocol recommendations, please visit the antibody protocols page.
| Application Name | Verified | Min Dilution | Max Dilution |
|---|---|---|---|
| ELISA |  |
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| Immunofluorescence | |
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| Immunohistology - Paraffin 1 | |
||
| Immunoprecipitation | |
||
| Western Blotting |
- 1This product requires protein digestion pre-treatment of paraffin sections using formic acid for 2-3 minutes.
Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls.
- Histology Positive Control Tissue
- Alzheimer's disease brain
References for Beta Amyloid antibody
-
(2011) The Human Protein Atlas : CAB000157
The Human Protein Atlas : CAB000157 -
Kitamoto, T. et al. (1987) Formic acid pretreatment enhances immunostaining of cerebral and systemic amyloids.
Lab Invest. 57 (2): 230-6. -
Lee, M.H. et al. (2010) TGF-β induces TIAF1 self-aggregation via type II receptor-independent signaling that leads to generation of amyloid β plaques in Alzheimer's disease.
Cell Death Dis. 1: e110. -
Koronyo-Hamaoui, M. et al. (2011) Identification of amyloid plaques in retinas from Alzheimer's patients and noninvasive in vivo optical imaging of retinal plaques in a mouse model.
Neuroimage. 54 Suppl 1: S204-17. -
Chang, J.Y. et al. (2012) TIAF1 self-aggregation in peritumor capsule formation, spontaneous activation of SMAD-responsive promoter in p53-deficient environment, and cell death.
Cell Death Dis. 3: e302. -
Chang, J.Y. et al. (2015) Trafficking protein particle complex 6A delta (TRAPPC6AΔ) is an extracellular plaque-forming protein in the brain.
Oncotarget. 6 (6): 3578-89.
MCA2172
0215
149336
160353
163956
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