Defects in APP are associated with the pathology of various types of Alzheimer’s disease. Specially, the defective amyloid-beta-APP 40-42 peptides, which MOAB-2 targets exclusively, are major constituents of extracellular plaques and contribute cytotoxic neuronal death.
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| University of Illinois Chicago |
| Cat. #: | 156374 |
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| Tool sub type: | Primary antibody |
| Unit size: | 100 ug |
| Research Fields: | Apoptosis and autophagy;Cell biology;Developmental biology |
| Application: | IHC ; WB |
| Target: | Amyloid-? Peptide |
| Reactivity: | Human |
| Host: | Mouse |
| Class: | Monoclonal |
| Alternate name: | AÄÂ? or Abeta |
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| Product description: | Defects in APP are associated with the pathology of various types of Alzheimer's disease. Specially, the defective amyloid-beta-APP 40-42 peptides, which MOAB-2 targets exclusively, are major constituents of extracellular plaques and contribute cytotoxic neuronal death. |
| Conjugation: | Unconjugated |
| Immunogen: | Human beta Amyloid. Recombinant oligomeric A?42. Epitope maps to residues 1-4 of human A?42 and A?40 (DAEF). |
| Target background: | Defects in APP are associated with the pathology of various types of Alzheimer's disease. Specially, the defective amyloid-beta-APP 40-42 peptides, which MOAB-2 targets exclusively, are major constituents of extracellular plaques and contribute cytotoxic neuronal death. |
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| Format: | Liquid |
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| Shipping conditions: | Dry ice |
| References: |
295587871 Fekete et al. 2019. Neuroscience. 405:35-46. PMID: 29522854. Scaringi et al. 2012. Anticancer Res. 32(10):4213-23. PMID: 23060541. Youmans et al. 2012. Mol Neurodegener. 7:8. PMID: 22423893. Youmans et al. 2012. Mol Neurodegener. 7:8. PMID: 22423893. |
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