beta Amyloid 1-16 (AA 1-16) anticorps
Aperçu rapide pour beta Amyloid 1-16 (AA 1-16) anticorps (ABIN724955)
Antigène
Reactivité
Hôte
Clonalité
Conjugué
Application
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Épitope
- AA 1-16
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Réactivité croisée
- Humain
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Purification
- Purified by Protein A.
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Immunogène
- KLH conjugated synthetic peptide of human beta-Amyloid(1-16)
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Isotype
- IgG
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Indications d'application
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WB 1:100-1000
IHC-P 1:100-500
IF(IHC-P) 1:50-200 -
Restrictions
- For Research Use only
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Format
- Liquid
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Concentration
- 1 μg/μL
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Buffer
- Aqueous buffered solution containing 1 % BSA, 50 % glycerol and 0.09 % sodium azide.
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Agent conservateur
- Sodium azide
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Précaution d'utilisation
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.
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Stock
- -20 °C
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Stockage commentaire
- Store at -20°C for 12 months.
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Date de péremption
- 12 months
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- beta Amyloid 1-16
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Sujet
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Synonyms: AAA, AD1, PN2, ABPP, APPI, CVAP, ABETA, PN-II, CTFgamma, Amyloid beta A4 protein, APP, Alzheimer disease amyloid protein, Cerebral vascular amyloid peptide, PreA4, Protease nexin-II, A4
Background: Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1. Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses.
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ID gène
- 351
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UniProt
- P05067
Antigène
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