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Amyloid-β Polyclonal Antibody

货号: YP-Ab-12870
促销价:

产品介绍

反应种属
Human;Mouse;Rat
应用范围
IF;WB;IHC;ELISA
抗体类型
多克隆抗体
基因名称(Gene Name)
APP A4 AD1
蛋白名称
Amyloid beta A4 protein, Amyloid-β, Aβ
分子量(DA)
87kD
免疫原
Synthesized peptide derived from Amyloid-β at AA range: 221-270
特异性
Amyloid-β Polyclonal Antibody detects endogenous levels of Amyloid-β
组成
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
来源
Polyclonal, Rabbit,IgG
稀释比例
IF: 1:50-200 WB 1:500-2000, ELISA 1:10000-20000 IHC 1:50-300
纯化工艺
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
浓度
1 mg/ml
储存
-20°C/1 year
其他名称
amyloid beta (A4) precursor protein
背景
This gene encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Some of these peptides are secreted and can bind to the acetyltransferase complex APBB1/TIP60 to promote transcriptional activation, while others form the protein basis of the amyloid plaques found in the brains of patients with Alzheimer disease. In addition, two of the peptides are antimicrobial peptides, having been shown to have bacteriocidal and antifungal activities. Mutations in this gene have been implicated in autosomal dominant Alzheimer disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy). Multiple transcript variants encoding several different isoforms have been found for this gene. [provided by RefSeq, Aug 2014],
功能
alternative products:Additional isoforms seem to exist. Experimental confirmation may be lacking for some isoforms,disease:Defects in APP are the cause of Alzheimer disease type 1 (AD1) [MIM:104300]. AD1 is a familial early-onset form of Alzheimer disease. It can be associated with cerebral amyloid angiopathy. Alzheimer disease is a neurodegenerative disorder characterized by progressive dementia, loss of cognitve abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituent of these plaques is the neurotoxic amyloid-beta-APP 40-42 peptide (s), derived proteolytically from the transmembrane precursor protein APP by sequential secretase processing. The cytotoxic C-terminal fragments (CTFs) and the caspase-cleaved products such as C31 derived from APP, are also implicated

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