β淀粉样肽1-28/β-Amyloid 1-28抗体

中文名称：β淀粉样肽1-28/β-Amyloid 1-28抗体

英文名称：beta Amyloid 1-28

别    名：β-Amyloid 1-28; beta Amyloid(1-28); beta-amyloid peptide; beta-Amyloid 1-28; beta-Amyloid 1-28; Amyloid 1-28; A4; AAA; ABETA; ABPP; AD1; Alzheimers Disease Amyloid Protein; Amyloid B; Amyloid Beta A4 Protein Precursor; Amyloid Beta; Amyloid of Aging and Alzheimer Disease; APP; APPI; B Amyloid; Beta APP; Cerebral Vascular Amyloid Peptide; CTFgamma; CVAP; PN II; PN2; PreA4; Protease nexin II; A beta; A4_HUMAN.  

分 子 量：4.3kDa

细胞定位：细胞浆 细胞膜 细胞外基质 

纯化方法：affinity purified by Protein A

储 存 液：0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.





产品介绍：与阿尔茨海默病相关的脑血管斑块主要由β淀粉样肽组成。 β 淀粉样蛋白来源于淀粉样蛋白前体蛋白的切割，长度从 39 到 43 个氨基酸不等。 β 淀粉样蛋白 [1-40]、β 淀粉样蛋白 [1-42] 和 β 淀粉样蛋白 [1-43] 肽分别由淀粉样蛋白前体蛋白在残基 40、42 和 43 后的切割产生。 在最后的淀粉样前体蛋白加工步骤中，γ-分泌酶进行切割。 β 淀粉样蛋白 [1-40]、β 淀粉样蛋白 [1-42] 和 β 淀粉样蛋白 [1-43] 肽是阿尔茨海默病中出现的斑块和缠结的主要成分。 β淀粉样蛋白抗体和肽已被开发为阐明阿尔茨海默病生物学的工具。

Function:
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. 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.
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. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity.
Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brai.
The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis.
N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).

注意：
所提供的本产品仅供研究使用，不得用于人类、治疗或诊断应用。