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Anti-Amyloid beta A4 Rabbit Monoclonal Antibody
Anti-Amyloid beta A4 Rabbit Monoclonal Antibody
- 中文名称:
- Anti-Amyloid beta A4 Rabbit Monoclonal Antibody
- 英文名称:
- Anti-Amyloid beta A4 Rabbit Monoclonal Antibody
- 品牌:
- AAA Biotech
- 品牌介绍:
- AAA Biotech专注于为全球生命科学研究提供高品质的蛋白质研究工具,核心产品包括经严格验证的抗体、重组蛋白及ELISA试剂盒。
- 货号:
- AAA46868
- 规格:
- 0.03 mL|0.1 mL|2x0.1 mL|3x0.1 mL|4x0.1 mL
- 保存建议:
- Store at -20 degree C for one year. After reconstitution, at 4 degree C for one month. It can also be aliquotted and stored frozen at -20 degree C for a longer time. Avoid repeated freezing and thawing.
- 货期:
- 6-8周
- 来源宿主:
- Rabbit
- 反应种属:
- Human, Mouse, Rat
- 应用:
- WB (Western Blot), ICC (Immunocytochemistry), IHC (Immunohistochemistry), IF (Immunofluorescence), IP (Immunoprecipitation), FCM/FACS (Flow Cytometry)
- 免责声明:
- *本产品仅供科研实验使用,不得用于临床诊断。*
- 其他:
克隆性:Monoclonal
同型:N/A
克隆号:N/A
特异性:N/A
纯度:Affinity-chromatography
形式:Liquid
浓度:N/A
- 说明书:
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.