炭疽杆菌菌体蛋白抗体elisa实验

炭疽杆菌菌体蛋白抗体英文名称  Anti-Bacillus anthraci protein 

中文名称  炭疽杆菌菌体蛋白抗体 

浓    度  1mg/1ml 

规 格  0.2ml/200μg  

抗体来源  Rabbit  

克隆类型  polyclonal 

炭疽杆菌菌体蛋白抗体交叉反应  Bacillusantci  

产品类型  一抗    

研究领域  免疫学 细菌及病毒  

性    状  Lyophilized or Liquid 

免 疫 原  KLH conjugated synthetic peptide derived from Ba Bacillus anthraci protein 

亚    型  IgG 

纯化方法  affinity purified by Protein A 

储 存 液  Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4 

产品应用   ELISA=1:500-1000  IP=1:20-100  IHC-P=1:100-500  IHC-F=1:100-500  ICC=1:100-500  IF=1:100-500 

（石蜡切片需做抗原修复） 

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

保存条件  Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. 

Important Note  This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 

产品介绍 Bacillus anthracis is an aerobic spore forming bacterium that causes anthrax, an acute infectious disease of cattle, sheep, goats, camels, antelopes and other herbivores. Infection can occur in humans when they are exposed to infected animals or tissue from infected animals via three routes: cutaneous, inhalation and gastrointestinal. B. anthracis spores persist in the soil for many years as they are resistant to heat, cold, radiation, desiccation, and d炭疽杆菌菌体蛋白抗体isinfectants. In vivo, B anthracis produces a polypeptide (polyglutamic acid) capsule that protects it from phagocytosis. The virulence factors of B anthracis are its capsule and three component toxin, both encoded on plasmids.

炭疽杆菌从损伤的皮肤、胃肠粘膜及呼吸道进入人体后，首先在局部繁殖，产生毒素而致组织及脏器发生出血性浸润、坏死和高度水肿，形成原发性皮肤炭疽、肠炭疽的肺炭疽等。当机体抵抗力降低时，致病菌即迅速沿淋巴管及血管向全身扩散，形成败血症和继发性脑膜炎。皮肤炭疽因缺血及毒素的作用，真皮的神经纤维发生变化，故病灶处常无明显的疼痛感。炭疽杆菌的毒素可直接损伤血管的内皮细胞，使血管壁的通透性增加，导致有效血容量减少，微循环灌注量下降，血液呈高凝状态，出现DIC和感染性休克。