α毒素
α毒素从
坏疽毒素梭状芽胞杆菌是一个家庭成员β-pore形成毒素(β-PFTs)和被确定为这种细菌的主要毒力因子。毒素的产生是单身、多肽、蛋白质分泌。七的毒素单体oligomerize哺乳动物细胞膜上创建一个ring-structured转移膜孔隙/通道。孔隙允许K +的流出和流入的Ca +导致渗透细胞溶菌作用和死亡。这亲水c .坏疽抗毒素α毒素产生的孔隙直径大约1.3 - -1.6 nm。各种有核哺乳动物细胞,包括IEC-6 (EC50 5.8 ng / ml),维罗(EC50 24.3 ng / ml),曹(EC50 24.3 ng / ml), MDCK (EC50 14.6 ng / ml),和MDBK (EC50 24.3 ng / ml),已报告这种毒素敏感。因为α毒素结合GPI-anchored蛋白质,包括表面抗原1 (SAG1)和SAG3一些原生动物寄生虫,毒素已经被用于理解GPI-anchored蛋白质合成和运输通过不寻常的寄生虫的triple-membrane结构薄膜质膜,GPI-anchored生物合成的分子遗传分析,GPI-anchored蛋白质贩卖。特别是,刚地弓形虫是发现是非常敏感的α毒素(EC50 0.2海里)。α毒素可用于癌症研究筛选和识别肿瘤抗原,如癌胚抗原、mesothelin,前列腺特异性干细胞抗原,和尿激酶纤溶酶原激活物受体,据报道也升高血浆的乳腺癌、卵巢、肾、肝和大脑癌症患者。α毒素已被用于捕捉这些记者抗原,其中一些已经被质谱分析,确定这是用于筛查和检测这些肿瘤抗原以及发现新的生物标记/各种癌症的目标。 Alpha Toxin can be used to develop immunoassays. As Alpha Toxin has been reported to be an immune dominant extracellular antigen, inactive toxin/toxoid, therefore, can be used to develop effective vaccines against C. septicum mediated diseases. Purified Alpha Toxin can also be used to understand the disease progression and in pharmacokinetic studies in animal models. C.
坏疽毒素α毒素在列表实验室是一个生产重组蛋白表达在大肠杆菌和高纯度的pro-toxin约50 kDa的蛋白质。pro-toxin已经被胰蛋白酶激活之前记下的45氨基酸残基糖基(KRRGKR398SVD)。
- 产品# 116α毒素从C。坏疽毒素冻结在提供20%甘油包含MES缓冲
ε毒素
ε分泌出毒素toxinotype B和D perfringens梭状芽胞杆菌菌株。ε毒素属于heptamericβ-pore-forming毒素家族包括aerolysin和c .坏疽抗毒素α毒素。ε毒素合成为一个单一的、分泌~ 33 kDa蛋白质活性很差,称为prototoxin。产生的蛋白酶c perfringens或出现在主机腔prototoxin转换为一个减小尺寸(~ 28.6 kDa)活跃ε毒素,使毒素oligomerize其heptamericβ-barrel形式。激活显著降低了π值从8.02到5.36,最有可能创建一个构象的变化。ε毒素受体尚未确定,然而,脂筏相关髓磷脂和淋巴细胞蛋白(MAL)提出了膜的受体ε毒素。ε毒素是更有效的比aerolysin (100 x), c .坏疽抗毒素α毒素。ε毒素被列为B类bio-threat代理潜在的恶意。在这方面,活动/活动/突变ε毒素疫苗开发潜力和在生物研究。高浓度的ε毒素诱导肠道黏膜的渗透性的增加,调解的毒素进入血液,传播和积累特别是在肾脏和大脑。 Epsilon Toxin efficiently increases the vascular permeability of rat mesentery microvessels or skin vessels after intradermal injection. In the kidney, Epsilon Toxin causes interstitial hemorrhage between tubules and degeneration of proximal and distal epithelium suggesting that kidney is one of the target organs for epsilon toxin. The toxin is able to alter the integrity of the blood brain barrier (BBB) resulting in prominent lesions consisting of perivascular edema described in mice, rats, sheep and calves, which in the acute state, develop foci of necrosis and hemmorhage. A direct and rapid Epsilon Toxin effect in the brain involves the stimulation of glutamate release from glutametargic neurons abundant in the CNS, which is probably the main cause of the neurological symptoms of excitation (convulsions) observed in Epsilon Toxin dependant enterotoxemia in sheep. Epsilon Toxin has also been shown to induce the release of other neurotransmitters such as dopamine. In that respect, Epsilon Toxin can be used as a reagent to stimulate glutametargic neurons where many bacterial neurotoxins inhibit the release of neurotransmitters. Epsilon Toxin has also been reported to be used as delivery vehicle to facilitate the transport of drugs through the BBB for the treatment of experimental malignant brain tumors in mice. There is a growing body of evidence that indicates Epsilon Toxin may be a potential trigger for human multiple sclerosis (MS), an inflammatory disease of the central nervous system characterized by disruption of blood brain barrier (BBB) and demyelination of the myelin sheath that insulates the neurons. Epsilon Toxin is known to bind and kill the brain’s endothelium cells and oligodendrocytes (myelin producing cells), the same cells that die in MS lesions. Epsilon Toxin has been found to bind to the retinal vasculature and kill meningeal cells; meningeal inflammation and subpial cortical lesions are known pathologies associated with MS. These findings are very important for future MS research, and epsilon toxin will be a valuable reagent and tool to understand the pathophysiology of MS. Active Epsilon Toxin is highly purified from native C. perfringens.
- 产品# 126ε毒素从c perfringens提供冻干PBS缓冲。
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