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从原料到标记,打造属于中国自己的流式抗体品牌abinScience 体内级抗体,年度锁价,低至 1200五大应用案例:Mustang Q 膜层析应用全解析1 个小工具,一次性搞定流程图、质粒图谱和信号通路图- 详细信息
- 文献和实验
- 技术资料
- 保存条件:
Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 6 months; -20°C, 1 month.
- 库存:
货期:1-2天
- 供应商:
MedChemExpress LLC
- CAS号:
332420-90-3
- 规格:
10 mM * 1 mL/5 mg/10 mg/25 mg/50 mg/100 mg
| 规格: | 10 mM * 1 mL | 产品价格: | ¥890.0 |
|---|---|---|---|
| 规格: | 5 mg | 产品价格: | ¥800.0 |
| 规格: | 10 mg | 产品价格: | ¥1200.0 |
| 规格: | 25 mg | 产品价格: | ¥2500.0 |
| 规格: | 50 mg | 产品价格: | ¥3800.0 |
| 规格: | 100 mg | 产品价格: | ¥5500.0 |
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C 87
CAS No. : 332420-90-3
MCE 国际站:C 87
产品活性:C 87 是一种新型小分子 TNFα 抑制剂; 高效抑制 TNFα 诱导的细胞毒性,IC50 值为 8.73 μM。
研究领域:Apoptosis
作用靶点:TNF Receptor
In Vitro: C 87 (C87) directly binds to TNFα, potently inhibits TNFα-induced cytotoxicity (IC50=8.73 μM) and effectively blocks TNFα-triggered signaling activities. C 87 exhibits good solubility and consistent dose-dependent functions in vitro. C 87 completely blocks TNFα-induced activation of caspase-3 and caspase-8. The activity of c-Jun N-terminal kinase (JNK) is significantly reduced by C 87 in L929 cells. C 87 also prevents the degradation of IκBα in cells treated with TNFα. C 87 potently blocks multiple signaling transduction pathways and downstream target gene activation triggered by TNFα.
In Vivo: C 87 (C87) attenuates TNFα-induced inflammation, thereby markedly reducing injuries to the liver and improving animal survival. C 87 injection delays the incidence of death and increases the survival rate by two folds compared with the vehicle control. The level of alanine transaminase and aspartate transaminase is consistently reduced in mice with C 87 treatment.
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文献和实验广义的细胞色素 c是含有血红素 c的细胞色素之总称。通常是指主要存在于高等动植物、酵母、霉菌等线粒体中的细胞色素 c,起着传递电子的作用。为分子量约 1.3万的碱性蛋白质,还原型的吸收带为 550、 520、 415毫微米,氧化型为 407毫微米。α 因此很早便被研究,并获得结晶。不仅一级结构而且立体结构也已清楚(图 1)。其结构基本上是生物界共有的。由细胞色素 c氧化酶〔细胞色素( a+ a3 )复合体〕氧化。在呼吸链中从细胞色素 c开始接受电子,各种还原酶都已清楚
实验87 华氏呼吸计 原理 动、植物细胞和组织的许多代谢过程,往往发生气体变化,其变化的速度,可以用测压计法来测定,华氏呼吸计是实验室中常用的测压法。测压法的原理是,在固定体积并保持温度一定的密闭系统中,气体数量上的变化(产生或消失),可以从此系统中气体压力的变化进行测量。气体产生或消失的总量,可以按照气体定律求得。 仪器的构造 国产SKW—2型
导致Val66Met突变,降低BDNF分泌量,从而缩短ALS患者的生存期。利用ALS致病基因FUS R521C敲入小鼠模型进一步证明,BDNF半剂量不足会导致寿命缩短、运动功能障碍加速以及运动神经元死亡加剧。重要的是,使用激动性抗体激活BDNF受体TrkB,能够有效挽救ALS相关表型,在其他ALS小鼠模型中,TrkB激活抗体也显示出优于目前ALS治疗药物利鲁唑的治疗效果。该研究表明BDNF不足可能是ALS进展的关键促成因素,激活BDNF-TrkB通路代表了一种有前景的ALS治疗新策略
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