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- 详细信息
- 文献和实验
- 技术资料
- 保存条件:
蛋白表达区间:Ala20-Phe152
- 保质期:
See instructions
- 英文名:
标签:N-6His
- 库存:
表达系统:E.coli
- 供应商:
上海经科化学科技有限公司
- 规格:
10ug/50ug/500ug/1mg
| 规格: | 10ug | 产品价格: | ¥840.0 |
|---|---|---|---|
| 规格: | 50ug | 产品价格: | ¥2520.0 |
| 规格: | 500ug | 产品价格: | ¥12320.0 |
| 规格: | 1mg | 产品价格: | ¥17600.0 |
- Always centrifuge tubes before opening.Do not mix by vortex or pipetting.
- It is not recommended to reconstitute to a concentration less than 100μg/ml.
- Dissolve the lyophilized protein in distilled water.
- Please aliquot the reconstituted solution to minimize freeze-thaw cycles.
- The product is shipped at ambient temperature.
- Upon receipt, store it immediately at the temperature listed below.
- Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt.
- Reconstituted protein solution can be stored at 2-8°C for 2-7 days.
- Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months.
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文献和实验Interleukin-3 (IL-3) is a potent growth promoting cytokine. IL-3 can stimulate the proliferation and differentiation of pluripotent hematopoietic stem cells as well as various lineage committed progenitors. IL-3 exerts its biological function through binding to specific cell surface receptors. The amino acid sequences of this protein among different species share relatively low identity and its activity is highly species-specific. IL-3 has also been shown to possess neurotrophic activity, and is thought to be associated with neurologic disorders.
Development of Conditionally Immortalized Epithelial Cell Lines from CF and Non-CF Mice
84) cells or heterologous expression systems (4 -9 ). Epithelial cells from other tissues affected by cystic fibrosis have received relatively little attention, primarily due to the lack of access to appropriate human material. The development of the CF
依赖关系;E2干预24~48小时促进MG-63细胞MT1-MMP蛋白质表达;激光共聚焦显微系统免疫荧光法证实E2促进MT1-MMP蛋白质表达增强,MT1-MMP蛋白质表达于细胞膜和细胞质中。E2对MG-63细胞MMP-2活性无影响。结论:E2可促进MG-63细胞MT1-MMP表达。雌激素不足可减少成骨样细胞MT1-MMP表达,此可能为绝经后OP的骨吸收增强机理之一。Abstract Part One Oberservation of the Differentiation of Human
Xenograft Model of the CF Airway
question. Hindering a firm answer to this question is a lack of animal models that mimic human CF airways disease at the molecular level and cellular levels.
技术资料






