Recombinant Human Activation-i
nduced TNFR member Ligand/TNFSF18-Recombinant Human Activation-induced TNFR member Ligand/TNFSF18- ￥33
- APExBIO
- 美国
- APE-P1280-005
- 2025年07月09日
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- 详细信息
- 文献和实验
- 技术资料
- 保存条件：
该Recombinant Human Activation-induced TNFR member Ligand/TNFSF18产品的保存方式具体查看产品。
- 保质期：
1年
- 英文名：
Recombinant Human Activation-induced TNFR member Ligand/TNFSF18
- 库存：
100
- 供应商：
艾美捷科技
- CAS号：
无
- 规格：
5ug
Recombinant Human Activation-induced TNFR member Ligand/TNFSF18，Recombinant Human Activation-induced TNFR member Ligand/TNFSF18，Recombinant Human Activation-induced TNFR member Ligand/TNFSF18,Recombinant Human Activation-induced TNFR member Ligand/TNFSF18
Recombinant Human Activation-induced TNFR member Ligand/TNFSF18-Recombinant Human Activation-induced TNFR member Ligand/TNFSF18
产品货号：APE-P1280-005
产品规格：5ug
重组人活化诱导的TNFR成员配体/TNFSF18
Peptides & Proteins|Recombinant Proteins
Recombinant Human Activation-induced TNFR member Ligand/TNFSF18-Recombinant Human Activation-induced TNFR member Ligand/TNFSF18该Recombinant Human Activation-induced TNFR member Ligand/TNFSF18产品的保存方式具体查看产品。
点击：Recombinant Human Activation-induced TNFR member Ligand/TNFSF18-Recombinant Human Activation-induced TNFR member Ligand/TNFSF18查看更详细产品说明，更多应用、储存、价格、货期等信息请垂询艾美捷科技有限公司。更多APExBIO公司特色小分子抑制剂等产品评论，请点击查看艾美捷特色产品中心。
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文献和实验TRAF‐Mediated TNFR‐Family Signaling
. Schwarz, H., Tuckwell, J., and Lotz, M. 1993. A receptor induced by lymphocyte activation (ILA): A new member of the human nerve‐growth‐factor/tumor‐necrosis‐factor receptor family. Gene 134:295‐298
Activation and Expansion of Human Treg Cells
to TCR/CD3 and CD28 for full activation and expansion of human Treg cells. 二、实验试剂 2 ml Dynabeads? Human Treg Expander 2 x 107 beads/ml in phosphate buffered saline (PBS), pH 7.4, w/ 0.1% human serum albumin (HSA). Magnet: Any Dynal MPC Buffer
Genetic Engineering in the Mouse: Tuning TNF/TNFR Expression
research tools for basic biomedical research and for genomic approaches for the development of new therapeutic treatments for human disease. Over the past ten years it has become possible to make essentially any mutation in the mouse by transgenesis
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