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Cynomolgus IL9 Protein, hFc Tag
Cynomolgus IL9 Protein, hFc Tag
- 中文名称:
- Cynomolgus IL9 Protein, hFc Tag
- 英文名称:
- Cynomolgus IL9 Protein, hFc Tag
- 品牌:
- AAA Biotech
- 品牌介绍:
- AAA Biotech专注于为全球生命科学研究提供高品质的蛋白质研究工具,核心产品包括经严格验证的抗体、重组蛋白及ELISA试剂盒。
- 货号:
- AAA47560
- 规格:
- 0.01 mg|0.05 mg|0.1 mg|2x0.1 mg|3x0.1 mg
- 保存建议:
- Store at -20 degree C to -80 degree C for 12 months in lyophilized form. After reconstitution, if not intended for use within a month, aliquot and store at -80 degree C (Avoid repeated freezing and thawing). Lyophilized proteins are shipped at ambient temperature.
- 货期:
- 6-8周
- 纯度:
- The purity of the protein is greater than 95% as determined by SDS-PAGE and Coomassie blue staining.
- 产品形式:
- Lyophilized from sterile PBS, pH7.4. Normally 5%-8% trehalose is added as protectants before lyophilization. Please see Certificate of Analysis for specific instructions.
- 免责声明:
- *本产品仅供科研实验使用,不得用于临床诊断。*
- 说明书:
Recombinant Cynomolgus IL9 protein with C-terminal human Fc tag
Interleukin 9, also known as IL-9, is a cytokine (cell signaling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-beta1 to differentiate naive CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and the absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.