分享产品介绍 评论(0)
宿主来源
Rat抗原名称
CD25分子别名
Interleukin-2 receptor subunit alpha; IL-2 receptor subunit alpha; IL-2-RA; IL-2R subunit alpha; IL2-RA; p55; Il2r; Il2ra细胞定位
MembraneAccession
P01590克隆号
PC-61.5.3抗体类型
Recombinant mAb抗体同种型
IgG1,λ同型对照
Invivo rat IgG1 Isotype control, anti-trinitrophenol反应种属 ?
Ms纯化方式
Protein G浓度
5 mg/ml纯度
>95%(Determined by SDS-PAGE)内毒素含量
<1EU/mg标记
Unconjugated性状
Liquid缓冲体系
PBS pH7.4, containing no preservative
储存条件
2 to 8 °C for 2 weeks under sterile conditions;
-20 °C for 3 months under sterile conditions;
-80 °C for 24 months under sterile conditions.
Please avoid repeated freeze-thaw cycles.应用
in vivo regulatory T cell depletion
ELISA
WB
稀释度
应用 稀释度 推荐种属 WB 1:1000 Ms
CD25, also known as the interleukin-2 receptor alpha chain (IL2RA), is a type I transmembrane glycoprotein that plays a crucial role in the immune system. It is primarily expressed on the surface of activated T cells and regulatory T cells (Tregs). CD25 is a key component of the high-affinity IL-2 receptor complex, which also includes the IL-2 receptor beta and gamma chains. By itself, CD25 can bind IL-2 with low affinity, but when combined with the beta and gamma chains, it forms a high-affinity receptor that initiates intracellular signaling pathways such as MAPK and JAK/STAT. This receptor complex is essential for the proliferation and activation of T cells, as well as the regulation of immune tolerance by controlling the activity of Tregs. Mutations in the IL2RA gene can lead to deficiencies in IL-2 receptor function, highlighting its importance in maintaining immune homeostasis.
验证数据
Tregs depletion efficacy of S0B7020 in MC38 tumor bearing C57 mice.
免疫印迹
WB result of Invivo Anti-Mouse CD25 (IL-2Rα) Recombinant mAb
Primary antibody: Invivo Anti-Mouse CD25 (IL-2Rα) Recombinant mAb at 1/1000 dilution
Lane 1: IL-2R alpha/CD25 His Tag Protein, Human 1 µg
Lane 2: IL-2R alpha/CD25 His Tag Protein, Mouse 1 µg
Secondary antibody: Goat Anti-rat IgG, (H+L), HRP conjugated at 1/10000 dilution
Predicted MW: 31 kDa
Observed MW: 40-55 kDa
评论(0)