EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72932_C
酪氨酸激酶抑制剂；抑制EGFR、HER2、JAK2、JAK3和STAT5a/b
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总览
AG-490是酪氨酸激酶小分子抑制剂tyrphostin家族的成员，可抑制包括EGFR （Gazit et al.）、HER2 （Gazit et al.）、JAK2 （Burger et al.）、JAK3 （Brown et al.）和STAT5a/b （Wang et al.）在内的多种酪氨酸激酶，IC₅₀值分别为0.1、13.5、11和12 μM。AG-490不抑制LCK、LYN、BTK、SYK或SRC酪氨酸激酶（Meydan et al.）。
分化
·和LIF和BMP4一起，诱导小鼠（OG2）胚胎干细胞分化（Chen et al.）。
癌症研究
·通过抑制JAK2，诱导程序性细胞死亡，阻断急性淋巴细胞白血病前B细胞的生长（Meydan et al.）。
·抑制宫颈癌细胞系的增殖（Soto-Cruz et al.）。
·抑制 STAT3 磷酸化，并诱导 β-catenin 向结肠癌细胞系 SW480 的胞质转移（Kawada et al.）。
·通过抑制JAK2诱导GL15胶质母细胞瘤细胞的S期阻滞（Sciaccaluga et al.）。
·抑制EGF依赖性NIH3T3细胞系的增殖（Gazit et al.）。
·阻断IL-2诱导的胸腺嘧啶在T细胞系中的结合（Wang et al.）。
细胞类型
癌细胞及细胞系，白血病/淋巴瘤细胞，多能干细胞，T 细胞
种属
人，小鼠，非人灵长类，其他物种，大鼠
应用
分化
研究领域
癌症，干细胞生物学
CAS 编号
133550-30-8
化学式
C₁₇H₁₄N₂O₃
纯度
≥98%
通路
JAK/STAT，酪氨酸激酶
靶点
EGFR，HER2，JAK2，JAK3，STAT5
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (2)
文献 (9)
JAK3, STAT, and MAPK signaling pathways as novel molecular targets for the tyrphostin AG-490 regulation of IL-2-mediated T cell response.
Journal of immunology (Baltimore,Md. : 1950) 1999 APR
Abstract
AG-490 is a member of the tyrphostin family of tyrosine kinase inhibitors. While AG-490 has been considered to be a Janus kinase (JAK)2-specific inhibitor,these conclusions were primarily drawn from acute lymphoblastic leukemia cells that lack readily detectable levels of JAK3. In the present study,evidence is provided that clearly demonstrates AG-490 potently suppresses IL-2-induced T cell proliferation,a non-JAK2-dependent signal,in a dose-dependent manner in T cell lines D10 and CTLL-2. AG-490 blocked JAK3 activation and phosphorylation of its downstream counterpart substrates,STATs. Inhibition of JAK3 by AG-490 also compromised the Shc/Ras/Raf/mitogen-activated protein kinase (MAPK) signaling pathways as measured by phosphorylation of Shc and extracellular signal-related kinase 1 and 2 (ERK1/2). AG-490 effectively inhibited tyrosine phosphorylation and DNA binding activities of several transcription factors including STAT1,-3,-5a,and -5b and activating protein-1 (AP-1) as judged by Western blot analysis and electrophoretic mobility shift assay. These data suggest that AG-490 is a potent inhibitor of the JAK3/STAT,JAK3/AP-1,and JAK3/MAPK pathways and their cellular consequences. Taken together,these findings support the notion that AG-490 possesses previously unrecognized clinical potential as an immunotherapeutic drug due to its inhibitory effects on T cell-derived signaling pathways.
Naphthyl ketones: a new class of Janus kinase 3 inhibitors.
Bioorganic & medicinal chemistry letters 2000 MAR
Abstract
Potent inhibition of Janus kinase 3 was found for a series of naphthyl(beta-aminoethyl)ketones (e.g. 7,pIC50 = 7.1+/-0.3). Further studies indicated that these compounds fragment in less than 1 h by retro-Michael reaction in the Jak3 in vitro ELISA assay procedure. The breakdown product of 7,2-naphthylvinyl ketone (22,pIC50 = 6.8+/-0.3) showed very similar inhibitory activity to 7. Compounds 7 (in neutral buffer) and 22 will be useful pharmacological tools for the investigation of the Janus tyrosine kinase Jak3.
Signal transducers and activators of transcription 3 activation is involved in nuclear accumulation of beta-catenin in colorectal cancer.
Cancer research 2006
Abstract
Nuclear accumulation of beta-catenin is a key event for the development of colorectal cancer. Little is known,however,about the mechanisms underlying translocation of beta-catenin from the cytoplasm or the membrane to the nucleus. The present study examined whether signal transducers and activators of transcription 3 (STAT3) activation is involved in the nuclear accumulation of beta-catenin in colorectal cancer cells. Of the 90 primary colorectal cancer tissues,40 (44.4%) were positive for nuclear staining of p-STAT3 and 63 (70.0%) were positive for nuclear staining of beta-catenin. The nuclear staining of both p-STAT3 and beta-catenin were observed predominantly in the periphery of the cancer tissues. Importantly,of the 40 tumors with p-STAT3 nuclear staining,37 (92.5%) were also positive for nuclear beta-catenin staining and there was a significant correlation between p-STAT3 and beta-catenin nuclear staining (P textless 0.01). Coexpression of nuclear p-STAT3 and beta-catenin was associated with lower patient survival (P textless 0.01). In an in vitro study using a human colon cancer cell line,SW480,inhibition of STAT3 by dominant negative STAT3 or the Janus kinase inhibitor,AG490,induced translocation of beta-catenin from the nucleus to the cytoplasm or membrane. Luciferase assays revealed that STAT3 inhibition resulted in significant suppression of beta-catenin/T-cell factor transcription in association with significant inhibition of cell proliferation (P textless 0.05). These findings suggest that in colorectal cancer,STAT3 activation is involved in the nuclear accumulation of beta-catenin,resulting in poor patient survival.
更多信息
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
|---|---|
| Cas Number | 133550-30-8 |
| Chemical Formula | C₁₇H₁₄N₂O₃ |
| 纯度 | ≥ 98% |
| Target | EGFR, HER2, JAK2, JAK3, STAT5 |
| Pathway | JAK/STAT, Tyrosine Kinase |
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