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- 文献和实验
- 技术资料
- 保存条件：
Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 6 months; -20°C, 1 month.
- 库存：
货期：1-2天
- 供应商：
MedChemExpress LLC
- CAS号：
1450881-55-6
- 规格：
10 mM * 1 mL/5 mg/10 mg/25 mg/50 mg
| 规格： | 10 mM * 1 mL | 产品价格： | ￥1320.0 |
|---|---|---|---|
| 规格： | 5 mg | 产品价格： | ￥1200.0 |
| 规格： | 10 mg | 产品价格： | ￥2050.0 |
| 规格： | 25 mg | 产品价格： | ￥4400.0 |
| 规格： | 50 mg | 产品价格： | ￥7400.0 |
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SAR-20347
CAS No. : 1450881-55-6
MCE 国际站：SAR-20347
产品活性：SAR-20347 是 TYK2，JAK1，JAK2 和 JAK3 的抑制剂，其 IC50 值分别为 0.6, 23, 26 和 41 nM。
研究领域：Epigenetics | Protein Tyrosine Kinase/RTK | JAK/STAT Signaling | Stem Cell/Wnt
作用靶点：JAK
In Vitro: When NK-92 cells are stimulated with IL-12, SAR-20347 potently inhibits IL-12-mediated STAT4 phosphorylation, a TYK2-dependent event, with an IC50 of 126 nM. SAR-20347 demonstrates a selectivity of TYK2>JAK1>JAK2>JAK3. Cells without IL-12 in the culture media have no measureable IFN-γ, while cells incubated with IL-12 and SAR-20347 demonstrate dose-dependent inhibition of IFN-γ production. SAR-20347 dose-dependently inhibits the production of secreted embryonic alkaline phosphatase (SEAP) with greatest inhibition occurring with 5 μM of SAR-20347 in these experiments.
In Vivo: 60 mg/kg SAR-20347 inhibits the production of IFN-γ in the serum by 91% compare to vehicle-treated animals, demonstrating that SAR-20347 can inhibit TYK2 signaling in vivo. SAR-20347 treatment significantly reduces IL-17 production as measured by average signal intensity, consistent with the gene expression analysis.
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文献和实验Heterologous SERCA1a Ca2+ -ATPase (sarco-endoplasmic reticulum Ca2+ -adenosine triphosphatase isoform 1a) from rabbit was expressed in yeast Saccharomyces cerevisiae as a fusion protein, with a biotin acceptor domain (BAD) linked to the SERCA
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21 日，北京大学刘颖及陈杰教授团队在 Nature 杂志上发表研究论文 SAR1B senses leucine levels to regulate mTORC1 signalling，该研究发现 SAR1B 是一种保守的亮氨酸感应器，能够调节 mTOR 复合物 1 从而响应细胞内亮氨酸的水平。图 5：来源 Nature6. Nature：肠道炎症影响嗅觉在以往的认知中，嗅觉与大脑、鼻子息息相关。2021 年 7 月 21 日，美国加州诺瓦托巴克老年研究所 Heinrich Jasper 教授
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活性 CBS3 对 DAG 激活的 TRPC3/6 电流同样产生调节作用。 结构显示在 FSGS 疾病中发现的 TRPC6 GOF 点突变都分布于胞内区亚基间相互作用的界面上，有可能破坏了亚基间的相互作用。为了验证此假说，作者们解析了 GOF 突变体的结构，并通过电生理和热稳定性实验发现 GOF 突变体减弱了抑制性 Ca2+ 结合位点（CBS1）的作用，使胞内区结构变得松散，从而打开了阳离子从胞质内空腔向胞质区流出的孔道。 最后作者们解析了 BTDM 以及 SAR7334 与 TRPC6 结合的高分
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