Anisomycin-Flagecidin_天然产物-MedChemExpress LLC

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产品简介 品牌 MedChemExpress (MCE) 货号 HY-18982 规格 10 mM * 1 mL ; 10 mg ; 50 mg ; 100 mg 供货周期 现货 应用领域 生物产业     Anisomycin是一种有效的蛋白质合成抑制剂，它通过抑制肽基转移酶或80S核糖体系统干扰蛋白质和DNA合成。
详细介绍 Anisomycin

产品活性：Anisomycin是一种有效的蛋白质合成抑制剂，它通过抑制肽基转移酶或80S核糖体系统干扰蛋白质和DNA合成。

研究领域：Cell Cycle/DNA Damage

作用靶点：DNA/RNA Synthesis

In Vitro: To examine whether JNK has a core role in colistin-induced neurotoxicity in PC-12 cells, an SP600125 (a highly selective inhibitor of JNK) and Anisomycin (a potent activator) are used in this study. In order to select an appropriate concentration, PC-12 cells are treated with a range of SP600125 (0-80 μM) and Anisomycin (0-20 μM) respectively for 24 h. The results show that the cells viability significantly decreases by SP600125 treatment in a concentration-dependent manner, observed at the concentrations greater than 20 μM (pIn Vivo: Disruption of TNFRp55/p75 attenuates Anisomycin-induced ventricular functional improvements. Anisomycin results in an improvement in left ventricular developed pressure (LVDP), which disappears in animals with disruption of TNFR p55/p75. In addition, the Anisomycin-induced improvement in LVEDP in wild-type animals is eliminated by deletion of TNFR p55/p75. Likewise, disruption of TNFR p55/p75 abrogates the recovery of rate pressure product (RPP) elicited by pretreatment of Anisomycin. TNFR p55/p75-/- mice without Anisomycin treatment do not show differences in cardiac functional recovery compared with the control wild-type mice. There are no significant differences in heart rate between wild-type and TNFR p55/p75-deficient mice. To see whether Nox2 is involved in Anisomycin-induced myocardial protection, Nox2-deficient mice are treated with Anisomycin. The improvement in the LVEDP in Anisomycin-treated mice is eliminated in Nox2-/- mice compared with wild-type mice. In addition, recovery of RPP in wild-type mice treated with Anisomycin is mitigated in Nox2-/- mice. Nox2-/- mice without Anisomycin treatment do not show the difference in cardiac functional recovery compared with wild-type control mice.

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