Hesperadin is an inhibitor of chromosome alignment and segregation. Hesperadin causes this phenotype by inhibiting the function of the mitotic kinase Aurora B. Mammalian cells treated with Hesperadin enter anaphase in the presence of numerous monooriented chromosomes, many of which may have both sister kinetochores attached to one spindle pole (syntelic attachment). Hesperadin also causes cells arrested by taxol or monastrol to enter anaphase within <1 h, whereas cells in nocodazole stay arrested for 3-5 h[3]. Hesperadin, an inhibitor of human Aurora B, prevented the phosphorylation of substrate with IC(50) of 40 nM. Hesperadin blocked nuclear division and cytokinesis but not other aspects of the cell cycle. Hesperadin provides neuroprotection against ICH (intracerebral hemorrhage) by inhibiting the MST4/AKT signaling pathway[4]. Hesperadin induces delayed transition from metaphase to anaphase, and early exit from mitosis after chromosome segregation. In addition, micronuclei were observed frequently and lagging chromosomes, caused by the delay and failure of sister chromatid separation, were observed at anaphase and telophase in Hesperadin-treated BY-2 cells[5]. Hesperadin inhibits multiple human clinical isolates of influenza A and B viruses with single to submicromolar efficacy, including oseltamivir-resistant strains. Mechanistic studies revealed that hesperadin inhibits the early stage of viral replication by delaying the nuclear entry of viral ribonucleoprotein complex, thereby inhibiting viral RNA transcription and translation as well as viral protein synthesis. Moreover, a combination of hesperadin with oseltamivir shows synergistic antiviral activity[6].
Hesperadin 细胞研究
细胞系
浓度
检测类型
检测时间
活动说明
数据源
HepG2 cells
Cytotoxicity assay
48 h
Cytotoxicity against human HepG2 cells after 48 hrs by MTT assay, TC50=0.2 μM
搜索
