前期染色体凝集
中文名称
通路描述
在有丝分裂前期，凝缩蛋白 II 复合物的作用使染色体初步凝集。凝缩蛋白 II 复合物的亚基 NCAPD3 结合单甲基化的组蛋白 H4（H4K20me1），从而与染色质结合（Liu et al. 2010）。凝缩蛋白 II 复合物与染色质的结合部分受 RB1 的存在控制（Longworth et al. 2008）。H4K20me1 在有丝分裂起始时积累的两个机制是：首先，SETD8 组蛋白甲基转移酶活性在 G2/M 过渡期达到高峰（Nishioka et al. 2002, Rice et al. 2002, Wu et al. 2010）。其次，CDK1 和 cyclin B1 复合物在有丝分裂开始时磷酸化 PHF8 组蛋白去甲基酶，将其从染色质上移除（Liu et al. 2010）。凝缩蛋白 II 复合物需要被 CDK1:CCNB1 复合物磷酸化，然后再被 PLK1 磷酸化，才能有效地凝集前期染色体（Abe et al. 2011）。
英文描述
Enterobacterial factors antagonize host defense This Reactome event describes mechanisms used by intracellular bacterial pathogens that deploy type III secretion system (T3SS) effectors to inhibit caspase-4 (CASP4)-mediated pyroptosis, a lytic form of cell death triggered during infection. Specifically, Shigella flexneri secretes OspC3, which catalyzes ADP-riboxanation of CASP4, thereby inhibiting its catalytic activity and blocking lipopolysaccharide (LPS)-induced pyroptosis (Kobayashi T et al., 2013; Li Z et al., 2021; Hou Y et al., 2023). Pathogenic Escherichia coli strains secrete the T3SS effector NleF, which directly binds and inhibits CASP4 as well as apoptotic caspases CASP8 and CASP9 (Blasche S et al., 2013). The crystal structure of the NleF:CASP9 complex revealed a novel inhibitory mechanism involving insertion of the NleF carboxy-terminus into the protease active site (Blasche S et al., 2013). Bacterial NleF blocks CASP4 activation in vitro and also inhibits CASP4 during enteropathogenic (EPEC) or enterohemorrhagic (EHEC) infection in epithelial cells (Pallett MA et al., 2017; Song T et al., 2017). During EPEC infection, NleF suppresses CASP4 activity and CASP4-dependent interleukin-18 (IL-18) processing (Pallett MA et al., 2017).
所含基因
15 个基因