Cover photograph: Proposed model of SubAB activities in cells. Locus for Enterocyte Effacement (LEE)‐negative Shiga‐toxigenic Escherichia coli (STEC)‐produced Subtilase cytotoxin (SubAB) binds to receptors, which are sialic carbohydrates‐modified glycoproteins (e.g., L1CAM, integrin) on the cell surface. After SubAB uptake into cells, it translocates to the Golgi compartment, followed by migration to the ER. In the ER, SubAB specifically cleaves chaperone protein BiP, which activates ER stress sensor protein PERK, followed by phosphorylation of eIF2α This phosphorylation not only inhibits protein synthesis transiently, but also causes formation of stress granules (SG). SubAB‐induced ER stress causes expression of a various transcription factors and apoptosis inducers, which are involved in unfolded protein response, metabolic processes and immune response pathways. In macrophages, SubAB suppresses LPS‐induced NO production through inactivation of NF‐κB. Bak/Bax are conformationally changed by SubAB and oligomerized on mitochondria, with release of cytochrome c from mitochondria and movement to the cytoplasm, followed by activation of apoptotic pathways. Overexpression of Bcl‐xL or PKC activator suppressed SubAB‐induced apoptosis. Microbiol Immunol: 64:657–665. Article link here

中文翻译：

---

发行信息–封面

封面照片：拟议的SubAB细胞活性模型。轨迹为肠抹杀（LEE）阴性志贺毒素的大肠杆菌（STEC）产生的枯草杆菌蛋白酶细胞毒素（SubAB）与受体结合，受体是唾液碳水化合物修饰的细胞表面糖蛋白（例如L1CAM，整联蛋白）。SubAB吸收到细胞中后，它易位到高尔基体区室，然后迁移到ER。在ER中，SubAB特异性裂解伴侣蛋白BiP，后者激活ER应激传感器蛋白PERK，随后eIF2α磷酸化。这种磷酸化不仅瞬时抑制蛋白质合成，而且导致形成应激颗粒（SG）。SubAB诱导的内质网应激导致多种转录因子和细胞凋亡诱导剂的表达，它们参与了未折叠的蛋白质反应，代谢过程和免疫反应途径。在巨噬细胞中，SubAB通过失活NF-κB抑制LPS诱导的NO产生。Subak改变了Bak / Bax的构象，并在线粒体上寡聚，从线粒体释放出细胞色素c并移至细胞质，随后激活了凋亡途径。Bcl-xL或PKC激活剂的过表达抑制了SubAB诱导的细胞凋亡。微生物免疫：64：657–665。文章链接在这里