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首页> 外文期刊>Biochimica et biophysica acta. Molecular cell research >Histidine-rich protein Hpn from Helicobacter pylori forms amyloid-like fibrils in vitro and inhibits the proliferation of gastric epithelial AGS cells.
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Histidine-rich protein Hpn from Helicobacter pylori forms amyloid-like fibrils in vitro and inhibits the proliferation of gastric epithelial AGS cells.

机译:来自幽门螺杆菌的富含组氨酸的蛋白Hpn在体外形成淀粉样蛋白原纤维,并抑制胃上皮AGS细胞的增殖。

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摘要

Helicobacter pylori causes various gastric diseases, such as gastritis, peptic ulcerations, gastric cancer and mucosa-associated lymphoid tissue lymphoma. Hpn is a histidine-rich protein abundant in this bacterium and forms oligomers in physiologically relevant conditions. In this present study, Hpn oligomers were found to develop amyloid-like fibrils as confirmed by negative stain transition electron microscopy, thioflavin T and Congo red binding assays. The amyloid-like fibrils of Hpn inhibit the proliferation of gastric epithelial AGS cells through cell cycle arrest in the G2/M phase, which may be closely related to the disruption of mitochondrial bioenergetics as reflected by the significant depletion of intracellular ATP levels and the mitochondrial membrane potential. The collective data presented here shed some light on the pathologic mechanisms of H. pylori infections.
机译:幽门螺杆菌引起各种胃疾病,例如胃炎,消化性溃疡,胃癌和与粘膜相关的淋巴组织淋巴瘤。 Hpn是在此细菌中富集的富含组氨酸的蛋白质,并在生理相关条件下形成寡聚物。在本研究中,发现Hpn低聚物会形成淀粉样样原纤维,这可通过负染色过渡电子显微镜,硫代黄素T和刚果红结合测定法得到证实。 Hpn的淀粉样样原纤维通过G2 / M期的细胞周期阻滞抑制胃上皮AGS细胞的增殖,这可能与线粒体生物能学的破坏密切相关,这反映在细胞内ATP水平和线粒体的显着消耗上。膜电位。这里介绍的集体数据为幽门螺杆菌感染的病理机制提供了一些启示。

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