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Regulation of transcription by eukaryotic-like serine-threonine kinases and phosphatases in Gram-positive bacterial pathogens

机译:革兰氏阳性细菌病原体中真核样丝氨酸-苏氨酸激酶和磷酸酶对转录的调控

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摘要

Bacterial eukaryotic-like serine threonine kinases (eSTKs) and serine threonine phosphatases (eSTPs) have emerged as important signaling elements that are indispensable for pathogenesis. Differing considerably from their histidine kinase counterparts, few eSTK genes are encoded within the average bacterial genome, and their targets are pleiotropic in nature instead of exclusive. The growing list of important eSTK/P substrates includes proteins involved in translation, cell division, peptidoglycan synthesis, antibiotic tolerance, resistance to innate immunity and control of virulence factors. Recently it has come to light that eSTK/Ps also directly modulate transcriptional machinery in many microbial pathogens. This novel form of regulation is now emerging as an additional means by which bacteria can alter their transcriptomes in response to host-specific environmental stimuli. Here we focus on the ability of eSTKs and eSTPs in Gram-positive bacterial pathogens to directly modulate transcription, the known mechanistic outcomes of these modifications, and their roles as an added layer of complexity in controlling targeted RNA synthesis to enhance virulence potential.
机译:细菌真核生物样丝氨酸苏氨酸激酶(eSTKs)和丝氨酸苏氨酸磷酸酶(eSTPs)已作为重要的信号转导元件,对于发病机理是必不可少的。与它们的组氨酸激酶对应物有很大不同,在普通细菌基因组中很少编码eSTK基因,并且它们的靶标在本质上是多效的而不是排他的。重要的eSTK / P底物清单不断增加,包括参与翻译,细胞分裂,肽聚糖合成,抗生素耐受性,对先天免疫的抵抗力和毒力因子控制的蛋白质。最近发现,eSTK / Ps还直接调节许多微生物病原体中的转录机制。这种新型的调节形式正在作为一种额外的方式出现,细菌可以通过这种方式响应宿主特定的环境刺激来改变其转录组。在这里,我们重点研究革兰氏阳性细菌病原体中eSTKs和eSTPs直接调节转录的能力,这些修饰的已知机理,以及它们作为控制靶RNA合成以增强毒性潜能的复杂性的附加作用。

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