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抗 PemK 毒素的全局蛋白质组反应。

Global Proteomic Response of Against PemK Toxin.

机构信息

Department of Biotechnology, Alagappa University, Karaikudi, India.

出版信息

Front Cell Infect Microbiol. 2019 May 31;9:172. doi: 10.3389/fcimb.2019.00172. eCollection 2019.

Abstract

Bacterial exotoxins are major causative agents that infect by promoting cell and tissue damages through disabling the invading host immune system. However, the mode of action by which toxins modulate host immune system and lead cell death is still not completely understood. The nematode, has been used as an attractive model host for toxicological studies. In this regard, the present study was undertaken to assess the impact of toxin (PemK) on the host through global proteomics approach. Our proteomic data obtained through LC-MS/MS, subsequent bioinformatics and biochemical analyses revealed that in response to PemK a total of 601 proteins of were differentially regulated in response to PemK. The identified proteins were found to mainly participate in ATP generation, protein synthesis, lipid synthesis, cytoskeleton, heat shock proteins, innate immune defense, stress response, neuron degeneration, and muscle assembly. Current findings suggested that involvement of several regulatory proteins that appear to play a role in various molecular functions in combating PemK toxin-mediated microbial pathogenicity and/or host immunity modulation. The results provided a preliminary view of the physiological and molecular response of a host toward a toxin and provided insight into highly complex host-toxin interactions.

摘要

细菌外毒素是主要的致病因子,通过使入侵宿主的免疫系统失能来促进细胞和组织损伤而感染。然而,毒素调节宿主免疫系统并导致细胞死亡的作用方式仍不完全清楚。线虫已被用作毒理学研究的有吸引力的模型宿主。在这方面,本研究旨在通过蛋白质组学方法评估毒素 (PemK) 对宿主的影响。我们通过 LC-MS/MS 获得的蛋白质组学数据、随后的生物信息学和生化分析表明,针对 PemK,总共 有 601 种蛋白质被 PemK 以不同的方式调节。鉴定出的蛋白质主要参与 ATP 生成、蛋白质合成、脂质合成、细胞骨架、热休克蛋白、先天免疫防御、应激反应、神经元变性和肌肉组装。目前的研究结果表明,涉及几种调节蛋白,这些调节蛋白似乎在对抗 PemK 毒素介导的微生物致病性和/或宿主免疫调节的各种分子功能中发挥作用。这些结果提供了宿主对毒素的生理和分子反应的初步观点,并深入了解了高度复杂的宿主-毒素相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e858/6555269/b184ddf43043/fcimb-09-00172-g0001.jpg

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