利什曼原虫巨噬细胞的信号网络通过集成系统生物学破译:数学建模方法。

Systems and Synthetic Biology Pub Date : 2013-12-01 Epub Date: 2013-07-04 DOI:10.1007/s11693-013-9111-9
Milsee Mol, Milind S Patole, Shailza Singh
{"title":"利什曼原虫巨噬细胞的信号网络通过集成系统生物学破译:数学建模方法。","authors":"Milsee Mol,&nbsp;Milind S Patole,&nbsp;Shailza Singh","doi":"10.1007/s11693-013-9111-9","DOIUrl":null,"url":null,"abstract":"<p><p>Network of signaling proteins and functional interaction between the infected cell and the leishmanial parasite, though are not well understood, may be deciphered computationally by reconstructing the immune signaling network. As we all know signaling pathways are well-known abstractions that explain the mechanisms whereby cells respond to signals, collections of pathways form networks, and interactions between pathways in a network, known as cross-talk, enables further complex signaling behaviours. In silico perturbations can help identify sensitive crosstalk points in the network which can be pharmacologically tested. In this study, we have developed a model for immune signaling cascade in leishmaniasis and based upon the interaction analysis obtained through simulation, we have developed a model network, between four signaling pathways i.e., CD14, epidermal growth factor (EGF), tumor necrotic factor (TNF) and PI3 K mediated signaling. Principal component analysis of the signaling network showed that EGF and TNF pathways can be potent pharmacological targets to curb leishmaniasis. The approach is illustrated with a proposed workable model of epidermal growth factor receptor (EGFR) that modulates the immune response. EGFR signaling represents a critical junction between inflammation related signal and potent cell regulation machinery that modulates the expression of cytokines. </p>","PeriodicalId":22161,"journal":{"name":"Systems and Synthetic Biology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11693-013-9111-9","citationCount":"4","resultStr":"{\"title\":\"Signaling networks in Leishmania macrophages deciphered through integrated systems biology: a mathematical modeling approach.\",\"authors\":\"Milsee Mol,&nbsp;Milind S Patole,&nbsp;Shailza Singh\",\"doi\":\"10.1007/s11693-013-9111-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Network of signaling proteins and functional interaction between the infected cell and the leishmanial parasite, though are not well understood, may be deciphered computationally by reconstructing the immune signaling network. As we all know signaling pathways are well-known abstractions that explain the mechanisms whereby cells respond to signals, collections of pathways form networks, and interactions between pathways in a network, known as cross-talk, enables further complex signaling behaviours. In silico perturbations can help identify sensitive crosstalk points in the network which can be pharmacologically tested. In this study, we have developed a model for immune signaling cascade in leishmaniasis and based upon the interaction analysis obtained through simulation, we have developed a model network, between four signaling pathways i.e., CD14, epidermal growth factor (EGF), tumor necrotic factor (TNF) and PI3 K mediated signaling. Principal component analysis of the signaling network showed that EGF and TNF pathways can be potent pharmacological targets to curb leishmaniasis. The approach is illustrated with a proposed workable model of epidermal growth factor receptor (EGFR) that modulates the immune response. EGFR signaling represents a critical junction between inflammation related signal and potent cell regulation machinery that modulates the expression of cytokines. </p>\",\"PeriodicalId\":22161,\"journal\":{\"name\":\"Systems and Synthetic Biology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2013-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1007/s11693-013-9111-9\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Systems and Synthetic Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/s11693-013-9111-9\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2013/7/4 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Systems and Synthetic Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s11693-013-9111-9","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2013/7/4 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 4

摘要

信号蛋白网络和感染细胞与利什曼原虫之间的功能相互作用,虽然不是很清楚,但可以通过重建免疫信号网络来计算破译。众所周知,信号通路是众所周知的抽象,它解释了细胞对信号作出反应的机制,信号通路的集合形成了网络,而网络中信号通路之间的相互作用,即串扰,使进一步复杂的信号行为成为可能。微扰可以帮助识别网络中敏感的串扰点,这些点可以进行药理学测试。在本研究中,我们建立了利什曼病免疫信号级联模型,并基于模拟得到的相互作用分析,我们建立了CD14、表皮生长因子(EGF)、肿瘤坏死因子(TNF)和pi3k介导的信号通路之间的模型网络。信号网络的主成分分析表明,EGF和TNF通路可能是抑制利什曼病的有效药理靶点。该方法是用一个可行的模型的表皮生长因子受体(EGFR),调节免疫反应说明。EGFR信号是炎症相关信号和调节细胞因子表达的有效细胞调节机制之间的关键连接。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Signaling networks in Leishmania macrophages deciphered through integrated systems biology: a mathematical modeling approach.

Signaling networks in Leishmania macrophages deciphered through integrated systems biology: a mathematical modeling approach.

Signaling networks in Leishmania macrophages deciphered through integrated systems biology: a mathematical modeling approach.

Signaling networks in Leishmania macrophages deciphered through integrated systems biology: a mathematical modeling approach.

Network of signaling proteins and functional interaction between the infected cell and the leishmanial parasite, though are not well understood, may be deciphered computationally by reconstructing the immune signaling network. As we all know signaling pathways are well-known abstractions that explain the mechanisms whereby cells respond to signals, collections of pathways form networks, and interactions between pathways in a network, known as cross-talk, enables further complex signaling behaviours. In silico perturbations can help identify sensitive crosstalk points in the network which can be pharmacologically tested. In this study, we have developed a model for immune signaling cascade in leishmaniasis and based upon the interaction analysis obtained through simulation, we have developed a model network, between four signaling pathways i.e., CD14, epidermal growth factor (EGF), tumor necrotic factor (TNF) and PI3 K mediated signaling. Principal component analysis of the signaling network showed that EGF and TNF pathways can be potent pharmacological targets to curb leishmaniasis. The approach is illustrated with a proposed workable model of epidermal growth factor receptor (EGFR) that modulates the immune response. EGFR signaling represents a critical junction between inflammation related signal and potent cell regulation machinery that modulates the expression of cytokines.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信