Phosphoproteomics Approach to Anaylse Differences of Phosphorylation Induced by Helicobacter Pylori Infection in AGS cells

碩士 === 臺灣大學 === 生物化學暨分子生物學研究所 === 96 === It has been found that Helicobacter pylori infection could result in a variety of gastroduodenal diseases such as gastritis, ulcer, and even gastric cancer. When H. pylori infection occurs, different kinds of host responses such as morphology changes, prolife...

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Bibliographic Details
Main Authors: Li-Chia Yang, 楊禮嘉
Other Authors: 周綠蘋
Format: Others
Language:zh-TW
Published: 2008
Online Access:http://ndltd.ncl.edu.tw/handle/56110472768411066556
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Summary:碩士 === 臺灣大學 === 生物化學暨分子生物學研究所 === 96 === It has been found that Helicobacter pylori infection could result in a variety of gastroduodenal diseases such as gastritis, ulcer, and even gastric cancer. When H. pylori infection occurs, different kinds of host responses such as morphology changes, proliferation, inflammation, and apoptosis would be induced. Because of this significant relationship between H. pylori and gastroduodenal diseases, many researches have focused on the regulation of signal transduction in host cells during H. pylori infection. Due to fast and reversible regulation, signal transduction through protein phosphorylation in host cells can react to stimulation in a real-time fashion. As a result, phosphproteomics tools were used to identify the phosphorylation regulation changes in host cell during H. pylori infection. After phosphoprotein enrichment and LC/MS-MS identification, the phosphorylated proteins specific in H. pylori infected host cells were analysed by the signal transduction database tool. In addition, quantitative technique of mass spectrometry was also used to accurately compare the differences of phosphorylation induced by infection. These identified phosphoproteins involve in cellular growth and proliferation, cell morphology, in-cell and cell-to-cell signaling and apoptosis. According to western blot validation and literature searches, it is found that H. pylori would induce phosphorylation of Akt and glycogen synthase kinase 3b, which might involve in cell proliferation. Besides, morphology changes and inflammation would also be induced through phosphorylation regulations of other proteins. However, the phosphorylation regulations and their physiological roles need to be further validated. This information may help to demonstrate more comprehensive pathogenic mechanisms of H. pylori infection.