URN |
etd-0824110-180422 |
Author |
Chang-Yi Weng |
Author's Email Address |
No Public. |
Statistics |
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Department |
Institute of Biomedical Sciences |
Year |
2009 |
Semester |
2 |
Degree |
Master |
Type of Document |
|
Language |
zh-TW.Big5 Chinese |
Title |
Association between SUMOs and p38 activation during Helicobacter pylori infection |
Date of Defense |
2010-07-27 |
Page Count |
137 |
Keyword |
SUMO
sumoylation
Helicobacter pylori
apoptosis
|
Abstract |
Diverse extracellular stimuli, including ultraviolet light, irradiation, heat shock, proinflammatory cytokines, trigger activation of MAPK pathway through phosphorylation on a TGY motif within the kinase activation loop. Protein MAPK appears to play a major role in apoptosis. It has been causally implicated in sepsis and arthritis. The translational small ubiquitin related modifier (SUMO) modification of proteins has been shown to play multiple functional roles in several cellular processes, including signal transduction, protein targeting, stabilization, transcriptional activation and apoptosis. Our previous study demonstrated that the expression levels of SUMO-1 rnRNA and proteins were enhanced in Helicobacter pylori infected human gastric epithelial cells. The activation of MAPK pathway and cellular apoptosis of AGS cell lines were increased during Helicobacter pylori infection. It was hypothesized that Helicobacter pylori functioning as a biological stress that induced MAPK mediated apoptosis which may be regulated by sumoylation. Results showed that MAPK phosphorylation and cellular apoptosis were enhanced in RFP-SUMOs or GFP-MAPK expressing cells, especially during Helicobacter pylori infection. It was inhibited by pretreatment of MAPK inhibitor. The enhanced phosphorylation and apoptosis were observed during GFP-MAPK overexpression. It’s suggested that MAPK is a target protein for SUMOs. |
Advisory Committee |
Ming-Hong Tai - chair
Hurng-Wern Huang - co-chair
Angela Chen - advisor
|
Files |
indicate not accessible |
Date of Submission |
2010-08-24 |