2000 Fiscal Year Final Research Report Summary
A study on cellualr redox regulation in response to cytokine stresses
Project/Area Number |
11671493
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
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Research Institution | KYOTO UNIVERSITY |
Principal Investigator |
YODOI Junji Kyoto University, Institute for Virus Research, Professor, ウイルス研究所, 教授 (80108993)
|
Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Hajime Kyoto University, Institute for Virus Research, Associate Professor, ウイルス研究所, 助教授 (70303914)
|
Project Period (FY) |
1999 – 2000
|
Keywords | redox / thioredoxin / glutaredoxin / cytokine / oxidative stress / cellular signal transduction |
Research Abstract |
Hypercytokinemia is one of the most threatening elements of stress responses against surgical insult, fulminate pancreatitis, trauma, burn, and sepsis. Now it is widely appreciated that reactive oxygen intermediates (ROIs) play critical roles in the pathophysiology of hypercytokinemia. The main aim of our project is to clarify the significance of oxido-reductive (redox) regulation of extra- and intra-cellular signaling transduction in neuronal, immunological, and endocrinological reactions. TRX system and its related molecules are one of key systems to control cellular redox status, as well as the glutathione system. In the intracellular molecular network TRX plays important roles in regulating cellular signaling and gene expressions. Further analysis of the role of TRX in the oxidative stress response and the mechanism of the TRX gene regulation by oxidative stress should help to elucidate how cells link the oxidative stress response to gene regulation. Because ROIs are involved in various diseases including not only inflammatory disease but also degenerative disease, further scrutiny is highly required.
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