2010 Fiscal Year Final Research Report
The mechanism of epithelial apical membrane domain development and diseases.
| Project/Area Number |
21790307
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tokai University |
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Principal Investigator |
HORIKOSHI Yosuke Tokai University, 医学部, 奨励研究員 (60448678)
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| Project Period (FY) |
2009 – 2010
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| Keywords | 細胞極性 / アピカルドメイン / aPKC-PAR複合体 |
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| Research Abstract |
Excessive productions of free radicals and oxidative stress are implicated in the pathogenesis of cancer and inflammatory bowel diseases. These diseases disturb the apical membrane domains and tissue architectures. However, the molecular mechanisms of oxidative stress-induced cell injuries and the effect of cell polarity remain to be clarified. The treatment of carbon tetrachloride (CCl4), which strongly promotes oxidative stress in rat liver, resulted in the disassembly of cell-cell junctions and also changes the localization of Par3 and aPKC from it to cytosol. Importantly, the Par3-aPKC interaction was inhibited by oxidative stress. Furthermore, phosphorylation level of aPKC Thr410/403 increased and it's regulating kinase, PI3-kinase signaling is activated. These results suggested that oxidative stress inhibit the interaction between Par3 and aPKC and consequently the hepatocyte polarity is disrupted.
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Research Products
(10 results)
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[Journal Article]2011
Author(s)
堀越洋輔、濱田明香、大野茂男、末次志郎
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Journal Title
Cell Structure and Function 36
Pages: 97-102
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