2013 Fiscal Year Final Research Report
Analysis of the molecular mechanism of disease based on the functional aberration of aPKC-PAR complex
| Project/Area Number |
23790379
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tottori University (2012-2013)
Tokai University (2011) |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Keywords | 細胞極性 / aPKC-PAR / アピカル膜ドメイン / 酸化ストレス / 管腔構造 |
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| Research Abstract |
Excessive productions of free radicals and oxidative stress are implicated in the pathogenesis of cancer, cirrhosis and inflammatory bowel diseases. However, the effect of oxidative stress on cell polarity or tissue morphology is still unknown.
Here we demonstrated that carbon tetrachloride (CCl4)-induced oxidative stress resulted in the loss of cell polarity in rat liver. Furthermore, the polarity regulating protein complex, aPKC-PAR complex (Par-3-aPKC-Par-6 ternary complex) formation was inhibited by aberrant activation of aPKC through CCl4 treatment. Our findings would contribute to understanding of molecular basis of oxidative stress-induced disease and to the innovation of diagnostic techniques.
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[Journal Article] Localization of aPKC lambda/iota and its interacting protein, Lgl2, is significantly associated with lung adenocarcinoma progression2013
Author(s)
Imamura N, Horikoshi Y, Matsuzaki T, Toriumi K, Kitatani K, Ogura G, Masuda R, Nakamura N, Takekoshi S, Iwazaki M
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Journal Title
Tokai J Exp Clin Med
Volume: 38(4)
Pages: 146-158
Peer Reviewed
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