PI3K-AKT Network Roles in Infectious Diseases
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- NOGUCHI Masayuki
- Division of Cancer Biology, Institute for Genetic Medicine, Hokkaido University
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- KINOWAKI Keiichi
- Division of Cancer Biology, Institute for Genetic Medicine, Hokkaido University
Bibliographic Information
- Other Title
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- 感染症におけるPI3K-AKTシグナル伝達の意義
- カンセンショウ ニ オケル PI3K AKT シグナル デンタツ ノ イギ
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Abstract
The PI3K-Akt network, which is activated by cytokines or growth factors, mediates intracellular signalsto regulate a variety of cellular responses, including antiapoptosis, proliferation, cell cycling, protein synthesis, glucose metabolism, and telomere activity. Genomic mutations, alterations of the PI3K-Akt regulatorynetwork, underlie such diseases as cancer, glucose intolerance (diabetes mellitus), schizophrenia, and/orautoimmune diseases. In addition to direct tumorigenesis involvement by genetically altering human cancer, the PI3K-Akt network underlies the clinical manifestation of different stages of tumorigenic viral infection, such as latent and chronic infection, and malignant transformation of Epstein-Barr, hepatitis C, hepatitis B, and human immunodeficiency virus (HIV) viruses. We summarize updated knowledge on the PI3K-AKTnetwork underlying different phathological viral and/or bacterial infections. Antiviral activity engenderedby suppressing of PI3K-Akt activity, rather than directly targeting anticancer activity via oncogenes, maythus open up ways to prevent malignant transformation by tumorigenic viral infection.
Journal
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- Kansenshogaku Zasshi
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Kansenshogaku Zasshi 82 (3), 161-167, 2008
The Japanese Association for Infectious Diseases
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Details 詳細情報について
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- CRID
- 1390282680025408896
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- NII Article ID
- 130004331429
- 10021928754
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- NII Book ID
- AN00047715
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- ISSN
- 1884569X
- 03875911
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- NDL BIB ID
- 9525496
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- Data Source
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed