2012 Fiscal Year Final Research Report
Disruption of transcription network of cellular genes by human T-cell leukemia virus type-1.
| Project/Area Number |
22501000
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Carcinogenesis
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| Research Institution | Tokushima Bunri University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2012
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| Keywords | ウイルス / HTLV-1 / 転写制御 / HBZ / 発がん / オートファジー / 細胞死 |
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| Research Abstract |
Human T-cell leukemia virus type-1 (HTLV-1) infection causes adult T-cell leukemia (ATL). Modulation of the transcriptional control of cellular genes by HTLV-1 is thought to be associated with the development of ATL. The viral protein HTLV-1 basic leucine-zipper factor (HBZ) has been shown to dysregulate the activity of cellular transcription factors. We evidence that HBZ reduced both IRF-1 DNA-binding activity and stability via a proteasome-dependent pathway. In addition, IRF-1-mediated apoptosis is significantly reduced by ectopic production of the HBZ. Also, we demonstrate that HBZ is exported from the nucleus to the cytoplasm, where it activates the mTOR signaling pathway through an association with growth arrest and DNA damage gene 34 (GADD34). Starvation-induced autophagy is significantly suppressed by the overexpression of HBZ.
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[Journal Article] Protein inhibitor of activated STAT, PIASy regulates alpha-smooth muscle actin expression by interacting with E12 inmesangial cells.2012
Author(s)
Kazuo Torikoshi, Hideharu Abe, Takeshi Matsubara, Takahiro Hirano, Takayuki Ohshima, Taichi Murakami, Makoto Araki, Akira Mima, Noriyuki Iehara, Atsushi Fukatsu, Toru Kita, Hideyuki Arai, and Toshio Doi.
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Journal Title
PLoS One
Volume: 7
Pages: e41186-41199
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