| Project/Area Number |
24790309
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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 | University of Tsukuba |
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Principal Investigator |
SAITO Shoko 筑波大学, 医学医療系, 助教 (70344885)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 核―細胞質間物質輸送 / 細胞がん化 / 核膜孔複合体 / 核外輸送 / CRM1/XPO1 / NF-kB / 核―細胞質間輸送 / 白血病 / XPO1/CRM1 / NXF1/TAP / リボソーム / NESタンパク質 / 核－細胞質間輸送 / エクスポーチン / mRNA |
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| Outline of Final Research Achievements |
To elucidate the relationship between aberrant nuclear-cytoplasmic transport and oncogenesis, we examined cellular functions of fusion proteins, SET-NUP214 and DEK-NUP214. NUP214 is one of the nuclear pore complex components, and critical for efficient nuclear-cytoplasmic export of macromolecules.
We found SET-NUP214 and DEK-NUP214 interact with not only XPO1/CRM1 but also NXF1/TAP preferentially among several nuclear transport receptors. We observed that nuclear accumulation of endogenous proteins harboring NES in cells expressing SET-NUP214 or DEK-NUP214. By contrast, nuclear accumulation of mRNA was not so clear in cells expressing SET-NUP214 or DEK-NUP214. We also observed that endogenous NF-κB complex, whose subcellular localization is regulated in a XPO1-dependent manner, accumulates in nuclei in cells expressing SET-,DEK-NUP214. NF-κB activity was partially suppressed in the presence of SET-,DEK-NUP214.
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