| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
Although the shape of the cell nucleus changes depending on physiological and pathological conditions, its underlying mechanisms remain unclear. We have found that inactive form of Rif, an intracellular protein involved in filopodia formation, induces degradation of the nuclear membrane protein, emerin, and nuclear deformation. In this study, we studied the mechanism of Rif-mediated emerin degradation and its role in pathological conditions. Our results suggest that inactive form of Rif itself is ubiquitinated and degraded, leading to degradation of emerin. We have also found that active form of Rif can suppress mislocalization and degradation of emerin, associated with Hutchinson-Gilford progeria syndrome. We have further shown that Rif is involved in growth and invasion of human lung adenocarcinoma cells.
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