| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
Dysbindin-1 is now widely accepted as a potential schizophrenia susceptibility gene. However, cellular functions of dysbindin-1 are largely unknown. To reveal novel functions of dysbindin-1, we tried to identify a new binding partner. We consulted with the protein interaction database and found cyclin D3 as a possible binding partner for dysbindin-1. Immunoprecipitation analysis revealed that dysbindin-1A preferentially complexes with cyclin D1 among various dysbindin-1 isoforms and D-type cyclins. Dysbindin-1 and cyclin D1 in NIH3T3 cells partially co-localized at the cytosol and the nucleus in a cell cycle progression-dependent manner. Co-expression of dysbindin-1A transferred the nuclear cyclin D1 to the cytosolic fraction in many cells. These results indicate that dysbindin-1 may control the cell cycle progression in concert with cyclin D1.
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