Dysbindin-1, a schizophrenia-related molecule, interacts with cyclin D1

2014 Fiscal Year Final Research Report

• Project/Area Number: 23590124
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Institute for Developmental Research, Aichi Human Service Center
• Principal Investigator: ITO Hidenori 愛知県心身障害者コロニー発達障害研究所, 神経制御学部, 主任研究員 (40311443)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: 統合失調症 / dysbindin / サイクリン

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.

Free Research Field

神経生物学、生物系薬学