Regulatory mechanism and physiological role of the CDK family member PCTK3

2015 Fiscal Year Final Research Report

• Project/Area Number: 25450131
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Applied biochemistry
• Research Institution: The University of Tokushima
• Principal Investigator: YUASA KEIZO 徳島大学, ソシオテクノサイエンス研究部, 准教授 (70363132)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 情報伝達

Outline of Final Research Achievements

1) The activity of PCTK3 was increased via interaction with cyclin A and phosphorylation at Ser12 by PKA. 2) PCTK3 knockdown HEK293T cells exhibited an increase in cell size and F-actin accumulation at the edges of cell membranes and increased cofilin phosphorylation at Ser3, suggesting that PCTK3 is involved in the regulation of actin reorganization. 3) PCTK3-knockdown HEK293T cells exhibited an increase in cell motility. 4) The activity of focal adhesion kinase 1 (FAK1), which is activated during early cell adhesion, was suppressed by PCTK3, suggesting that PCTK3 might act as a negative regulator of FAK1.

Free Research Field

農学