Elucidation of abnormal epigenetic mechanisms through S-phse of the cell cycle in the psoriatic epidermal keratinocytes

2014 Fiscal Year Final Research Report

• Project/Area Number: 23591617
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• Research Institution: Nagoya University
• Principal Investigator: SUGIURA Kazumitsu 名古屋大学, 医学(系)研究科(研究院), 准教授 (70335032)
• Co-Investigator(Kenkyū-buntansha): MURO Yoshinao 名古屋大学, 大学院医学系研究科, 准教授 (80270990)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: 乾癬 / 表皮角化細胞 / 細胞周期 / エピジェネティクス / LEDGF / RanBP2 / RanGaP1 / トランスジェニックマウス

Outline of Final Research Achievements

We indicated that RanBP2 and RanGAP1 are overexpressed and that the phosphorylation of S53 in MCM2 is significantly upregulated not only in the spinous layers but also in the basal layers of psoriatic epidermis. We also suggest that RanBP2 and RanGAP1 regulate the intracellular localization of LEDGF and phosphorylated Y705 STAT3 via the PI3K/Akt and MAPK /Erk1/2 pathways in our psoriatic model systems of HaCaT cells. These findings suggest that RanBP2 and RanGAP1 may play pivotal roles in the pathogenesis of psoriasis via translocation of LEDGF and phosphorylated Y705 STAT3 into the nucleus in psoriatic KCs Moreover, we created a KC speficif LEDGF transgenic mouse.

Free Research Field

皮膚科学