GALNT3 functions in phosphate homeostasis and bone biology

• Project/Area Number: 21791404
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Single-year Grants
• Research Field: Orthopaedic surgery
• Research Institution: Nagasaki University
• Principal Investigator: YOSHIDA CarolinaAndrea Nagasaki University, 大学院・医歯薬総合研究科, 助教 (50437828)
• Project Period (FY): 2009 – 2010
• Project Status: Completed (Fiscal Year 2010)
• Budget Amount: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000); Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000); Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
• Keywords: Galnt3 / 骨 / リン代謝 / 骨格 / 骨代謝

Research Abstract

Loss of function mutations in the GALNT3 gene result in under-glycosylation and subsequent proteolysis of FGF23, leading to hype rostosis-hype rphosphatemi a syndrome or tumoral calcinosis. Using Galnt3 null (^<-/->) mice, we corroborated the roles of GALNT3 in the maintenance of active FGF23, thus in Pi homeostasis and we analyzed its functions in bone and testis biology. We found that Galnt3' mice had increased bone volume and a trabecular bone with cartilage inclusions, despite the facts that osteoblast differentiation and osteoclast activity were normal. GALNT3 is also important for sperm production and maturation, as evidenced by the apoptosis seen in the epydimis of the Galnt3^<-/-> mice.

Research Products

• [Journal Article] Akt regulates skeletal development through GSK3, mTOR, and FoxOs (2009)
  • Author(s): O Rokutanda S, Fujita T, Kanatani N, Yoshida CA, Komori H, Liu W, Mizuno A, Komori T
  • Journal Title: Dev Biol Vol.328, No.1 Pages: 78-93
  • Peer Reviewed
• [Journal Article] Akt regulates skeletal development through GSK3, mTOR, and FoxOs. (2009)
  • Author(s): S.Rokutanda
  • Journal Title: Dev Biol 328 Pages: 78-93
  • Peer Reviewed