| Project/Area Number |
24659039
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Kobe Pharmaceutical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
NADANAKA Satomi 神戸薬科大学, 薬学部, 講師 (60378578)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | プロテオグリカン / 糖転移酵素 / 硫酸化糖鎖 / ノックアウトマウス / ガン抑制遺伝子 / ストレス応答 / リン酸化 / 脱リン酸化 / 癌抑制遺伝子 / ゴルジ体 |
|---|
| Research Abstract |
Glycosaminoglycans (GAGs) are components of proteoglycans (PGs), which are abundant on the surfaces of most cells and in extracellular matrices. PGs are known to function as cofactors in a variety of biological processes. Most biological activities of PGs are attributed to the GAG side chains that interact with diverse protein ligands via specific saccharide sequences. EXTL2, a member of the EXT family of tumor suppressors, functions to suppress any GAG biosynthesis that is enhanced by a xylose kinase, and thus lack of EXTL2 causes GAG overproduction and structural changes to GAGs. These poor-quality GAGs have effects on the cell signaling such as HGF-mediated and BMP-mediated signaling, and consequently disturb liver regeneration and blood vessel remodeling. Therefore, the EXTL2-dependent mechanism that regulates GAG biosynthesis might be a "quality control system" for PGs and GAGs produced in the absence of EXTL2 can be closely associated with diseases.
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