2013 Fiscal Year Final Research Report
The functional analysis of the nucleotide-sugar transporter SLC35D1 and SLC35D2 in cartilage using knockout mice model.
| Project/Area Number |
21390428
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kobe Pharmaceutical University (2012-2013)
National Research Institute for Child Health and Development (2009-2011) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
ASAHARA Hiroshi 東京医科歯科大学, 大学院医歯学総合研究科, 教授 (70294460)
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| Project Period (FY) |
2009-04-01 – 2013-03-31
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| Keywords | 糖ヌクレオチド輸送体 / 軟骨疾患 / コンドロイチン硫酸 |
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| Research Abstract |
The chondroitin sulfate (CS) is required for various cartilage functions. The nucleotide-sugar transporter SLC35D1 and SLC35D2 supply substrates to polymerize CS. I analyzed compound mutant mice harboring in SLC35D1 KO and hypomorphic, and SLC35D2 KO mutations. As a result of investigations, I clarified that both transporters play the essential role for CS synthesis of proteoglycans in cartilage, (2) various combinations of mutant alleles of both coding genes induce to step wise reduction of CS producing level in cartilage, (3) the skeletal abnormalities are observed in response to the reduction level of CS synthesis. I also investigated SLC35D1 function using Flox mutant of SLC35d1 mice. I observed critical loss of intestinal functions in adult mice lacking SLC35D1 by inducible gene disruption strategy. The nobel function of SLC35D1 in intestine is useful to survey unidentified leaky-type mutations of SLC35D1 in human, which may survive during perinatal period.
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Research Products
(11 results)
