2015 Fiscal Year Final Research Report
Dysregulation of Sulfated Glycosaminoglycan Biosynthesis is Implicated in Inflammatory Response
| Project/Area Number |
25460080
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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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) |
Kitagawa Hiroyuki 神戸薬科大学, 薬学部, 教授 (40221915)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | proteoglycan / glycosaminoglycan |
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| Outline of Final Research Achievements |
GAGs (glycosaminoglycans) are abundant on the surfaces of most cells and in extracellular matrices as components of PGs (proteoglycans). PGs play important roles in homoeostasis at the cellular and tissue level because they function as cofactors in a variety of biological processes, including cell growth, and cell differentiation. These functions of PGs are mediated by interactions between GAG chains and bioactive proteins. In addition, diverse protein ligands recognize the specific saccharide sequences of the GAG side chains. Thus abnormal GAG biosynthesis causes disordered cellular function and various disease conditions. EXTL2 (exostosin-like 2) is one of a regulator to regulate in vivo GAG biosynthesis. Thus, loss of EXTL2 causes a change in amount and structure of GAGs, and the resulting aberrant GAGs are linked to pathological conditions. In this study, we have demonstrated that abnormal GAGs produced in the absence of EXTL2 induce inflammatory response and how they do so.
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| Free Research Field |
glycobiology
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