| Project/Area Number |
23792128
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional basic dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 味覚 / 甘味受容体 / 味覚修飾物質 / グルマリン / ギムネマ酸 / ミラクリン |
|---|
| Research Abstract |
Gymnemic acid (GA) and gurmarin (Gur) are known as selective inhibitors for sweet taste responses in mammals. To clarify the mechanisms of sweet-suppressing effects, we examined potential effects of these inhibitors on HEK293 cell responses heterologously expressed T1r2+T1r3. The results showed that similar to previous studies in humans and mice, GA and Gur inhibited the [Ca2+]i responses of HEK293 cells expressing human and mouse T1r2+T1r3 to various sweeteners and these effects were inhibited by γ- and β-CD, respectevely. We examined the responses of mouse/human chimeras of T1r2 and T1r3 to identify the interaction sites for GA and Gur. Our results suggest that the main target for GA’s action is transmembrane region of human T1r3 and Gur interacts with amino terminal region of mouse T1r3. Our mutation analysis indicate that the molecular basis for strain-specific sensitivity to Gur depends on a site within amino terminal region of mouse T1r2. In our models, GA is predicted to dock to a binding pocket within the transmembrane region of human T1r3 and Gur docks with amino terminal regions of mouse T1r2 and T1r3
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