| Project/Area Number |
24790314
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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 |
Pathological medical chemistry
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| Research Institution | Kyoto University |
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Principal Investigator |
ITO Shinji 京都大学, 医学(系)研究科(研究院), 特定助教 (50362512)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | Ｐｅｒｉｐｌａｋｉｎ / 肝臓 / 胆汁鬱滞 / 糖代謝 / Periplakin |
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| Research Abstract |
We sought the functional roles of periplakin in homeostasis. Periplakin-interacting proteins were screened in normal- and cholestatic mouse liver. Several candidates were identified in cholestatic liver. The gene- and protein expression profiles were also examined. The loss of periplakin function influenced on the expressions of several hepatic molecules during cholestasais; however, the difference were highly susceptible to the genetic background and breeding conditions. These results indicate that the roles of periplakin in cholestatic liver might be limited; otherwise, the functional redundancy for periplakin may exist in mouse liver. Interestingly, the fasting blood glucose levels were reproducibly lowered in periplakin-null mice compared to the gender-matched wild-type littermates. Thus, a functional role of periplakin in fasting blood glucose metabolism was suggested.
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