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The role of TORC signal on impaired glucose tolerance and cloning the new protein binding with TORC.

The role of TORC signal on impaired glucose tolerance and cloning the new protein binding with TORC.
TORC 信号对葡萄糖耐量受损的作用以及克隆与 TORC 结合的新蛋白。
批准号:
20591050
负责人:
SAKODA Hideyuki
金额:
$3.08万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2008
资助国家:
日本
项目状态:
已结题
起止时间:
2008 至 2010

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中文摘要
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英文摘要
Excess nutrient intake leads to activation of mTORC1 and mTORC1 inhibits insulin signal transduction, such that activation of mTOR signaling may lead to insulin resistance and even diabetes mellitus. In the case of insulin action, mTORC1 and mTORC2 have contradictory effects on insulin signaling. Conversely, mTOR also activates Akt, a key molecule in the actions of insulin. Thus, we consider it essential to perform these studies focusing on alterations in the total LST8 amount as well as changes in mTORC1 and mTORC2 to elucidate the pathogenesis of various disorders including cancer and the metabolic syndrome.
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LST8 level controls basal p70 S6 kinase and Akt phosphorylations, and mTORC1 and mTORC2 negatively regulate each other by competing for association with LST8.
LST8 水平控制基础 p70 S6 激酶和 Akt 磷酸化,mTORC1 和 mTORC2 通过与 LST8 竞争关联而相互负向调节。
DOI: 10.1016/j.orcp.2011.10.002
发表时间: 2012
期刊: Obesity Research and Clinical Practice
影响因子: 4.3
作者: [Kikuchi T, Zhang J, Sakoda H, Koketsu Y, Fujishiro M, Kushiyama A, Nakatsu Y, Kamata H, Inoki K, Takahashi S, Kurihara H, Hideki K, Oka Y, Asano T]
通讯作者: Asano T
Paraquat-induced oxidative stress represses PI 3-kinase activities leading to impaired glucose uptake in 3T3-L1 adipocytes.
百草枯诱导的氧化应激会抑制 PI 3 激酶活性,导致 3T3-L1 脂肪细胞的葡萄糖摄取受损。
DOI: --
发表时间: 2010
期刊: J Biol Chem. 285(27)
影响因子: --
作者: [Nakatsu Y, Sakoda H, Kushiyama A, Ono H, Fujishiro M, Horike N, Yoneda M, Ohno H, Kamata H, Tahara H, Isobe T, Nishimura F, Katagiri H, Oka Y, Fukushima T, Takahashi SI, Kurihara H, Uchida T, Asano T., Shibata M.; Hakuno F.; Yamanaka D.; Okajima H.; Fukushima T.; Hasegawa T.; Ogata T.; Toyoshima Y.; Chida K.; Kimura K.; Sakoda H.; Takenaka A.; Asano,T ; Takahashi S.I.]
通讯作者: Shibata M.; Hakuno F.; Yamanaka D.; Okajima H.; Fukushima T.; Hasegawa T.; Ogata T.; Toyoshima Y.; Chida K.; Kimura K.; Sakoda H.; Takenaka A.; Asano,T ; Takahashi S.I.
Pin1 associates with and induces translocation of CRT C2 to the cytosol, thereby suppressing CRE transcriptional activity
Pin1 与 CRT C2 结合并诱导其易位至胞质溶胶,从而抑制 CRE 转录活性
DOI: --
发表时间: 2010
期刊: J Biol Chem
影响因子: 4.8
作者: [Nakatsu Y, sakoda h, et.al]
通讯作者: et.al
DOI: 10.1016/j.diabres.2010.10.008
发表时间: 2011-02
期刊: Diabetes research and clinical practice
影响因子: 5.1
作者: [H. Sakoda;S. Ito;H. Kanda;M. Fujishiro;J. Osuga;K. Tsukamoto;K. Ueki;T. Kadowaki]
通讯作者: H. Sakoda;S. Ito;H. Kanda;M. Fujishiro;J. Osuga;K. Tsukamoto;K. Ueki;T. Kadowaki
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