Role of INTS6 in the adipose differentiation
Role of INTS6 in the adipose differentiation
批准号:
24659445
负责人:
ASANO Tomoichiro
金额:
$2.41万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Challenging Exploratory Research
财政年份:
2012
资助国家:
日本
项目状态:
已结题
起止时间:
2012-04-01 至 2014-03-31
中文摘要
我们发现,在3T3-L1细胞中,整合子复合体的亚基fints6和IntS11的表达水平在细胞达到ed汇合并分化为脂肪细胞时升高,而在分化完成后则降至基础水平。利用sirna抑制3t3 - l1前脂肪细胞中IntS6或IntS11的表达可显著抑制成熟脂肪细胞的分化。这些发现表明,在脂肪分化过程中,整合子复合体亚基的表达增加是不可或缺的。虽然需要进一步的研究来阐明其潜在的机制,但U1, U2小核rna的加工可能参与了细胞分化的步骤。
英文摘要
We demonstrated that expression levels ofIntS6 and IntS11, subunits ofthe Integrator complex, were increased in 3T3-L1 cells in the period when the cells reach edconfluenceand differentiated into adipocytes, while being reduced tobasal levels after the completion ofdifferentiation. Suppre ssion of IntS6 or IntS11 expression using siRNAs in3T3-L1 pre-adipocytes markedly inhibited differentiation into mature adipocytes. These findings demonstrate that increased expression of Integrator complex subunits is an indispensable event in adipose differentiation. Although further study is necessary to elucidate the underlying mechanism, the processing of U1, U2 small nuclear RNAs may be involved in cell differentiation steps.
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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
脂肪酸合成酵素におけるPin1の作用
Pin1 对脂肪酸合酶的作用
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[山本屋武, 中津祐介, 松永泰花, 新城尊徳, 西村英紀, 迫田秀之, 櫛山暁史, 鎌田英明, 内田隆史, 浅野知一郎]
通讯作者:
浅野知一郎
プロリン異性化酵素Pin1はAMPKとPPARαを制御して脂質代謝に関与する
脯氨酸异构酶 Pin1 通过调节 AMPK 和 PPARα 参与脂质代谢
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[中津祐介, 大久保博史, 大谷裕一郎, 松永泰花, 山本屋武, 藤城緑, 鎌田英明, 内田隆史, 浅野知一郎]
通讯作者:
浅野知一郎
DPP4阻害薬SK-0403はマクロファージ共培養系における脂肪細胞の炎症遺伝子の発現を抑制する
DPP4抑制剂SK-0403抑制巨噬细胞共培养系统中脂肪细胞炎症基因的表达
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[新城尊徳, 岩下未咲, 中津祐介, 迫田秀之, 藤城緑, 櫛山暁史, 菊池貴子, 西村英紀, 浅野知一郎]
通讯作者:
浅野知一郎
キサンチンオキシダーゼ阻害剤による動脈硬化予防の可能性
黄嘌呤氧化酶抑制剂预防动脉硬化的可能性
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[Xu M, Iwasaki T, Shimokawa N, Sajdel- Sulkowska EM, Koibuchi N., 浅野 知一郎]
通讯作者:
浅野 知一郎
共 51 条
Elucidation of molecular mechanism underlying insulin resistane and inflammation
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批准号:23390242
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$5.16万
-
财政年份:2011
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负责人:ASANO Tomoichiro
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依托单位:
Elucidation of the role of Pin1 on the adipose differentiation
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批准号:22659175
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项目类别:Grant-in-Aid for Challenging Exploratory Research
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资助金额:$2.07万
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财政年份:2010
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负责人:ASANO Tomoichiro
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依托单位:
Elucidation of the molecular mechanisms underlying insulin resistance and metabolic disorders using a proteomics technology
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批准号:20390258
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$12.23万
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财政年份:2008
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负责人:ASANO Tomoichiro
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依托单位:
Elucidation of the molecular mechanisms underlying metabolic disorders using protemomics analysis
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批准号:18390271
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$11.14万
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财政年份:2006
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负责人:ASANO Tomoichiro
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依托单位:
Elucidation of the molecular mechanisms underlying insulin and exercise-induced effects on metabolism and vascular cells
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批准号:16390262
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$9.22万
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财政年份:2004
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负责人:ASANO Tomoichiro
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依托单位:
Molecular mechanisms of insulin-and exercise-induced glucose uptake
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批准号:14370334
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$9.6万
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财政年份:2002
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负责人:ASANO Tomoichiro
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依托单位:
Molecular mechanism underlying the GLUT4 translocation and its abnormality in diabetes mellitus
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批准号:12470224
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$10.43万
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财政年份:2000
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负责人:ASANO Tomoichiro
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依托单位:
The role of PI 3-kinase on insulin action and its alteration in diabetic condition
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批准号:09470214
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$8.19万
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财政年份:1997
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负责人:ASANO Tomoichiro
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依托单位:
海外基金