Regulation of cellular growth and differentiation by novel kinase like proteins, TRB family

新型激酶样蛋白 TRB 家族对细胞生长和分化的调节

基本信息

  • 批准号:
    18590067
  • 负责人:
  • 金额:
    $ 2.57万
  • 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:
    2006
  • 资助国家:
    日本
  • 起止时间:
    2006 至 2007
  • 项目状态:
    已结题

项目摘要

We recently found that a novel pseudokinase TRB3 was induced by endoplasmic reticulum (ER) stress and regulated the ER stress-inducible apoptosis. It was recently reported that TRB3 was highly expressed in some kind of cancers. Then we examined the function of TRB3 in the cell proliferation from the viewpoint of the cell cycle. The expression level of ectopic CDC25A, one of the cell cycle associated phosphatases, was down-regulated by TRB3 in HeLa cells. On the other hand, endogenous CDC25A level was increased when TRB3 was knockdowned by using the RNAi method. We have observed that TRB3 expressed in a cell cycle dependent manner and this expression pattern was reversely correlated with that of CDC25A at the G2/M phase. When we examined the effect of TRB3 knockdown on the cell cycle, its progression was delayed at the G2/M phase and the down-regulation of CDC25A at the M/G1 phase was significantly suppressed. These results suggest that TRB3 is a modulator of cell cycle progression at t … More he G2/M phase and that the inhibition of CDC25A expression will be one of the targets of TRB3.Next, the influence on the cell differentiation was examined. When we had examined the expression level of the endogenous TRB3 in the adipocyte differentiation process using a mouse preadipocyte cell line, 3T3-L1 cell, its expression have temporarily decreased at the early stage, and then have gradually increased according to the cell differentiation at mRNA and protein level. This expression profile was closely related to the appearance of the stress-inducible transcription factor CHOP10/gadd153. When TRB3 was over-expressed in 3T3-L1 cells, the gross amount of intracellular triglyceride and the mRNA expression level of the downstream targets of PPARγ, which is one of the mastering regulator of adipocyte differentiation. On the other hand, when TRB3 mRNA level was impaired by shRNA method, the adipocyte differentiation was potently obstructed. Moreover, TRB3 and PPARγ were associated each other in the cells, and the adipocyte differentiation induced by PPARγ overexpression was strongly suppressed by the ectopic expression of TRB3. It was shown that TRB3 regulates the adipocyte differentiation by negatively controlling the transcriptional activity of PPARγ. Less
我们最近发现了一种新的假性蛋白TRB3,它是由内质网(ER)应激诱导的,调节内质网应激诱导的细胞凋亡。最近有报道称,TRB3在某些肿瘤中高表达。然后我们从细胞周期的角度研究了TRB3在细胞增殖中的作用。TRB3下调细胞周期相关磷酸酶CDC25A在HeLa细胞中的表达。另一方面,用RNAi方法将TRB3基因敲除后,内源性CDC25A水平升高。我们观察到TRB3以细胞周期依赖的方式表达,并且这种表达模式与CDC25A在G2/M期的表达模式呈负相关。当我们检测TRB3基因敲除对细胞周期的影响时,它的进程被延迟在G2/M期,CDC25A在M/G1期的下调被显著抑制。这些结果表明trb3在t…是细胞周期进程的调节器。抑制CDC25A的表达将是TRB3作用的靶点之一。我们用小鼠前脂肪细胞系3T3-L1细胞检测了内源性TRB3在脂肪细胞分化过程中的表达水平,其表达在早期暂时降低,然后随着细胞分化在mRNA和蛋白质水平上逐渐升高。这种表达谱与胁迫诱导转录因子CHOP10/Gadd153的出现密切相关。当TRB3在3T3-L1细胞中过表达时,细胞内甘油三酯总量和脂肪细胞分化的主要调控因子之一的PPARγ下游靶点的基因表达水平发生变化。另一方面,当用shRNA方法抑制TRB3mRNA水平时,脂肪细胞的分化被有效地阻止。此外,TRB3和PPARγ在细胞内相互关联,PPARγ过表达诱导的脂肪细胞分化受到TRB3异位表达的强烈抑制。结果表明,TRB3通过负调控PPARγ的转录活性来调节脂肪细胞的分化。较少

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Functional analysis of a pseudokinase, TRB3 during the M phase.
M 期假激酶 TRB3 的功能分析。
  • DOI:
  • 发表时间:
    2008
  • 期刊:
  • 影响因子:
    0
  • 作者:
    S. sakai;et. al.
  • 通讯作者:
    et. al.
Novel regulatory mechanism of PGC-la activity by TRB3
TRB3对PGC-1α活性的新调控机制
  • DOI:
  • 发表时间:
    2007
  • 期刊:
  • 影响因子:
    0
  • 作者:
    N. Ohoka;et. al.
  • 通讯作者:
    et. al.
Functional analysis of novel regulators of the cell cycle associated phosphatase CDC25A
细胞周期相关磷酸酶CDC25A新型调节剂的功能分析
  • DOI:
  • 发表时间:
    2006
  • 期刊:
  • 影响因子:
    0
  • 作者:
    S. Sakai;et. al.
  • 通讯作者:
    et. al.
Regulation of TGFβ signaling by a novel stress sensor protein, TRB3
新型应激传感器蛋白 TRB3 对 TGFβ 信号传导的调节
  • DOI:
  • 发表时间:
    2007
  • 期刊:
  • 影响因子:
    0
  • 作者:
    H. Hayashi;et. al.
  • 通讯作者:
    et. al.
細胞周期関連ホスファターゼCDC25Aの新規発現制御因子の機能解析
细胞周期相关磷酸酶CDC25A新型表达调节因子的功能分析
  • DOI:
  • 发表时间:
    2006
  • 期刊:
  • 影响因子:
    0
  • 作者:
    酒井 聡;ら
  • 通讯作者:
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HAYASHI Hidetoshi其他文献

HAYASHI Hidetoshi的其他文献

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{{ truncateString('HAYASHI Hidetoshi', 18)}}的其他基金

Immune related gene-expression profiling for the combination of chemotherapy and PD-1/PD-L1 inhibition.
化疗和 PD-1/PD-L1 抑制相结合的免疫相关基因表达谱。
  • 批准号:
    19K07785
  • 财政年份:
    2019
  • 资助金额:
    $ 2.57万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Resistance mechanis of molecular targeted therapy and tumor micro environment as the immune-checkpoint inhibitor's biomarker
分子靶向治疗的耐药机制和作为免疫检查点抑制剂生物标志物的肿瘤微环境
  • 批准号:
    16K21506
  • 财政年份:
    2016
  • 资助金额:
    $ 2.57万
  • 项目类别:
    Grant-in-Aid for Young Scientists (B)
Molecular bases of cellular stress and disease development regulated by by stress inducible molecules, TRB1 and TRB3
应激诱导分子 TRB1 和 TRB3 调节细胞应激和疾病发展的分子基础
  • 批准号:
    24590085
  • 财政年份:
    2012
  • 资助金额:
    $ 2.57万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Crosstalk between stress and cytokine signaling in metabolic syndrome
代谢综合征中压力与细胞因子信号传导之间的串扰
  • 批准号:
    21590067
  • 财政年份:
    2009
  • 资助金额:
    $ 2.57万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular mechanism of CHOP dependent cell death induced by extracellular stresses
细胞外应激诱导CHOP依赖性细胞死亡的分子机制
  • 批准号:
    16590057
  • 财政年份:
    2004
  • 资助金额:
    $ 2.57万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Control of TGFβ signaling by degradation of Smads, TGFβ signal transducers
通过降解 Smads、TGFβ 信号转导器来控制 TGFβ 信号传导
  • 批准号:
    13672294
  • 财政年份:
    2001
  • 资助金额:
    $ 2.57万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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研究泛素化调节的细胞周期事件支撑疟疾传播
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    MR/X023087/1
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细胞周期机制的发育调控
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    10714634
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核膜对细胞周期进程的调节
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