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首页> 外文期刊>Cell metabolism >SREBP activity is regulated by mTORC1 and contributes to Akt-dependent cell growth.
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SREBP activity is regulated by mTORC1 and contributes to Akt-dependent cell growth.

机译：SREBP活性受mTORC1调节，并有助于Akt依赖的细胞生长。

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摘要

Cell growth (accumulation of mass) needs to be coordinated with metabolic processes that are required for the synthesis of macromolecules. The PI3-kinase/Akt signaling pathway induces cell growth via activation of complex 1 of the target of rapamycin (TORC1). Here we show that Akt-dependent lipogenesis requires mTORC1 activity. Furthermore, nuclear accumulation of the mature form of the sterol responsive element binding protein (SREBP1) and expression of SREBP target genes was blocked by the mTORC1 inhibitor rapamycin. We also show that silencing of SREBP blocks Akt-dependent lipogenesis and attenuates the increase in cell size in response to Akt activation in vitro. Silencing of dSREBP in flies caused a reduction in cell and organ size and blocked the induction of cell growth by dPI3K. Our results suggest that the PI3K/Akt/TOR pathway regulates protein and lipid biosynthesis in an orchestrated manner and that both processes are required for cell growth.
机译：细胞生长（质量积累）需要与大分子合成所需的代谢过程协调。 PI3-激酶/ Akt信号通路通过激活雷帕霉素靶标（TORC1）的复合物1诱导细胞生长。在这里，我们显示依赖Akt的脂肪生成需要mTORC1活性。此外，mTORC1抑制剂雷帕霉素可阻止成熟形式的固醇响应元件结合蛋白（SREBP1）的核积累和SREBP目标基因的表达。我们还显示，SREBP沉默可阻止Akt依赖的脂肪生成，并在体外响应Akt激活而减弱细胞大小的增加。果蝇中dSREBP的沉默导致细胞和器官大小的减少，并阻止dPI3K诱导细胞生长。我们的结果表明，PI3K / Akt / TOR途径以协调的方式调节蛋白质和脂质的生物合成，并且这两个过程都是细胞生长所必需的。

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