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B细胞生长受磷脂酰肌醇3激酶依赖性诱导的Rel/NF-κB调控的c-myc转录控制。

B cell growth is controlled by phosphatidylinosotol 3-kinase-dependent induction of Rel/NF-kappaB regulated c-myc transcription.

作者信息

Grumont Raelene J, Strasser Andreas, Gerondakis Steve

机构信息

The Walter and Eliza Hall Institute of Medical Research, P.O. Box The Royal Melbourne Hospital, 3050, Victoria, Australia.

出版信息

Mol Cell. 2002 Dec;10(6):1283-94. doi: 10.1016/s1097-2765(02)00779-7.

Abstract

Rel/NF-kappaB transcription factors regulate the division and survival of B lymphocytes. Here we show that B cells lacking NF-kappaB1 and c-Rel fail to increase in size upon mitogenic stimulation due to a reduction in induced c-myc expression. Mitogen-induced B cell growth, although not markedly impaired by FRAP/mTOR or MEK inhibitors, required phosphatidylinositol 3-kinase (PI3K) activity. Inhibition of PI3K-dependent growth coincided with a block in the nuclear import of NF-kappaB1/c-Rel dimers and a failure to upregulate c-myc. In addition, PI3K was shown to be necessary for a transcription-independent increase in c-Myc protein levels that accompanies mitogenic activation. Collectively, these findings establish a role for Rel/NF-kappaB signaling in the mitogen-induced growth of mammalian cells, which in B lymphocytes requires a PI3K/c-myc-dependent pathway.

摘要

Rel/NF-κB转录因子调节B淋巴细胞的增殖和存活。我们在此表明,缺乏NF-κB1和c-Rel的B细胞在有丝分裂原刺激后无法增大体积,这是由于诱导的c-myc表达减少所致。有丝分裂原诱导的B细胞生长虽然未被FRAP/mTOR或MEK抑制剂显著损害,但需要磷脂酰肌醇3-激酶(PI3K)的活性。PI3K依赖性生长的抑制与NF-κB1/c-Rel二聚体的核输入受阻以及c-myc上调失败同时发生。此外,PI3K被证明对于有丝分裂原激活时伴随的c-Myc蛋白水平的转录非依赖性增加是必需的。总的来说,这些发现确立了Rel/NF-κB信号在哺乳动物细胞有丝分裂原诱导生长中的作用,在B淋巴细胞中这需要一条PI3K/c-myc依赖性途径。

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