IRS-2, but not IRS-1, can sustain proliferation and rescue UBF stabilization in InR or InR defective signaling of 32D myeloid cells.

Wu S; Zhou B; Xu L; Sun H

首页> 外文期刊>Cell cycle >IRS-2, but not IRS-1, can sustain proliferation and rescue UBF stabilization in InR or InR defective signaling of 32D myeloid cells.

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IRS-2, but not IRS-1, can sustain proliferation and rescue UBF stabilization in InR or InR defective signaling of 32D myeloid cells.

机译：IRS-2（而非IRS-1）可以在32D髓样细胞的InR或InR缺陷信号中维持增殖并拯救UBF稳定。

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Despite both IRS-1 and IRS-2 are two important adaptor molecules essential for intracellular signaling of insulin and IGF-I, the distinct biological pattern of IRS-2 versus IRS-1 remains as a concernful issue to be clarified. We demonstrated here an important evidence that in 32D myeloid cells expressing the insulin receptor (InR) or selected mutants of the InR, IRS-2, but not IRS-1, is required for promoting the proliferation and inhibiting the granulocytic differentiation, thus restore ERKs phosphorylation and UBF1 stabilization. In addition, unlike IRS-1, IRS-2 can effectively compensate the InR defective signaling and lead to the activation of cell cycle progression and proliferation genes in 32D myeloid cells. These results indicate a predominant role of IRS-2 involved in InR signaling of 32D myeloid cells.

机译：尽管IRS-1和IRS-2都是胰岛素和IGF-1的细胞内信号转导必不可少的两个重要衔接子分子，但IRS-2与IRS-1的不同生物学模式仍然是一个有待澄清的问题。我们在这里证明了一个重要的证据，在表达胰岛素受体（InR）或InR的选定突变体的32D髓样细胞中，IRS-2而非IRS-1是促进增殖和抑制粒细胞分化从而恢复ERK所必需的磷酸化和UBF1稳定化。此外，与IRS-1不同，IRS-2可有效补偿InR缺陷信号传导并导致32D髓样细胞中细胞周期进程和增殖基因的激活。这些结果表明，IRS-2在32D髓样细胞的InR信号传导中起主要作用。

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《Cell cycle》 |2009年第19期|共9页
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Wu S; Zhou B; Xu L; Sun H;
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正文语种 eng
中图分类细胞生物学;
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1. IRS-2, but not IRS-1, can sustain proliferation and rescue UBF stabilization in InR or InR defective signaling of 32D myeloid cells. [J] . Wu S, Zhou B, Xu L, Cell cycle . 2009,第19期

机译：IRS-2（而非IRS-1）可以在32D髓样细胞的InR或InR缺陷信号中维持增殖并拯救UBF稳定。
2. Reduction of insulin signalling pathway IRS-1/IRS-2/AKT/mTOR and decrease of epithelial cell proliferation in the prostate of glucocorticoid-treated rats [J] . CostaM.M., ViolatoN.M., TabogaS.R., International Journal of Experimental Pathology . 2012,第3期

机译：减少胰岛素信号通路IRS-1 / IRS-2 / AKT / mTOR和糖皮质激素治疗大鼠前列腺前列腺内上皮细胞增殖降低
3. Differential signaling by insulin receptor substrate 1 (IRS-1) and IRS-2 in IRS-1-deficient cells. [J] . J C Brüning, J Winnay, B Cheatham, Molecular and Cellular Biology . 1997,第3期

机译：胰岛素受体底物1（IRS-1）和IRS-2在IRS-1缺陷细胞中的差异信号。
4. Differential signaling by insulin receptor substrate 1 (IRS-1) and IRS-2 in IRS-1-deficient cells. [O] . J C Brüning, J Winnay, B Cheatham, 1997

机译：胰岛素受体底物1（IRS-1）和IRS-2在IRS-1缺陷细胞中的差异信号。
5. IRS-2, but not IRS-1, can sustain proliferation and rescue UBF stabilization in InR or InR defective signaling of 32D myeloid cells [O] . Shufang Wu, Bo Zhou, Lin Xu, 2009

机译：IRS-2，但不是IRS-1，可以在32D骨髓细胞中维持INR或INR缺陷信号传导的增殖和救援UBF稳定

IRS-2, but not IRS-1, can sustain proliferation and rescue UBF stabilization in InR or InR defective signaling of 32D myeloid cells.

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