期刊文献

FoxO 收藏

的FoxO

原文求助发布源

作者

Karen CArden;

作者单位

Ludwig Institute for Cancer Research and University of California San Diego, School of Medicine, San Diego, CA USA[*]Correspondence: Karen C. Arden, 858 534 7812 (phone), 858 534 7750 (fax)

发布日期

21 May 2004

页码

416-418

DOI

10.1016/S1097-2765(04)00213-8

来源信息

Molecular Cell ISSN：1097-2765, 2004年, 14卷, 4期, 416-418页

摘要

Two recent reports (Seoane et al., 2004; Hu et al., 2004) reveal new roles for FoxO proteins in cell proliferation and tumorigenesis. Seoane and colleagues show that FoxO proteins play key roles in the TGFβ-dependent activation of p21Cip1 by partnering with Smad3 and Smad4. FoxG1, a protein from a distinct Fox subfamily, binds FoxO/Smad complexes and blocks p21Cip1 expression. These interactions establish a relationship between the PI3K pathway, FoxG1, and the TGFβ/Smad pathways. The second report identifies IκB kinase as a negative regulator of FoxO proteins, suggesting a mechanism for relieving negative regulation of cell cycle and promoting tumor cell proliferation.

摘要译文

最近的两个报道（Seoane等，2004; Hu等，2004）揭示了FoxO蛋白在细胞增殖和肿瘤发生中的新作用。 Seoane及其同事通过与Smad3和Smad4配合，发现FoxO蛋白在TGFβ依赖性激活p21Cip1过程中发挥重要作用。 FoxG1是一种独特的Fox亚家族的蛋白质，与FoxO / Smad复合物结合并阻断p21Cip1的表达。这些相互作用建立了PI3K途径，FoxG1和TGFβ/ Smad途径之间的关系。第二份报告将IκB激酶鉴定为FoxO蛋白的负调控因子，提示了减轻细胞周期负调控和促进肿瘤细胞增殖的机制。

Karen CArden;. FoxO[J]. Molecular Cell, 2004,14(4): 416-418