D53 (TPD52L1) is a cell cycle-regulated protein maximally expressed at the G2-M transition in breast cancer cells
D53 (TPD52L1) is a cell cycle-regulated protein maximally expressed at the G2-M transition in breast cancer cells
复制标题
DOI：
10.1016/j.yexcr.2005.07.009
复制
发表时间：
2005-10-15
影响因子：
3.7
通讯作者：
Byrne, JA
中科院分区：
文献类型：
--
作者：
Boutros, R;Byrne, JA
细胞在G2-M转换期间致力于分裂，并且有丝分裂进入的时间必须严格调节以确保正确的染色体分离。鉴定所有的蛋白质和分子事件，协调G2-M过渡将需要一个完整的理解细胞分裂周期，以及如何其失调有助于细胞转化。我们以前曾报道过D53，肿瘤蛋白D52家族的成员，是乳腺癌细胞中的一种新的14-3-3伴侣蛋白。我们现在报道，在乳腺癌细胞系中，D53的表达在G2-M过渡期高度上调，其中D53是内源性或外源性表达的。D53表达的时间和亚细胞定位与cyclin 131相似，并且D53表达在转录后和翻译后水平上受到类似的调控。D53和14-3-3之间的相互作用，G2-M转换的负调节，增加了同步化的群体中富集的细胞在G2/M期，与G1/S停滞的细胞。两个EGFP标记的D53亚型和相关蛋白D52的强制表达产生高比例的多核MDA-MB-231乳腺癌细胞。这些结果将D53鉴定为细胞周期调节蛋白，其失调表达可不利地影响有丝分裂的完成。(c)2005年爱思唯尔公司All rights reserved.
The cell commits to dividing during the G2-M transition, and timing of mitotic entry must be tightly regulated to ensure correct chromosome segregation. Identification of all proteins and molecular events that orchestrate the G2-M transition will be required for a complete understanding of the cell division cycle, and how its deregulation contributes to cell transformation. We have previously reported D53, a member of the tumor protein D52 family, to be a novel 14-3-3 partner protein in breast cancer cells. We now report that D53 expression is highly upregulated at the G2-M transition in breast cancer cell lines in which D53 is endogenously or exogenously expressed. The timing and subcellular localization of D53 expression paralleled that of cyclin 131, and D53 expression was similarly regulated at both post-transcriptional and post-translational levels. Interactions between D53 and 14-3-3, a negative regulator of the G2-M transition, were increased in synchronized populations enriched for cells in G2/M phases, compared with G1/S arrested cells. Enforced expression of two EGFP-tagged D53 isoforms and the related protein D52 produced high proportions of multinucleated MDA-MB-231 breast carcinoma cells. These results identify D53 as a cell cycle-regulated protein whose deregulated expression can adversely affect the completion of mitosis. (c) 2005 Elsevier Inc. All rights reserved.