细胞周期蛋白E与哺乳动物SWI-SNF复合物的组分BAF155和BRG1相结合，并改变BRG1诱导生长停滞的能力。
Cyclin E associates with BAF155 and BRG1, components of the mammalian SWI-SNF complex, and alters the ability of BRG1 to induce growth arrest.
作者信息
Shanahan F, Seghezzi W, Parry D, Mahony D, Lees E
机构信息
Cell Signaling Department, DNAX Research Institute, Palo Alto, California 94304, USA.
出版信息
Mol Cell Biol. 1999 Feb;19(2):1460-9. doi: 10.1128/MCB.19.2.1460.
Abstract
SWI-SNF complexes have been implicated in transcriptional regulation by chromatin remodeling. We have identified an interaction between two components of the mammalian SWI-SNF complex and cyclin E, an essential cell cycle regulatory protein required for G1/S transition. BRG1 and BAF155, mammalian homologs of yeast SWI2 and SWI3, respectively, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase activity. In this report, we show that overexpression of BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which can be overcome by cyclin E. Our results suggest that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.
摘要
SWI-SNF复合物通过染色质重塑参与转录调控。我们已经确定了哺乳动物SWI-SNF复合物的两个组分与细胞周期蛋白E之间的相互作用，细胞周期蛋白E是G1/S期转换所必需的一种重要细胞周期调节蛋白。酵母SWI2和SWI3的哺乳动物同源物BRG1和BAF155分别存在于细胞周期蛋白E复合物中，并被细胞周期蛋白E相关激酶活性磷酸化。在本报告中，我们表明BRG1的过表达导致生长停滞和衰老相关β-半乳糖苷酶活性的诱导，而细胞周期蛋白E可以克服这种情况。我们的结果表明，细胞周期蛋白E可能调节SWI-SNF装置的活性，以维持染色质处于转录允许状态。
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