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首页> 外文期刊>Journal of Cellular Physiology >Mechanisms of transforming growth factor beta induced cell cycle arrest in palate development.
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Mechanisms of transforming growth factor beta induced cell cycle arrest in palate development.

机译：转化生长因子β的机制诱导细胞周期阻滞在口感的发展。

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Immaculate and complete palatal seam disintegration, which takes place at the last phase of palate development, is essential for normal palate development. And in absence of palatal midline epithelial seam (MES) disintegration, cleft palate may arise. It has been established that transforming growth factor (TGF) beta induces both epithelial mesenchymal transition (EMT) and/or apoptosis during MES disintegration. It is likely that MES might cease cell cycle to facilitate cellular changes prior to undergoing transformation or apoptosis, which has never been studied before. This study was designed to explore whether TGFbeta, which is crucial for palatal MES disintegration, is capable of inducing cell cycle arrest. We studied the effects of TGFbeta1 and TGFbeta3, potent negative regulators of the cell cycle, on p15ink4b activity in MES cells. We surprisingly found that TGFbeta1, but not TGFbeta3, plays a major role in activation of the p15ink4b gene. In contrast, following successful cell cycle arrest by TGFbeta1, it is TGFbeta3 but not TGFbeta1 that causes later cellular morphogenesis, such as EMT and apoptosis. Since TGFbeta signaling activates Smads, we analyzed the roles of three Smad binding elements (SBEs) on the p15ink4b mouse promoter by site specific mutagenesis and found that these binding sites are functional. The ChIP assay demonstrated that TGFbeta1, not TGFbeta3, promotes Smad4 binding to two 5' terminal SBEs but not the 3' terminal site. Thus, TGFbeta1 and TGFbeta3 play separate yet complimentary roles in achieving cell cycle arrest and EMT/apoptosis and cell cycle arrest is a prerequisite for later cellular changes.
机译：完美和完整的腭骨发生在最后瓦解口感发展的阶段,是至关重要的口感的正常发展。腭中线上皮缝(MES)可能出现解体,腭裂。转化生长因子建立了(TGF)β诱导上皮间充质过渡(EMT)在MES和/或凋亡解体。细胞周期促进细胞变化之前进行转换或凋亡以前从未被研究过。旨在探索是否TGFbeta,腭MES解体,是至关重要的能够诱导细胞周期阻滞。TGFbeta1和TGFbeta3的影响,有效的在细胞周期的负调控因子在MES p15ink4b活动细胞。发现,但不是TGFbeta3 TGFbeta1扮演p15ink4b基因的激活的主要角色。相比之下,成功的细胞周期阻滞通过TGFbeta1, TGFbeta3但不是TGFbeta1EMT等原因后细胞形态发生和细胞凋亡。三个Smad Smads,我们分析了角色绑定元素(某人)p15ink4b鼠标启动子定点诱变和发现这些绑定网站功能。试验表明,TGFbeta1,不是TGFbeta3,促进Smad4绑定两个5 '末端某人但不是3 '末端的网站。TGFbeta3发挥独立却互补的作用实现细胞周期阻滞和EMT /凋亡和细胞周期阻滞是一个先决条件细胞的变化。

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