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Bcl2 enhances c-Myc-mediated MMP-2 expression of vascular smooth muscle cells

机译:Bcl2增强c-Myc介导的血管平滑肌细胞MMP-2表达

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摘要

Matrix metalloproteinases (MMPs) are a major group of enzymes that regulate cell matrix composition. In this paper, our results show that c-Myc significantly induced vascular smooth muscle cells (VSMCs) migration and invasion, compared with the results, the T58A had more effectively than WTc-Myc, which was associated with c-Myc increased MMP-2 gene expression and activity. Silenced c-Myc led to reduce MMP-2 gene expression and activity, as well as decrease VSMC migration and invasion, indicating c-Myc is required for MMP-2 mediated VSMC migration and invasion. However, S62A had no effect on VSMC migration and invasion, which was in line with S62A had no effect on the c-Myc transcriptional activity. To better understand whether Bcl2 cooperate with c-Myc on MMP-2 function, our data show that although Bcl2 had no effect on the MMP-2 activity, the coexpressing c-Myc and Bcl2 significantly increased MMP-2 gene expression and activity. Our results suggest that phosphorylation of Bcl2 (T70E and EEE) had more effectively on the MMP-2 activity, which resulted from T70E and EEE severely increased c-Myc transcriptional activity by directly binding to c-Myc. The findings show that phosphorylation of Bcl2 enhanced c-Myc-mediated MMP-2 activity. Crown Copyright
机译:基质金属蛋白酶(MMP)是调节细胞基质组成的主要酶类。在本文中,我们的结果表明c-Myc显着诱导了血管平滑肌细胞(VSMC)迁移和侵袭,与结果相比,T58A比WTc-Myc更有效,这与c-Myc增加MMP-2有关基因表达和活性。沉默的c-Myc导致MMP-2基因表达和活性降低,以及VSMC迁移和侵袭减少,表明c-Myc是MMP-2介导的VSMC迁移和侵袭所必需的。但是,S62A对VSMC的迁移和侵袭没有影响,这与S62A对c-Myc转录活性没有影响。为了更好地了解Bcl2是否与c-Myc在MMP-2功能上协同作用,我们的数据显示,尽管Bcl2对MMP-2活性没有影响,但是共表达c-Myc和Bcl2显着增加了MMP-2基因的表达和活性。我们的结果表明,Bcl2的磷酸化(T70E和EEE)对MMP-2活性具有更有效的作用,这是由于T70E和EEE通过直接结合c-Myc严重增强了c-Myc转录活性所致。该发现表明,Bcl2的磷酸化增强了c-Myc介导的MMP-2活性。皇冠版权

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