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首页> 外文期刊>Journal of Cellular Physiology >Nuclear Translocation of p65 is Controlled by Sec6 via the Degradation of IB
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Nuclear Translocation of p65 is Controlled by Sec6 via the Degradation of IB

机译：核易位p65由Sec6控制通过IB的退化

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摘要

Nuclear factor-B (NF-B) is an inducible transcription factor that mediates immune and inflammatory responses. NF-B pathways are also involved in cell adhesion, differentiation, proliferation, autophagy, senescence, and protection against apoptosis. The deregulation of NF-B activity is found in a number of disease states, including cancer, arthritis, chronic inflammation, asthma, neurodegenerative diseases, and heart disease. The 90kDa ribosomal S6 kinase (p90RSK) family, which is serine/threonine kinases, is phosphorylated by extracellular signal-regulated kinase1/2 (ERK1/2) and is related to NF-B pathways. Our previous studies revealed that Sec6, a component of the exocyst complex, plays specific roles in cell-cell adhesion and cell cycle arrest. However, the mechanism by which Sec6 regulates the NF-B signaling pathway is unknown. We demonstrated that Sec6 knockdown inhibited the degradation of IB and delayed the nucleus-cytoplasm translocation of p65 in HeLa cells transfected with Sec6 siRNAs after treatment with tumor necrosis factor alpha (TNF-). Furthermore, the binding of p65 and cAMP response element binding protein (CREB) binding protein (CBP) or p300 decreased and NF-B related genes which were inhibitors of NF-B alpha (IB), A20, B cell lymphoma protein 2 (Bcl-2), and monocyte chemoattractant protein-1 (MCP-1) were low in cells transfected with Sec6 siRNAs in response to TNF- stimulation. Sec6 knockdown decreased the expression of p90RSKs and the phosphorylation of ERK or p90RSK1 at Ser380 or IB at Ser32. The present study suggests that Sec6 regulates NF-B transcriptional activity via the control of the phosphorylation of IB, p90RSK1, and ERK. J. Cell. Physiol. 231: 719-730, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：核因子b (NF-B)是一种可诱导的转录因子,介导免疫炎症反应。参与细胞粘附、分化、扩散、自噬、衰老和防止细胞凋亡。NF-B活动中发现许多疾病州,包括癌症、关节炎、慢性炎症、哮喘、神经退行性疾病,和心脏病。家人(p90RSK),这是丝氨酸/苏氨酸激酶的磷酸化是细胞外signal-regulated kinase1/2 (ERK1/2)和NF-B通路有关。显示,Sec6 exocyst的组件复杂,在信息中扮演特定的角色粘附和细胞周期阻滞。机制Sec6 NF-B调节信号通路是未知的。Sec6击倒抑制退化nucleus-cytoplasm IB和延迟易位的p65海拉细胞转染后与Sec6 siRNAs治疗肿瘤坏死因子-α(TNF)。绑定p65和营地响应元素的绑定蛋白(分子)结合蛋白(CBP)或p300减少和NF-B相关基因NF-Bα抑制剂(IB)、A20 B细胞淋巴瘤蛋白2 (bcl - 2)和单核细胞化学引诱物蛋白1 (MCP-1)较低细胞转染Sec6 siRNAs回应肿瘤坏死因子-刺激。p90RSKs和磷酸化的表情ERK或p90RSK1 Ser380或在Ser32 IB。本研究表明,Sec6调节NF-B通过控制转录活动IB的磷酸化,p90RSK1,兵。杂志。231:719 - 730年,2016年。期刊、公司。

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