三四脯氨酸
免疫沉淀
基因沉默
基因敲除
信使核糖核酸
细胞生物学
生物
蛋白质亚单位
分子生物学
RNA结合蛋白
免疫学
基因
生物化学
抗体
作者
Jun Shi,Jia‐Shu Li,Rong Hu,Xincheng Zhao,Chengcheng Liang,Xiaomin Li,Hong Wang,Yi Shi,Xin Su
出处
期刊:Molecular Medicine Reports
[Spandidos Publications]
日期:2018-06-22
被引量:2
标识
DOI:10.3892/mmr.2018.9213
摘要
Subunit 1 is the scaffold protein of the carbon catabolite repressor protein 4 (CCR4)‑negative on TATA (NOT) complex (CNOT1). In our previous study, it was reported that tristetraprolin (TTP) could recruit subunit 7 of the CCR4‑NOT complex (CNOT7) to induce the degradation of intercellular adhesion molecule‑1 (ICAM‑1) and interleukin‑8 (IL‑8) mRNA in human pulmonary microvascular endothelial cells (HPMECs). It was additionally demonstrated that TTP, CNOT7 and CNOT1 formed a complex in HPMECs. However, whether CNOT1 is involved in TTP‑mediated ICAM‑1 and IL‑8 mRNA decay remains unclear. The present study demonstrated that CNOT1 knockdown improved ICAM‑1 and IL‑8 mRNA stabilization and protein expression levels. The immunofluorescence results demonstrated that CNOT1, CNOT7 and TTP are co‑localized in the cytoplasm. CNOT1 silencing abolished CNOT7 and TTP coimmunoprecipitation. However, CNOT7 silencing did not influence CNOT1 and TTP coimmunoprecipitation, and TTP silencing additionally did not influence CNOT1 and CNOT7 coimmunoprecipitation. These results together with the authors' previous study, have identified that CNOT1 provides a platform for the recruitment of TTP and CNOT7, and is involved in TTP‑mediated ICAM‑1 and IL‑8 mRNA decay.
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