CNOT7/hCAF1 is involved in ICAM-1 and IL-8 regulation by tristetraprolin.
作者： Jia-Xin Shi , Jia-Shu Li , Rong Hu , Yi Shi , Xin Su
DOI: 10.1016/J.CELLSIG.2014.07.020
关键词:
摘要: Tristetraprolin (TTP) is an RNA-binding protein which can bind to the AU-rich elements (AREs) at 3'-untranslated region (3'-UTR) of target mRNA and promote deadenylation degradation. We have shown in a previous study that TTP regulates tumor necrosis factor-α (TNF-α)-induced expression intercellular adhesion molecule-1 (ICAM-1) interleukin-8 (IL-8), both whose mRNAs AREs 3'-UTR, human pulmonary microvascular endothelial cells (HPMEC) through destabilizing mRNAs, nevertheless, mechanism by promotes decay remains unclear. Observations indicated interact with CAF1 (CNOT7/hCAF1 human), subunit CCR4-NOT complex deadenylase activity. Another illustrated directly CNOT1, scaffold complex. The present showed bound ICAM-1 IL-8 was coimmunoprecipitated intracellular mRNAs. TTP, CNOT7 CNOT1 were HPMEC. silencing stabilized increased production following TNF-α stimulation. These results, together our study, suggest CNOT7/hCAF1 involved regulation
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