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        SAMHD1 controls cell cycle status, apoptosis and HIV-1 infection in monocytic THP-1 cells

        Bonifati, S.,Daly, M.B.,St. Gelais, C.,Kim, S.H.,Hollenbaugh, J.A.,Shepard, C.,Kennedy, E.M.,Kim, Dong.Hyun.,Schinazi, R.F.,Kim, B.,Wu, L. 3M Company 2016 Virology Vol.495 No.-

        <P>SAMHD1 limits HIV-1 infection in non-dividing myeloid cells by decreasing intracellular dNTP pools. HIV-1 restriction by SAMHD1 in these cells likely prevents activation of antiviral immune responses and modulates viral pathogenesis, thus highlighting a critical role of SAMHD1 in HIV-1 physiopathology. Here, we explored the function of SAMHD1 in regulating cell proliferation, cell cycle progression and apoptosis in monocytic THP-1 cells. Using the CRISPR/Cas9 technology, we generated THP-1 cells with stable SAMHD1 knockout. We found that silencing of SAMHD1 in cycling cells stimulates cell proliferation, redistributes cell cycle population in the G(1)/G(0) phase and reduces apoptosis. These alterations correlated with increased dNTP levels and more efficient HIV-1 infection in dividing SAMHD1 knockout cells relative to control. Our results suggest that SAMHD1, through its dNTPase activity, affects cell proliferation, cell cycle distribution and apoptosis, and emphasize a key role of SAMHD1 in the interplay between cell cycle regulation and HIV-1 infection. (C) 2016 Elsevier Inc. All rights reserved.</P>

      • Simulation Research on Control System of Main Converter Unit

        Li Xingyu,Zheng Zhongxiang,Wu Dali 제어로봇시스템학회 2019 제어로봇시스템학회 국제학술대회 논문집 Vol.2019 No.10

        The main converter unit needs to provide high-quality AC and DC power for the ship AC/DC hybrid power system. The reliability of its control system is very important. In order to study and optimize the control system of the converter unit, it is very meaningful to model and simulate it. The working characteristics and operation requirements of the converter unit in the ship hybrid power system are introduced. According to the control system structure, the corresponding simulation model is built. The simulation results meet the unit operation requirements and provide technical support for optimizing the converter unit control system.

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        A Novel Human BTB-kelch Protein KLHL31, Strongly Expressed in Muscle and Heart, Inhibits Transcriptional Activities of TRE and SRE

        Weishi Yu,Yuequn Wang,Yongqing Li,Yun Deng,Zequn Wang,Wuzhou Yuan,Dali Li,Chuanbing Zhu,Xueying Zhao,Xiaoyang Mo,Wen Huang,Na Luo,Yan Yan,Karen Ocorr,Rolf Bodmer,Xiushan Wu 한국분자세포생물학회 2008 Molecules and cells Vol.26 No.5

        The Bric-a-brac, Tramtrack, Broad-complex (BTB) domain is a protein-protein interaction domain that is found in many zinc finger transcription factors. BTB containing proteins play important roles in a variety of cellular functions including regulation of transcription, regulation of the cytoskeleton, protein ubiquitination, angiogenesis, and apoptosis. Here, we report the cloning and characterization of a novel human gene, KLHL31, from a human embryonic heart cDNA library. The cDNA of KLHL31 is 5743 bp long, encoding a protein product of 634 amino acids containing a BTB domain. The protein is highly conserved across different species. Western blot analysis indicates that the KLHL31 protein is abundantly expressed in both embryonic skeletal and heart tissue. In COS-7 cells, KLHL31 proteins are localized to both the nucleus and the cytoplasm. In primary cultures of nascent mouse cardiomyocytes, the majority of endogenous KLHL31 proteins are localized to the cytoplasm. KLHL31 acts as a transcription repressor when fused to GAL4 DNA-binding domain and deletion analysis indicates that the BTB domain is the main region responsible for this repression. Overexpression of KLHL31 in COS-7 cells inhibits the transcriptional activities of both the TPA-response element (TRE) and serum response element (SRE). KLHL31 also significantly reduces JNK activation leading to decreased phosphorylation and protein levels of the JNK target c-Jun in both COS-7 and Hela cells. These results suggest that KLHL31 protein may act as a new transcriptional repressor in MAPK/JNK signaling pathway to regulate cellular functions.

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