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Hye-Ra Lee Jaba Mitra Stacy Lee Shou-Jiang Gao Tae-Kwang Oh Myung Hee Kim Taekjip Ha Jae U. Jung 《Journal of virology》2016,90(2):1139-1143
Kaposi''s sarcoma-associated herpesvirus (KSHV) infection modulates the host cell cycle to create an environment optimal for its viral-DNA replication during the lytic life cycle. We report here that KSHV vIRF4 targets the β-catenin/CBP cofactor and blocks its occupancy on the cyclin D1 promoter, suppressing the G1-S cell cycle progression and enhancing KSHV replication. This shows that KSHV vIRF4 suppresses host G1-S transition, possibly providing an intracellular milieu favorable for its replication. 相似文献
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Kaposi''s sarcoma (KS) is common in Africa, but economic constraints hinder successful treatment in most patients. Propranolol, a generic β-adrenergic antagonist, decreased proliferation of KS-associated herpesvirus (KSHV)-infected cells. Downregulation of cyclin A2 and cyclin-dependent kinase 1 (CDK1) recapitulated this phenotype. Additionally, propranolol induced lytic gene expression in association with downregulation of CDK6. Thus, propranolol has diverse effects on KSHV-infected cells, and this generic drug has potential as a therapeutic agent for KS. 相似文献
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Haidai Hu Jiazhen Dong Deguang Liang Zengqiang Gao Lei Bai Rui Sun Hao Hu Heng Zhang Yuhui Dong Ke Lan 《Journal of virology》2016,90(3):1158-1168
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