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A systems biology approach identified different regulatory networks targeted by KSHV miR-K12-11 in B cells and endothelial cells

机译:系统生物学方法确定了B细胞和内皮细胞中KSHV miR-K12-11靶向的不同调控网络

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摘要

BackgroundKaposi’s sarcoma associated herpes virus (KSHV) is associated with tumors of endothelial and lymphoid origin. During latent infection, KSHV expresses miR-K12-11, an ortholog of the human tumor gene hsa-miR-155. Both gene products are microRNAs (miRNAs), which are important post-transcriptional regulators that contribute to tissue specific gene expression. Advances in target identification technologies and molecular interaction databases have allowed a systems biology approach to unravel the gene regulatory networks (GRNs) triggered by miR-K12-11 in endothelial and lymphoid cells. Understanding the tissue specific function of miR-K12-11 will help to elucidate underlying mechanisms of KSHV pathogenesis.
机译:背景卡波西氏肉瘤相关疱疹病毒(KSHV)与内皮和淋巴样起源的肿瘤有关。在潜伏感染期间,KSHV表达了miR-K12-11,这是人类肿瘤基因hsa-miR-155的直系同源基因。两种基因产物均为microRNA(miRNA),它们是重要的转录后调节因子,有助于组织特异性基因表达。目标识别技术和分子相互作用数据库的发展已使系统生物学方法能够揭示内皮细胞和淋巴样细胞中由miR-K12-11触发的基因调控网络(GRN)。了解miR-K12-11的组织特异性功能将有助于阐明KSHV发病机理的潜在机制。

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