潜伏期基因座补充体内 MicroRNA 155 的缺失。
Latency locus complements MicroRNA 155 deficiency in vivo.
机构信息
Department of Microbiology and Immunology, Program in Global Oncology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
出版信息
J Virol. 2013 Nov;87(21):11908-11. doi: 10.1128/JVI.01620-13. Epub 2013 Aug 21.
Abstract
MicroRNA-155 (miR-155) is expressed in many cancers. It also executes evolutionary conserved functions in normal B cell development. We show that the Kaposi's sarcoma-associated herpesvirus (KSHV) latency locus, which contains an ortholog of miR-155, miR-K12-11, complements B cell deficiencies in miR-155 knockout mice. Germinal center (GC) formation was rescued in spleen, lymph node, and Peyer's patches. Immunoglobulin levels were restored. This demonstrates that KSHV can complement the normal, physiological function of miR-155.
摘要
MicroRNA-155（miR-155）在许多癌症中表达。它在正常 B 细胞发育中也执行进化保守的功能。我们表明，卡波济肉瘤相关疱疹病毒（KSHV）潜伏部位包含 miR-155 的同源物，miR-K12-11，可弥补 miR-155 敲除小鼠中 B 细胞的缺陷。生发中心（GC）在脾脏、淋巴结和派尔氏斑中得到挽救。免疫球蛋白水平得到恢复。这表明 KSHV 可以弥补 miR-155 的正常生理功能。
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