Role of the cellular microRNA, miR-155, in EBV type III latency signaling

细胞 microRNA miR-155 在 EBV III 型潜伏信号传导中的作用

基本信息

  • 批准号:
    8455707
  • 负责人:
  • 金额:
    $ 28.19万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2009
  • 资助国家:
    美国
  • 起止时间:
    2009-07-01 至 2014-04-30
  • 项目状态:
    已结题

项目摘要

The Epstein Barr virus (EBV) is an oncogenic herpesvirus that is intimately involved in a number of malignancies in humans. The genetic basis of EBV associated oncogenesis is the concerted action of EBV latency associated genes and varying cellular genetic alterations. In immuno-competent individuals only minimal EBV latency gene expression can be tolerated due to the immunogeneticity of several EBV encoded latency gene products. In AIDS patients, however, expression of the full repertoire of latency genes (referred to as type III latency) can sometimes be tolerated and expression of these genes provide many essential elements of tumor cell development. In this setting, fewer cellular genetic alterations are required to give rise to malignant cell populations and this probably partly explains the greatly increased susceptibility of AIDS patients to EBV associated non-Hodgkin's lymphomas. The cellular microRNA, miR-155, is one of the most highly implicated microRNAs in cancer. miR-155 is induced by the EBV type III latency program (but not the type I latency program) suggesting a possible role for miR-155 in modulating type III latency signal transduction. Further evidence that miR-155 signaling is relevant to herpesvirus biology has been provided by Rolf Renne's lab and by Bryan Cullen's lab who both showed recently that the Kaposi's Sarcoma Herpes virus (KSHV) encodes a functional homologue of miR- 155. Two mouse miR-155 knock out papers recently showed that miR-155 is important for B cell activation responses following immune challenge. We hypothesize that induction of miR-155 by EBV type III latency plays a role in facilitating EBV mediated B cell activation and that miR-155 modulates signal transduction pathways that contribute to EBV associated maligancies in AIDS patients.
eb病毒(EBV)是一种致癌的疱疹病毒,与许多疾病密切相关

项目成果

期刊论文数量(8)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
miRNA-mRNA correlation-network modules in human prostate cancer and the differences between primary and metastatic tumor subtypes.
  • DOI:
    10.1371/journal.pone.0040130
  • 发表时间:
    2012
  • 期刊:
  • 影响因子:
    3.7
  • 作者:
    Zhang W;Edwards A;Fan W;Flemington EK;Zhang K
  • 通讯作者:
    Zhang K
Expanding the conversation on high-throughput virome sequencing standards to include consideration of microbial contamination sources.
扩大有关高通量病毒组测序标准的讨论,以纳入对微生物污染源的考虑。
  • DOI:
    10.1128/mbio.01989-14
  • 发表时间:
    2014
  • 期刊:
  • 影响因子:
    6.4
  • 作者:
    Strong,MichaelJ;Lin,Zhen;Flemington,ErikK
  • 通讯作者:
    Flemington,ErikK
Epstein - Barr virus Latent Membrane Protein 1 suppresses reporter activity through modulation of promyelocytic leukemia protein-nuclear bodies.
Epstein-Barr 病毒潜伏膜蛋白 1 通过调节早幼粒细胞白血病蛋白核体来抑制报告基因活性。
  • DOI:
    10.1186/1743-422x-8-461
  • 发表时间:
    2011
  • 期刊:
  • 影响因子:
    4.8
  • 作者:
    Sides,MarkD;Block,GregoryJ;Chadwick,ReidW;Shan,Bin;Flemington,ErikK;Lasky,JosephA
  • 通讯作者:
    Lasky,JosephA
Microbial contamination in next generation sequencing: implications for sequence-based analysis of clinical samples.
  • DOI:
    10.1371/journal.ppat.1004437
  • 发表时间:
    2014-11
  • 期刊:
  • 影响因子:
    6.7
  • 作者:
    Strong MJ;Xu G;Morici L;Splinter Bon-Durant S;Baddoo M;Lin Z;Fewell C;Taylor CM;Flemington EK
  • 通讯作者:
    Flemington EK
The sequence structures of human microRNA molecules and their implications.
  • DOI:
    10.1371/journal.pone.0054215
  • 发表时间:
    2013
  • 期刊:
  • 影响因子:
    3.7
  • 作者:
    Fang Z;Du R;Edwards A;Flemington EK;Zhang K
  • 通讯作者:
    Zhang K
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ERIK K FLEMINGTON其他文献

ERIK K FLEMINGTON的其他文献

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{{ truncateString('ERIK K FLEMINGTON', 18)}}的其他基金

EBV reactivation causes widespread host de novo promoter transcription and transcriptional interference
EBV 重新激活导致广泛的宿主从头启动子转录和转录干扰
  • 批准号:
    10647826
  • 财政年份:
    2022
  • 资助金额:
    $ 28.19万
  • 项目类别:
EBV reactivation causes widespread host de novo promoter transcription and transcriptional interference
EBV 重新激活导致广泛的宿主从头启动子转录和转录干扰
  • 批准号:
    10548370
  • 财政年份:
    2022
  • 资助金额:
    $ 28.19万
  • 项目类别:
Programmed splicing derangement as new EBV host cell shut-off mechanism
程序性剪接紊乱作为新的 EBV 宿主细胞关闭机制
  • 批准号:
    10580068
  • 财政年份:
    2022
  • 资助金额:
    $ 28.19万
  • 项目类别:
Programmed splicing derangement as new EBV host cell shut-off mechanism
程序性剪接紊乱作为新的 EBV 宿主细胞关闭机制
  • 批准号:
    10446536
  • 财政年份:
    2022
  • 资助金额:
    $ 28.19万
  • 项目类别:
RPMS1 circular RNAs in EBV malignancies
EBV 恶性肿瘤中的 RPMS1 环状 RNA
  • 批准号:
    10397562
  • 财政年份:
    2019
  • 资助金额:
    $ 28.19万
  • 项目类别:
RPMS1 circular RNAs in EBV malignancies
EBV 恶性肿瘤中的 RPMS1 环状 RNA
  • 批准号:
    10612751
  • 财政年份:
    2019
  • 资助金额:
    $ 28.19万
  • 项目类别:
RPMS1 circular RNAs in EBV malignancies
EBV 恶性肿瘤中的 RPMS1 环状 RNA
  • 批准号:
    10153734
  • 财政年份:
    2019
  • 资助金额:
    $ 28.19万
  • 项目类别:
Project 2: Joint Transcriptomic and Epigenomic Studies for Male Osteoporosis
项目2:男性骨质疏松症的转录组和表观基因组联合研究
  • 批准号:
    10180819
  • 财政年份:
    2017
  • 资助金额:
    $ 28.19万
  • 项目类别:
"Core B" Viral RNA-seq and bioinformatics Core
“核心 B”病毒 RNA-seq 和生物信息学核心
  • 批准号:
    10403019
  • 财政年份:
    2017
  • 资助金额:
    $ 28.19万
  • 项目类别:
"Core B" Viral RNA-seq and bioinformatics Core
“核心 B”病毒 RNA-seq 和生物信息学核心
  • 批准号:
    10646252
  • 财政年份:
    2017
  • 资助金额:
    $ 28.19万
  • 项目类别:

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