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Identifying synergistic therapeutic targets in RA using systems biology

Identifying synergistic therapeutic targets in RA using systems biology
利用系统生物学确定 RA 的协同治疗靶点
批准号：
9164023
负责人：
GARY S FIRESTEIN
金额：
$20.46万
依托单位：
UNIVERSITY OF CALIFORNIA, SAN DIEGO
依托单位国家：
美国
项目类别：
财政年份：
2016
资助国家：
美国
项目状态：
已结题
起止时间：
2016-09-15 至 2018-06-30
来源：
https://reporter.nih.gov/project-details/9164023
关键词：
AffectArthritisBehavioral MechanismsBiological AssayCartilage MatrixCell AdhesionCell LineCellsComputer SimulationDNA MethylationDataData SetDiseaseDrug TargetingEnvironmental Risk FactorEpigenetic ProcessFibroblastsGene ExpressionGene Expression RegulationGene ProteinsGenesGeneticImmune responseInvadedJointsLightMeasuresMesenchymalMethodsModelingMolecular ProfilingNetwork-basedNormal CellPathogenesisPathway interactionsPatientsPatternPhenotypePlayRegulationRheumatoid ArthritisRoleSynovitisSystems BiologyTestingTherapeuticTrainingWorkabstractingbasecomputer based statistical methodseffective therapyexperienceimprintimprovedjoint destructionjoint injuryknock-downnetwork modelsnew therapeutic targetnovelresearch studyrisk varianttherapeutic targettranscriptome sequencingtranscriptomicstumor

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中文摘要
翻译
摘要 类风湿关节炎(RA)关节损害和滑膜炎症受遗传因素影响 以及环境因素。在我们之前的研究中，我们已经确定了一组基因和 通过将DNA甲基化数据与 转录组学和类风湿性关节炎风险基因数据。在这些结果的基础上，我们将构建一个基因 由RA相关基因组成的网络，其表达谱代表RA的发病机制。 我们将开发一种新的系统生物学方法来寻找协同治疗靶点 这个基因网络。一旦完成，这项拟议的工作不仅将确定药物目标 对类风湿关节炎的有效治疗也有助于理解其调节机制 疾病的形成。
英文摘要
Abstract Joint damage and synovial inflammation in rheumatoid arthritis (RA) are influenced by genetic and environmental factors. In our previous studies, we have identified a panel of genes and pathways that could be targeted for RA by integrating DNA methylation data with transcriptomics and RA risk gene data. Built upon these results, we will construct a gene network composed of RA relevant genes whose expression profiles represent RA pathogenesis. We will develop a novel systems biology method to search for synergistic therapeutic targets in this gene network. Once completed, this proposed work will not only identify drug targets for effective treatment of RA but also shed light into understanding the regulatory mechanisms of disease formation.
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