Phenotypic characterization of itm2a-deficiency in T cells
T 细胞 itm2a 缺陷的表型特征
基本信息
- 批准号:8424870
- 负责人:
- 金额:$ 8.69万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2012
- 资助国家:美国
- 起止时间:2012-02-15 至 2014-01-31
- 项目状态:已结题
- 来源:
- 关键词:AffectAntibodiesAutoimmune DiseasesBacteriaBiological MarkersBiologyCell Differentiation processCellsClinicalDataDevelopmentDiseaseGene TargetingGoalsImmuneIntegral Membrane ProteinInvadedLaboratoriesLeadLeukocytesLupusMediatingMolecularMouse StrainsMultiple SclerosisMusOrganPathway interactionsPeripheralPhenotypePhysiologicalPlayProcessProteinsPsoriasisPublishingReagentRheumatoid ArthritisRoleSurfaceT-LymphocyteTh2 CellsTherapeuticThymocyte DevelopmentViruscrosslinkneoplastic cellnovelpathogentherapeutic targetthymocytetranscription factor
项目摘要
DESCRIPTION (provided by applicant): T lymphocytes (T cells) are a subset of white blood cells and are essential for eradicating invading bacteria, virus, and tumor cells. However, T cells can also initiate and propagate many autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, psoriasis, and lupus, if their function is not regulated properly. Better understanding of how the development and function of T cells is regulated can lead to novel treatments for many diseases. Preliminary data gathered at Dr. Ho's laboratory has suggested that a novel protein, namely itm2a, plays a critical role in regulating the development and function of T cells. In this project, Dr. Ho's team plans to study the impact of itm2a deficiency on T cells. Results generated from this project will establish itm2a as a rich therapeutic target in many clinical settings.
描述(由申请人提供):T淋巴细胞(T细胞)是白细胞的一个亚群,对于根除入侵的细菌、病毒和肿瘤细胞是必不可少的。然而,如果T细胞的功能调节不当,它们也可以启动和传播许多自身免疫性疾病,如类风湿性关节炎、多发性硬化症、牛皮癣和狼疮。更好地了解T细胞的发育和功能是如何调节的,可以为许多疾病带来新的治疗方法。何博士实验室收集的初步数据表明,一种名为ITM2A的新蛋白质在调节T细胞的发育和功能方面发挥着关键作用。在这个项目中,何博士的团队计划研究ITM2A缺陷对T细胞的影响。该项目产生的结果将使ITM2A在许多临床环境中成为丰富的治疗靶点。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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I-CHENG HO其他文献
I-CHENG HO的其他文献
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{{ truncateString('I-CHENG HO', 18)}}的其他基金
Regulatory roles of peptidylarginine deimination in elastogenisis
肽基精氨酸脱亚胺化在弹性生成中的调节作用
- 批准号:
10442830 - 财政年份:2022
- 资助金额:
$ 8.69万 - 项目类别:
Regulatory roles of peptidylarginine deimination in elastogenisis
肽基精氨酸脱亚胺化在弹性生成中的调节作用
- 批准号:
10605290 - 财政年份:2022
- 资助金额:
$ 8.69万 - 项目类别:
Functional analysis of SIRPG, a T cell-specific autoimmune gene
T细胞特异性自身免疫基因SIRPG的功能分析
- 批准号:
10425493 - 财政年份:2022
- 资助金额:
$ 8.69万 - 项目类别:
Functional analysis of SIRPG, a T cell-specific autoimmune gene
T细胞特异性自身免疫基因SIRPG的功能分析
- 批准号:
10557874 - 财政年份:2022
- 资助金额:
$ 8.69万 - 项目类别:
Proteome-wide assessment of the impact of citrullination on the activityof transcription factors in Th2 cells
瓜氨酸化对 Th2 细胞转录因子活性影响的全蛋白质组评估
- 批准号:
10493375 - 财政年份:2021
- 资助金额:
$ 8.69万 - 项目类别:
Proteome-wide assessment of the impact of citrullination on the activityof transcription factors in Th2 cells
瓜氨酸化对 Th2 细胞转录因子活性影响的全蛋白质组评估
- 批准号:
10349195 - 财政年份:2021
- 资助金额:
$ 8.69万 - 项目类别:
Causes and Roles of Hypercitrullination in Preclinical Rheumatoid Arthritis
临床前类风湿性关节炎中瓜氨酸过度化的原因和作用
- 批准号:
9980794 - 财政年份:2017
- 资助金额:
$ 8.69万 - 项目类别:
Causes and Roles of Hypercitrullination in Preclinical Rheumatoid Arthritis
临床前类风湿性关节炎中瓜氨酸过度化的原因和作用
- 批准号:
10218058 - 财政年份:2017
- 资助金额:
$ 8.69万 - 项目类别:
Phenotypic characterization of itm2a-deficiency in T cells
T 细胞 itm2a 缺陷的表型特征
- 批准号:
8227163 - 财政年份:2012
- 资助金额:
$ 8.69万 - 项目类别:
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