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FASEB SRC on Protein Aggregation, from Structural Variants to in Vivo Sequela

FASEB SRC on Protein Aggregation, from Structural Variants to in Vivo Sequela
FASEB SRC 关于蛋白质聚集,从结构变异到体内后遗症
批准号:
9752814
负责人:
Christina Sigurdson
金额:
$1.5万
依托单位国家:
美国
项目类别:
财政年份:
2019
资助国家:
美国
项目状态:
已结题
起止时间:
2019-06-01 至 2020-05-31

项目摘要

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中文摘要
翻译
项目摘要 蛋白质聚集是与多种神经系统和全身性疾病相关的关键特征, 衰老,但分子机制,在疾病中的确切作用,以及抑制或逆转聚集的治疗, 形成仍然知之甚少。最近的研究表明,蛋白质聚集和自我- 组装可能是正常细胞组织和调节的关键组成部分,这就提出了一个问题: 这些“功能组装”过程是受控的,以及为什么疾病相关的聚集没有减轻, 同样的方式。这项R13提案寻求FASEB夏季研究会议的核心支持, 聚集,从结构变异到体内后遗症”。第十二届会议在一系列开始, 1995年,我们的计划旨在利用蛋白质,系统和方法的广度,以促进 我们对与蛋白质聚集和组装有关的各种生物现象的理解, 最终干预这些过程的目标。该会议将于6月6日在科罗拉多州斯诺马斯举行 9 - 14日,2019年,并将提供一个论坛,介绍和讨论新出现的进展, 建立合作关系,以应对该领域的重大挑战。小尺寸(通常 150名与会者),并创新性地代表了全方位的研究 正常细胞功能和疾病中的聚集和自组装提供了独特的机会, 捕捉和整合这一过程的复杂性,并协同推进该领域。
英文摘要
Project summary Protein aggregation is a key feature associated with a wide range of neurological and systemic diseases of aging, yet the molecular mechanisms, precise role in disease, and therapy to inhibit or reverse aggregate formation remain poorly understood. Recent discoveries have shown that protein aggregation and self- assembly may be a key component of normal cellular organization and regulation, raising the question of how these ‘functional assembly’ processes are controlled, and why disease-related aggregation is not alleviated in the same way. This R13 proposal seeks core support for a FASEB Summer Research Conference on “Protein Aggregation, from Structural Variants to In Vivo Sequela”. The twelfth conference in a series that began in 1995, our program seeks to leverage the breadth of proteins, systems, and approaches available to advance our understanding of the full range of biological phenomena linked to protein aggregation and assembly with the goal of ultimately intervening in these processes. The conference will be held in Snowmass, CO, on June 9th-14th, 2019, and will provide a forum for the presentation and discussion of newly arising advances and for establishing collaborative relationships to address the grand challenges in the field. The small size (typically 150 participants) of this conference and its innovative representation of the full range of research on aggregation and self-assembly in both normal cellular function and disease provides a unique opportunity to capture and integrate the complexity of this process and synergistically advance the field.
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会议论文
Determining pathogenic PrPC-induced signaling pathways in human iPSC-induced neurons
Mechanisms of Prion Spread and Neuronal Toxicity
Molecular basis of prion protein-induced neurodegeneration
Molecular basis of prion protein-induced neurodegeneration
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