CSHL 2022 Protein Homeostasis in Health and Disease Conference

冷泉港实验室会议 健康与疾病中的蛋白质稳态 2022年4月26日至30日 摘要 该提案是为一次关于蛋白质稳态的会议提供财政支持的请求。 健康与疾病将于2022年4月26日至30日在冷泉港实验室举行。 这次会议是介绍这一领域新成果的首要国际论坛， 参加会议的有来自该领域几乎所有主要实验室的代表。爆炸 关于蛋白质折叠状态如何在体内获得和维持的新信息， 这一过程与健康老龄化和神经变性，癌症， 新陈代谢保证了这次会议的兴奋和紧迫。因为最近 关于衰老和疾病中压力信号的发展，我们将以这个新的 第二天的会议是关于衰老中的蛋白质聚集的会议， 神经退行性疾病，然后结束会议， 衰老和疾病中的蛋白质稳态。其他会议将讨论以下方面的关系： 蛋白质合成、折叠、转运和降解的分子机制 分子伴侣功能的机制，降解机制和空间质量控制， 细胞器蛋白质稳态会议还将介绍另一个关于压力的新会议 颗粒和相变带来了许多关于应激生理学的新概念， 调节生物学和大分子相互作用的新形式。这些基本问题 是蛋白质稳定生物学的核心， 以及蛋白质错误折叠疾病中的蛋白质稳态失败，包括阿尔茨海默病，ALS， 帕金森病和亨廷顿病。衰老、蛋白质稳定失败和 蛋白质错误折叠的疾病在整个会议中得到了很好的整合， 蛋白质客户端相互作用和替代蛋白质构象的原则将是 主要展示。区室使用的不同蛋白质质量控制策略 以确保分泌和细胞器途径的完整性， 蛋白质折叠应力将由空间质量控制的新兴主题表示， cell.热休克蛋白和分子伴侣的领域呈指数增长， 它不仅吸引了基础科学中传统科学学科的兴趣， 生物医学研究的不同领域，包括神经退行性疾病，传染病， 癌症、心脏病和衰老。会议将有八个讲座，两个海报 会议期间，两次快速演讲会和一次关于科学出版的小组讨论会。 会议包括：1）生物学，衰老和疾病中的综合应激信号; 2）蛋白质 衰老和神经退行性疾病中的聚集; 3） 分子伴侣; 4）自噬和蛋白酶体降解机制; 5）内源性 失调蛋白质、相变和应激颗粒; 6）核糖体折叠和 分类机制; 7）衰老和衰老中的细胞器蛋白质稳态和空间质量控制 疾病;和8）恢复衰老和疾病中的蛋白质稳态。每届会议将包括八个 将由一名特邀发言者主持。一般来说，两名发言人将 每届会议预先邀请，其余部分从提交的摘要中选出，因此约60- 65%的演讲者将来自提交的摘要，以确保初级研究者的平衡， 妇女和各种形式的多样性。同时，我们将有两个快速射击会议，每个10 -2 分钟讲座，以提高海报会议的知名度。这种谈判的平衡使 会议的特点介绍了领先的科学家，以响应令人兴奋的新 发展，并鼓励承认新的调查人员的多元化参与。

Cold Spring Harbor Laboratory Conference on Protein Homeostasis in Health and Disease April 26 - 30, 2022 ABSTRACT This proposal is a request for financial support for a meeting on PROTEIN HOMEOSTASIS IN HEALTH AND DISEASE to be held at Cold Spring Harbor Laboratory from April 26 - 30, 2022. This meeting is the premier international forum for presentation of new results in this area, and is attended by representatives from virtually every major laboratory in the field. The explosion of new information on how the folded state of proteins is acquired and maintained in vivo and the relevance of this process to healthy aging and risk for diseases of neurodegeneration, cancer, and metabolism guarantees an excitement and urgency of this meeting. Because of the recent developments on stress signaling in aging and disease, we will open the meeting with this new session followed the next day with a session on protein aggregation in aging and neurodegenerative diseases and then closing the meeting with a session on correcting proteostasis in aging and disease. Additional sessions will address the relationship between protein synthesis, folding, translocation and degradation by discussing the molecular mechanisms of chaperone function, degradative mechanisms and on spatial quality control and organellar proteostasis. The meeting will also introduce another new session on stress granules and phase transitions that has brought many new concepts on stress physiology, regulatory biology and novel forms of macromolecular interaction. These fundamental questions are at the heart of biology of proteostasis that will be complemented by the sessions on aging and proteostasis failure in diseases of protein misfolding including Alzheimer's disease, ALS, Parkinson's disease and Huntington's disease. The themes of aging, proteostasis failure, and diseases of protein misfolding are well integrated throughout the meeting, and emerging principles on protein client interactions and alternate protein conformations will be predominantly displayed. The diverse protein quality control strategies used by compartments of the cell to ensure the integrity of the secretory and organellar pathways during times of protein folding stress will be represented by emerging topics on spatial quality control within a cell. The field of heat shock proteins and molecular chaperones has grown exponentially and draws interest not only from traditional scientific disciplines in the basic sciences but also from diverse areas of biomedical research including neurodegenerative disease, infectious diseases, cancer, heart disease and aging. The meeting will have eight lecture sessions, two poster sessions, two rapid-fire presentation sessions, and a panel discussion on scientific publishing. The sessions include: 1) Integrative Stress Signaling in Biology, Aging and Disease; 2) Protein Aggregation in Aging and Neurodegenerative Diseases; 3) Molecular Mechanisms of Chaperones; 4) Mechanisms of Autophagy and Proteasome Degradation; 5) Intrinsically Disorder Proteins, Phase Transitions and Stress Granules; 6) Folding at the Ribosome and Triage Mechanisms; 7) Organellar Proteostasis and Spatial Quality Control in Aging and Disease; and 8) Restoring Proteostasis in Aging and Disease. Each session will consist of eight to nine oral presentations and will be chaired by an invited speaker. Generally, two speakers will be pre-invited per session with the remainder to be selected from submitted abstracts, thus ~60- 65% of speakers will be from submitted abstracts to ensure balance of junior investigators, women and all forms of diversity. As well, we will have two rapid fire sessions, each with ten-2 min. talks to increase the visibility from the poster sessions. This balance of talks allows the meeting to feature presentations by leading scientists, to be responsive to exciting new developments, and to encourage diverse participation that recognizes new investigators.