Stress Proteins in Growth, Development & Disease 2007Gordon Research Conference

所有生物都暴露于应激条件下，包括环境应激，如高温和辐射，生理应激，如代谢反应引起的氧化应激，或病理生理应激，如药理学作用，感染和炎症。这些应激条件导致蛋白质错误折叠、聚集、细胞功能障碍和细胞死亡。最近的研究强烈表明，通过激活信号转导途径、转录因子和在蛋白质稳态中起作用的基因产生来感知和响应应激信号的能力，对于正常生长、发育和预防包括癌症、心血管疾病和蛋白质折叠疾病（如阿尔茨海默氏病、亨廷顿氏病和朊病毒疾病）在内的疾病至关重要。此外，模型系统的研究已经建立了寿命与建立强大的应激反应能力之间的强烈相关性。会议将强调该领域的许多前沿进展，包括对自噬途径在应激条件下重塑细胞的重要性的日益认识，以及对使用建模方法在系统水平上理解应激调节的日益重视。“生长、发育和疾病中的应激蛋白”戈登研究会议将于2007年8月19日至24日在英国牛津的马德伦学院举行。组织者是Peter Walter，主席（加州大学旧金山分校）和Bernd Bukau，副主席（海德堡大学分子生物学中心）。我们将着重讨论以下方面的最新进展：应激感应、信号和基因表达、蛋白质构象疾病、应激基因在代谢、生长和发育中的作用、应激基因对感染的调节、应激细胞生物学以及应激在衰老中的作用。计划举行8次会议，其中大部分为新研究者、实习生和最近取得的突破预留了演讲机会。迄今为止，所有受邀的33位演讲者（其中42%是女性）都已确认有意参加。演讲者、博士后和研究生之间将有大量的机会进行详细的、非正式的讨论，在海报会议和会议期间的额外时间，以加强互动和信息传递。本申请要求为戈登研究会议提供部分支持。本次会议将加深我们对应激信号，应激蛋白的功能和作用机制，以及应激在人类健康，疾病和衰老中的作用的理解。细胞采用各种机制来帮助保护它们免受所有生物体不断暴露的压力，包括环境压力，如高温和辐射，生理压力，如代谢反应引起的氧化应激，或病理生理压力，如药物作用，感染和炎症。这种压力条件的分子后果是蛋白质错误折叠，细胞功能障碍和细胞死亡，表现为衰老和多种人类疾病。

DESCRIPTION (provided by applicant): GRC on Stress Proteins in Growth, Development and Disease All organisms are exposed to stressful conditions including environmental stresses such as elevated temperatures and irradiation, physiological stress such as oxidative stress due to metabolic reactions, or pathophysiological stresses such as pharmacological agents, infection and inflammation. These stressful conditions lead to protein misfolding, aggregation, cellular dysfunction and cell death. Recent studies strongly suggest that the ability to sense and respond to stress signals, through the activation of signal transduction pathways, transcription factors and gene productions that function in protein homeostasis is critical for normal growth, development and in the protection against diseases that include cancer, cardiovascular disease and protein folding diseases such as Alzheimer's Huntington's and prion-based disease. Furthermore, studies in model systems have established a strong correlation between longevity and the ability to mount robust stress responses. The meeting will highlight the many cutting- edge advances in the field, including the mounting appreciation of the importance of autophagy pathways to remodel cells under stress conditions and the increasing emphasis on using modeling approaches to understand stress regulation at a systems level. This Gordon Research Conference on "Stress Proteins in Growth, Development and Disease" will be held August 19-24, 2007 at Magdelan College in Oxford, UK. The organizers are Peter Walter, Chair (University of California, San Francisco), and Bernd Bukau, Vice-Chair (Universit¿t Heidelberg, Zentrum f¿r Molekulare Biologie). We will emphasize vigorous discussions of recent developments in stress sensing, signaling and gene expression, diseases of protein conformation, roles of stress genes in metabolism, growth and development, stress gene modulation of infection, the cell biology of stress and the roles of stress in aging. Eight sessions are planned, most with speaking opportunities reserved for new investigators, trainees and recent breakthroughs. All 33 speakers invited to date, of which 42% are women, have confirmed their intention to attend. There will be abundant opportunities for detailed, informal discussions among speakers, postdoctoral fellows and graduate students at poster sessions and additional times during the meeting to enhance interactions and information transmission. This application requests partial support for this Gordon Research Conference. GRC on Stress Proteins in Growth, Development and Disease This meeting will enhance our understanding of stress signaling, stress protein function and mechanism of action, and the role of stress in human health, disease and in aging. Cells employ various mechanisms that help protect them from stresses to which all organisms are constantly exposed, including environmental stresses such as elevated temperatures and irradiation, physiological stress such as oxidative stress due to metabolic reactions, or pathophysiological stresses such as pharmacological agents, infection and inflammation. The molecular consequences of such stressful conditions are protein misfolding, cellular dysfunction, and cell death, manifesting itself as aging and a multitude of human diseases.