2014 Notch Signaling in Development & Disease Gordon Research Conference/Seminar

2014 Notch Signaling 开发中

基本信息

批准号：
8716109
负责人：
Stephen C. Blacklow
金额：
$ 0.9万
依托单位：
GORDON RESEARCH CONFERENCES
依托单位国家：
美国
项目类别：
财政年份：
2014
资助国家：
美国
起止时间：
2014-05-10 至 2015-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8716109
关键词：
Academia Address Adult Alagille Syndrome Alzheimer&apos s Disease Animal Model Antibodies Area Attention Biology Boxing CADASIL Cancer Biology Chronic Clinical Collaborations Communication Communities Development Developmental Biology Developmental Cell Biology Disease Drosophila genus Drug Industry Dysostoses Education Environment Event Exposure to Faculty Future Goals Health Heart Valves Human In Vitro Industry International Lead Leadership Life Location Maine Malignant Neoplasms Mediator of activation protein Memory Mentors Multiple Sclerosis Muscular Dystrophies Natural regeneration Nature Notch Signaling Pathway Onset of illness Organ Organism Outcome Participant Pathology Pathway interactions Peptide Hydrolases Physics Physiology Play Postdoctoral Fellow Regulation Reliance Research Research Personnel Retina Role Scientist Signal Pathway Signal Transduction Students Syndrome System Technology Therapeutic Thinking Time Tissues Toxic effect Training Travel Work abstracting aortic valve disorder base body system cancer initiation cancer prevention career cell type cohesion college cost drug development experience frontier gain of function genome-wide graduate student human disease in vivo inhibitor/antagonist interest intestinal epithelium loss of function malformation meetings notch protein novel novel therapeutics posters programs public health relevance secretase stem cell biology success symposium tumor

项目摘要

DESCRIPTION (provided by applicant): The second Notch Signaling in Development, Regeneration & Disease meeting, to be held July 19-25, 2014 at Bates College, Maine, will address an unmet need in the scientific community, both academic and industrial. The broad and long-term goal of this conference is to enhance cross-disciplinary discussions and collaborations in this rapidly expanding field and to better address the myriad of mechanistic, developmental, organismal, clinical and therapeutic challenges met by practitioners in the field. The Notch signaling pathway is a central mediator of short-range inter-cellular communication in metazoans, under study since 1917 in Drosophila, in other model organisms since the 1980's, and in human health since 1991. More recent studies have established that alterations in Notch activity underlie several developmental syndromes (Alagille's Syndrome, Spondylocostal Dysostosis, aortic valve disease), adult onset diseases (CADASIL, various heart and valve malformations, muscular dystrophy, multiple sclerosis) and cause or contribute to cancer initiation, promotion or progression in a tissue-dependent manner. These pathologies reflect both loss of function (e.g., Alagille's, CADASIL) and gain of function (e.g., cancer). Because the Notch signaling pathway is unique in its reliance on proteases, in the paucity of signal modulators, and because it is repeatedly used in many organs throughout adult life, the road to chronic management of Notch signaling in disease is obscured by many untoward outcomes with available therapies. The main strategy currently practiced in anti-tumor campaigns is based on g-secretase inhibitors or antagonistic antibodies; however, due to their indiscriminate inhibition of Notch receptors in all organs, toxicity upon chronic administration remains a formidable challenge. Expanding the interest in this pathway beyond developmental biology and cancer prevention is the realization that a great hurdle in Alzheimer's disease research is the difficulty in developing reliable Notch-sparing g-secretase inhibitors capable of inhibiting APP cleavage. Solving these puzzles requires "outside the box" thinking. The Specific Aims for this interdisciplinary yet pathway-focused meeting is to bring together a diverse community of scientists working in every model organism and on nearly every organ system from academia, biotech and the pharmaceutical industry. The participants represent diverse approaches to study Notch function and regulation in normal and pathological contexts, which will further facilitate discovery and drug development efforts. The 40 projected speakers represent a blend of established world leaders with vast institutional memory and future leaders with exciting new findings to present. Significantly, the informal and confidential environment in Gordon conferences (GRCs), and the time provided for informal interactions, will create a forum in which cutting edge technologies, ideas and discoveries can be freely exchanged, stimulating new ideas. Most importantly, the combined GRC/GRS format excels in integrating students, postdocs and investigators wishing to enter a new field, such as the study of this important signaling pathway.

描述（由申请人提供）：第二届发育、再生和疾病中的 Notch 信号传导会议将于 2014 年 7 月 19 日至 25 日在缅因州贝茨学院举行，将解决科学界（学术界和工业界）未满足的需求。本次会议的广泛和长期目标是加强这个快速扩展领域的跨学科讨论和合作，并更好地解决该领域从业者遇到的无数机械、发育、组织、临床和治疗挑战。 Notch 信号通路是后生动物中短程细胞间通讯的核心介体，自 1917 年以来一直在果蝇中进行研究，自 20 世纪 80 年代以来在其他模式生物中进行研究，自 1991 年以来在人类健康中进行研究。最近的研究已经证实，Notch 的改变活动是多种发育综合征（阿拉吉尔综合征、脊椎肋骨发育不全、主动脉瓣疾病）、成人发病疾病的基础（CADASIL、各种心脏和瓣膜畸形、肌营养不良、多发性硬化症）并以组织依赖性方式导致或促成癌症的发生、促进或进展。这些病理反映了功能丧失（例如阿拉吉尔氏病、CADASIL）和功能获得（例如癌症）。由于Notch信号通路的独特之处在于它对蛋白酶的依赖、信号调节剂的缺乏，并且由于它在成年后的许多器官中被重复使用，因此在疾病中对Notch信号通路进行长期管理的道路被许多不良后果所掩盖。可用的疗法。目前抗肿瘤的主要策略是基于g-分泌酶抑制剂或拮抗抗体；然而，由于它们对所有器官中的Notch受体不加区别的抑制，长期给药的毒性仍然是一个艰巨的挑战。人们认识到阿尔茨海默病研究的一大障碍是难以开发出能够抑制 APP 裂解的可靠的、保留 Notch 的 g 分泌酶抑制剂，从而将人们对这一途径的兴趣扩展到发育生物学和癌症预防之外。解决这些难题需要“跳出框框”思维。这次跨学科但以途径为重点的会议的具体目标是汇集来自学术界、生物技术和制药行业的各种模型生物和几乎每个器官系统的不同科学家群体。参与者代表了研究正常和病理背景下 Notch 功能和调节的不同方法，这将进一步促进发现和药物开发工作。预计的 40 位演讲者包括拥有丰富机构记忆的知名世界领导人和将展示令人兴奋的新发现的未来领导人。值得注意的是，戈登会议 (GRC) 的非正式和保密环境以及提供的非正式互动时间将创建一个论坛，让尖端技术、想法和发现可以自由交流，激发新想法。最重要的是，GRC/GRS 组合格式擅长整合希望进入新领域（例如这一重要信号通路的研究）的学生、博士后和研究人员。