Cell Death

细胞死亡

• 批准号: 7329446
• 负责人: TERRI I. GRODZICKER
• 金额: $ 0.5万
• 依托单位: COLD SPRING HARBOR LABORATORY
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-09-14 至 2012-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7329446
• 关键词: Acquired Immunodeficiency Syndrome; Address; Apoptosis; Autoimmunity; Biochemical Pathway; Biochemical Process; Biochemical Reaction; Biochemistry; Biological Assay; Biological Models; Cell Cycle Regulation; Cell Death; Cell physiology; Cells; Cellular biology; DNA Damage; Development; Developmental Biology; Disease; Environment; Fostering; Genes; Goals; Homeostasis; Human; Infectious Disease Immunology; Invertebrates; Link; Lower Organism; Malignant Neoplasms; Mammals; Mitochondria; Molecular; Mutagenesis; Neurobiology; Neurodegenerative Disorders; Pathology; Pathway interactions; Proteins; Range; Receptor Signaling; Regulation; Regulator Genes; Research Personnel; Role; Scientist; Stroke; Tissues; Transcriptional Regulation; Tumor Suppressor Genes; Virus; Virus Diseases; Work; accomplished suicide; interest; novel therapeutics; posters; reconstitution; response; structural biology; symposium; tumorigenesis

DESCRIPTION (provided by applicant): Programmed Cell Death encompasses many molecular and biochemical processes that were evolutionarily selected to promote self-elimination of cells. Programmed cell death is required for normal development and tissue homeostasis. Abnormalities in the regulation of cell death contribute to a wide variety of human disorders, including cancer, AIDS, stroke, autoimmunity and neurodegenerative disorders. Most if not all cells have the capacity to commit suicide, and key components of various cell death programs have been conserved in lower organisms, thereby providing powerful model systems for study. Some of the genes that regulate programmed cell death include oncogenes and tumor suppressor genes, providing a link between deregulation of cell death pathways and cancer. Many viruses encode genes that promote or inhibit cell death, indicating that subversion of this cellular process is an aspect of the pathology of virus infections. Rapid advancements in recent years have led to the identification of numerous genes and gene products involved in controlling programmed cell death, and the biochemical pathways that regulate cell death have begun to emerge. New evidence strengthens the link between cell death mechanisms and mitochondrial energetics. Model systems have permitted directed mutagenesis of cell death regulatory genes mammals, invertebrates and lower organisms, demonstrating the role of cell death in a wide range of cellular responses and disease states. The development of cell-free assays and the reconstitution of biochemical reactions from purified components have served to delineate some of the details of cell death pathways. Researchers in the field of cell death are a diverse group whose interests span invertebrate to mammalian developmental biology, neurobiology, tumorigenesis, immunology, infectious diseases, biochemistry, cell biology, structural biology, cell cycle control, transcription regulation, receptor signaling and DNA damage pathways. The Cold Spring Harbor conference on Programmed Cell Death will be held on September 26-30, 2007. The objective of this conference is to bring together researchers working in the diverse aspects of programmed cell death and to facilitate new discoveries. The meeting plan includes an opening address, eight plenary and three poster sessions, in which participation by junior scientists will be facilitated. The overall goal is to create a meeting environment suitable for the open exchange of information and ideas that will foster advancement of the field toward a full understanding and development of new therapeutic approaches.

描述（由申请人提供）：程序性细胞死亡包括许多分子和生物化学过程，这些过程在进化上被选择以促进细胞的自我消除。细胞程序性死亡是正常发育和组织稳态所必需的。 细胞死亡调控的异常导致多种人类疾病，包括癌症、艾滋病、中风、自身免疫和神经退行性疾病。 大多数细胞（如果不是所有的话）都有自杀的能力，各种细胞死亡程序的关键组成部分在低等生物中被保存下来，从而为研究提供了强大的模型系统。 一些调控程序性细胞死亡的基因包括癌基因和肿瘤抑制基因，它们在细胞死亡途径的失调和癌症之间提供了联系。 许多病毒编码促进或抑制细胞死亡的基因，表明这种细胞过程的破坏是病毒感染病理学的一个方面。 近年来的快速进展已经导致鉴定了参与控制程序性细胞死亡的许多基因和基因产物，并且调节细胞死亡的生化途径已经开始出现。 新的证据加强了细胞死亡机制和线粒体能量学之间的联系。 模型系统已经允许对哺乳动物、无脊椎动物和低等生物的细胞死亡调节基因进行定向诱变，证明了细胞死亡在广泛的细胞反应和疾病状态中的作用。 无细胞分析的发展和纯化组分的生化反应的重建已经用于描绘细胞死亡途径的一些细节。 细胞死亡领域的研究人员是一个多元化的群体，其兴趣涵盖无脊椎动物到哺乳动物发育生物学、神经生物学、肿瘤发生、免疫学、传染病、生物化学、细胞生物学、结构生物学、细胞周期控制、转录调节、受体信号传导和DNA损伤途径。 关于细胞程序性死亡的冷泉港会议将于2007年9月26-30日举行。 本次会议的目的是汇集研究人员在程序性细胞死亡的各个方面的工作，并促进新的发现。 会议计划包括一次开幕词、八次全体会议和三次海报展示会，将为年轻科学家的参与提供便利。 总体目标是创造一个适合公开交流信息和想法的会议环境，促进该领域的发展，以充分理解和开发新的治疗方法。