Cell Death Pathways: Beyond Apoptosis
Cell Death Pathways: Beyond Apoptosis
批准号:
8257455
负责人:
James Wavell Aiken
金额:
$1.0万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2011
资助国家:
美国
项目状态:
已结题
起止时间:
2011-09-30 至 2012-08-31
关键词:
AddressAdultAlberta provinceApoptosisAreaAutophagocytosisBioenergeticsBioinformaticsBiologyBiomedical ResearchCanadaCaspaseCell DeathCell Death InductionCellsCellular biologyCessation of lifeClinicalComplexDefectDegenerative DisorderDisabled PersonsDiseaseEnvironmentEventFamilyFunctional disorderGeneticInterventionJointsKnowledgeMalignant NeoplasmsMindMitochondriaModalityMolecularMolecular BiologyMutateNatureNerve DegenerationNeurosciencesNormal tissue morphologyOutcomePathogenesisPathway interactionsPeptide HydrolasesPersonal SatisfactionPhenotypePlayPostdoctoral FellowQuality ControlRegulationRelative (related person)Request for ProposalsResearchResearch PersonnelRoleScienceSignal PathwaySignal TransductionStudentsSystems BiologyTherapeuticWorkagedanticancer researchbasebench to bedsidecohortmeetingsmitochondrial dysfunctionneoplastic cellpreventresponsesymposiumtool
中文摘要
描述(由申请人提供):本提案请求支持由Serge Przedborski和Richard J.Youle组织的题为细胞死亡路径:超越细胞凋亡的Keystone研讨会,该会议将于2012年3月19-24日在加拿大艾伯塔省班夫举行。越来越多的证据表明,疾病中的细胞死亡是发生在退化细胞内(细胞自主)和退化细胞外(非细胞自主)的分子机制之间复杂相互作用的结果。在这些不同的信号通路的交叉点上发现了线粒体,它通过适当的线粒体动力学和自噬(即有丝分裂)调节线粒体的消除,在维持细胞的健康方面发挥着关键作用。本次会议将集中讨论细胞死亡的一般机制,包括Bcl-2家族和caspase蛋白酶,线粒体动力学和有丝分裂的作用,生物信息学在解开死亡途径方面的作用,非细胞自主机制对细胞死亡的贡献,以及防止细胞死亡的治疗策略。同时举行的线粒体动力学和功能会议将显著增加跨学科互动的机会,该会议将与本次会议举行一次主旨演讲和两次全体会议。
公共卫生相关性:在健康的成人中,每秒有100多万个细胞死亡,以避免多余的、异位的、受损的、老化的或突变的细胞积累。因此,细胞死亡及其调控对于许多层面的生物医学研究具有重要意义:对于了解正常组织生物学和许多疾病的发病机制,对于防止细胞不当死亡的药物干预,以及对肿瘤细胞的治疗性破坏。关于细胞死亡途径:超越细胞凋亡的Keystone研讨会将汇聚来自许多不同领域的研究人员,以促进关于细胞死亡可被操纵用于治疗目的的新想法。
英文摘要
DESCRIPTION (provided by applicant): This proposal requests support for a Keystone Symposia meeting entitled Cell Death Pathways: Beyond Apoptosis, organized by Serge Przedborski and Richard J. Youle, which will be held in Banff, Alberta, Canada from March 19 - 24, 2012. Mounting evidence indicates that cell death in diseases results from complex interactions between molecular mechanisms taking place within the degenerating cells (cell-autonomous) and outside the degenerating cells (non-cell autonomous). At the cross road of these diverse signaling pathways are found the mitochondria which, through proper mitochondrial dynamics and regulated mitochondrial elimination by autophagy (i.e., mitophagy), play a crucial role in maintaining the well-being of the cells. This meeting will focus on the general mechanisms of cell death including the Bcl-2 family and caspase proteases, the role of mitochondrial dynamics and mitophagy, the usefulness of bioinformatics to unravel death-pathways, the contribution of non-cell autonomous mechanisms to cell death, and on therapeutic strategies to protect against cell death. Opportunities for interdisciplinary interactions will be significantly enhanced by the concurrent meeting on Mitochondrial Dynamics and Function, which will share a keynote address and two plenary sessions with this meeting.
PUBLIC HEALTH RELEVANCE: In the healthy human adult, more than one million cells die each second to avoid the accumulation of superfluous, ectopic, damaged, aged or mutated cells. Hence, cell death and its regulation are of central importance for biomedical research at many levels: for understanding normal tissue biology and the pathogenesis of numerous diseases, for pharmacological interventions that prevent unwarranted cell death, as well as for the therapeutic destruction of tumor cells. The Keystone Symposia meeting on Cell Death Pathways: Beyond Apoptosis will bring together investigators from many distinct fields in order to facilitate new ideas regarding the means by which cell death can be manipulated for therapeutic purposes.
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