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CELL FREE APOPTOSIS--FACTORS AND MECHANISMS

CELL FREE APOPTOSIS--FACTORS AND MECHANISMS
无细胞凋亡--因素和机制
批准号：
6138478
负责人：
DONALD DAVID NEWMEYER
金额：
$20.86万
依托单位：
LA JOLLA INSTITUTE FOR IMMUNOLOGY
依托单位国家：
美国
项目类别：
财政年份：
1997
资助国家：
美国
项目状态：
已结题
起止时间：
1997-01-01 至 2001-06-30
来源：
https://reporter.nih.gov/project-details/6138478
关键词：
DNA Xenopus oocyte affinity chromatography alternatives to animals in research antibody apoptosis biological models cell cycle cell free system ceramides cytoplasm enzyme activity model design /development molecular cloning protease inhibitor protein degradation protein kinase protooncogene

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DESCRIPTION (adapted from investigator's abstract): The investigator has developed a novel cell -free system based on extracts from eggs of the frog, Xenopus laevis. Such egg extracts are able to reproduce many of the features of apoptosis, including chromatin condensation, endonucleolytic DNA cleavage and the shrinkage and fragmentation of the nuclei. Lysates from baculovirus-infected cells expression the oncogene bcl-2 can suppress nuclear fragmentation. This system provides an excellent means to dissect the molecular mechanisms of apoptosis and protective function of bcl-2. The applicant proposes to identify and characterize some of the cytoplasmic events of apoptosis. Such cell-free systems offer the opportunity to reconstitute the apoptotic process from fractionated components.
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ACTIVATION OF MITOCHONDRIAL OUTER MEMBRANE PERMEABILIZATION BY BH3-ONL
Mitochondria, apoptosis and the Bcl-2 family
  • 批准号：
    8077521
  • 项目类别：
  • 资助金额：
    $8.49万
  • 财政年份：
    2010
  • 负责人：
    DONALD DAVID NEWMEYER
  • 依托单位：
    LA JOLLA INSTITUTE FOR IMMUNOLOGY
ACTIVATION OF MITOCHONDRIAL OUTER MEMBRANE PERMEABILIZATION BY BH3-ONL
ACTIVATION OF MITOCHONDRIAL OUTER MEMBRANE PERMEABILIZATION BY BH3-ONL
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