DOWNREGULATION OF AUTOPHAGY BY HERPESVIRUS BCL-2 HOMOLOGS

疱疹病毒 BCL-2 同源物下调自噬

• 批准号: 7715511
• 负责人: Chang-Seng Liang
• 金额: $ 3.24万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-06-05 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7715511
• 关键词: Acquired Immunodeficiency Syndrome; Apoptosis; Autophagocytosis; Cells; Computer Retrieval of Information on Scientific Projects Database; Down-Regulation; Funding; Grant; Herpesviridae; Homologous Gene; Institution; Pathogenesis; Pathway interactions; Proteins; Research; Research Personnel; Resources; Role; Satellite Viruses; Simplexvirus; Source; Staging; United States National Institutes of Health; Viral; Virus; Virus Diseases; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The critical role of the cellular autophagy pathway in viral infection and pathogenesis has become increasingly apparent. Mounting evidences suggest that viruses have developed different strategies to meticulously modulate intracellular autophagy for their own benefits, thereby either promoting efficient viral replication or facilitating viral persistence. While our understanding of these strategies is still in its incipient stage, recent advances demonstrate that gamma herpesvirus Bcl-2 homolog (vBcl-2), which protects virus-infected cells from apoptosis, also suppresses cellular autophagy pathway through its direct interaction with autophagy protein Beclin1. Intriguingly, vBcl-2 has evolved to harbor the enhanced anti-autophagic activity compared to its host counterpart, suggesting an important role of cellular autophagy in response to viral infection and virus-associated pathogenesis. AIDS related.

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