ATTENUATED FREE CHOLESTEROL LOADING-INDUCED APOPTOSIS BUT PRESERVED PHOSPHLIPID

游离胆固醇负荷诱导的细胞凋亡减弱但磷脂保留

• 批准号: 7953977
• 负责人: S BAO
• 金额: $ 0.12万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-02-01 至 2010-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7953977
• 关键词: Apoptosis; Attenuated; Cholesterol; Computer Retrieval of Information on Scientific Projects Database; Exhibits; Funding; Grant; Institution; Knockout Mice; Mass Spectrum Analysis; Mus; Phospholipases A; Research; Research Personnel; Resources; Source; Stress; United States National Institutes of Health; biomedical resource; cell type; human PLA2G6 protein; macrophage

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. Previous studies suggest that Group VIA Phospholipase A(2) (iPLA(2)beta) participates in ER-stress induced apoptosis, and mouse macrophages undergo ER stress and apoptosis upon free cholesterol loading (FCL). We recently generated iPLA(2)beta-null mice, and here we demonstrate that iPLA(2)beta-null macrophages have reduced sensitivity to FCL-induced apoptosis, although they and wild-type (WT) cells exhibit similar increases in the transcriptional regulator CHOP.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 先前的研究表明，VIA族磷脂酶A（2）（iPLA（2）β）参与ER应激诱导的细胞凋亡，并且小鼠巨噬细胞在游离胆固醇负荷（FCL）时经历ER应激和细胞凋亡。我们最近产生了iPLA（2）β-null小鼠，在这里我们证明iPLA（2）β-null巨噬细胞对FCL诱导的凋亡的敏感性降低，尽管它们和野生型（WT）细胞在转录调节因子CHOP中表现出类似的增加。