EFFECTS OF ENDOPLASMIC RETICULUM STRESS ON GROUP VIA PHOSPHOLIPASE A2

内质网应激对磷脂酶 A2 组的影响

• 批准号: 8361443
• 负责人: JOHN W TURK
• 金额: $ 0.81万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361443
• 关键词: Apoptosis; Arachidonic Acids; Blood Vessels; Cells; Funding; Glycerophospholipids; Grant; Hydrolysis; Lysophospholipids; Mass Spectrum Analysis; Membrane; Muscle Cells; National Center for Research Resources; Nonesterified Fatty Acids; Phospholipase A2; Phospholipases A; Phospholipids; Positioning Attribute; Principal Investigator; Process; Reporting; Research; Research Infrastructure; Resources; Source; Transcriptional Regulation; United States National Institutes of Health; biomedical resource; cost; endoplasmic reticulum stress; human PLA2G6 protein; inhibitor/antagonist; insulin secretion

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The Group VIA phospholipase A(2) (iPLA(2)¿) hydrolyzes glycerophospholipids at the sn-2-position to yield a free fatty acid and a 2-lysophospholipid, and iPLA(2)¿ has been reported to participate in apoptosis, phospholipid remodeling, insulin secretion, transcriptional regulation, and other processes. Induction of endoplasmic reticulum (ER) stress in ¿-cells and vascular myocytes with SERCA inhibitors activates iPLA(2)¿, resulting in hydrolysis of arachidonic acid from membrane phospholipids, by a mechanism that is not well understood.

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 该组通过磷脂酶A(2)(iPLA(2)？)将sn-2-位的甘油磷脂水解成游离脂肪酸和2-溶血磷脂，已有报道ipla(2)？参与细胞凋亡、磷脂重塑、胰岛素分泌、转录调节等过程。用SERCA抑制剂诱导内质网(ER)应激可激活iPLA(2)，导致膜磷脂中花生四烯酸的水解，其机制尚不清楚。