THE GROUP VIA CALCIUM-INDEPENDENT PHOSPHOLIPASE A2 PARTICIPATES IN ER STRESS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 由于细胞凋亡，β细胞的生长和死亡之间的平衡调节了β细胞的质量。我们以前曾报道，通过钙非依赖性磷脂酶A2(iPLA2β)抑制Ins-1胰岛素瘤细胞由thapsigarin诱导的内质网应激所致的细胞凋亡，并伴随神经酰胺生成水平的增加，并且在iPLA2β高表达的INS-1细胞(OE INS-1细胞)中，ER应激的影响被放大。

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. Beta-cell mass is regulated by a balance between beta-cell growth and beta-cell death, due to apoptosis. We previously reported that apoptosis of INS-1 insulinoma cells due to thapsigargin-induced ER stress was suppressed by inhibition of the group VIA Ca2+-independent phospholipase A2 (iPLA2beta), associated with an increased level of ceramide generation, and that the effects of ER stress were amplified in INS-1 cells in which iPLA2beta was overexpressed (OE INS-1 cells).