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。 由于细胞凋亡，β细胞质量受β细胞生长和β细胞死亡之间的平衡调节。我们以前报道过，由于毒胡萝卜素诱导的内质网应激，INS-1胰岛素瘤细胞的凋亡受到VIA组钙非依赖性磷脂酶A2（iPLA 2 β）抑制的抑制，与神经酰胺生成水平的增加有关，并且内质网应激的影响在iPLA 2 β过表达的INS-1细胞（OE INS-1细胞）中被放大。

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).