Activation of the unfolded protein response of the endoplasmic reticulum (UPRER) by aberrant Ca2+ signals (A21*)

内质网（ER）是蛋白质折叠、脂质代谢和Ca2+稳态的关键细胞器。这些功能在本质上是相互联系的。这些功能的任何扰动都可能引起内质网应激，并随之激活未折叠蛋白反应（UPR）。本项目旨在确定异常Ca2+信号激活UPR的机制，并建立UPR换能器信号相互作用的分子规则。使用先进的细胞器和最先进的脂质组学的免疫分离协议，应激内质网和异常Ca2+信号的脂质指纹应建立与亚细胞分辨率。

The endoplasmic reticulum (ER) is a key organelle of protein folding, lipid metabolism, and Ca2+ homeostasis. These functions are intrinsically connected to each other. Perturbation with any of these functions can cause ER-stress and followed by an activation of the unfolded protein response (UPR). This project aims to identify the mechanism of UPR activation by aberrant Ca2+ Signals and to establish the molecular rules underlying signal interaction by UPR transducers. Using sophisticated protocols for the immuno-isolation of organelles and state-of-the-art lipidomics, the lipid fingerprints of a stressed ER and of aberrant Ca2+ signals shall be established with subcellular resolution.