作者: Michael W. Harr , Clark W. Distelhorst
DOI: 10.1007/978-1-60327-381-7_7
关键词: Cell biology 、 Mitochondrion 、 Chemistry 、 STIM1 、 Apoptosis 、 Calcium in biology 、 Unfolded protein response 、 Endoplasmic reticulum 、 Calcium signaling 、 Signal transduction
摘要: Virtually all organisms adapt to stress in order prolong their survival. At the subcellular level, endoplasmic reticulum (ER) responds by inducing ER-specific signaling pathways reestablish homeostasis between protein synthesis and processing, a mechanism called unfolded response (UPR). However, when cells endure persistent irreversible state of ER stress, they undergo apoptosis. Apoptosis initiated at is distinct from mitochondrial or death receptor-mediated apoptosis but may involve require cross-talk intrinsic extrinsic pathways. Two functions are facilitate maturation newly synthesized proteins maintain stores intracellular calcium. Therefore, induced frequently characterized perturbations processing transport and/or loss calcium homeostasis. Additionally, because mitochondria reside close proximity one another, pro- antiapoptotic proteins, such as Bcl-2 family members, localize regulate stress. This chapter summarizes key associated with cell survival apoptotic context aberrant signaling.