2023年7月3日,中国科学院动物研究所唐铁山团队和北京基因组所郭彩霞团队在Cell & Bioscience上发表了题为“ER Ca2+overload activates the IRE1α signaling and promotes cell survival”的文章,揭示了内质网钙过载在UPR激活过程中的重要作用,发现TMCO1是IRE1α的一个新调节因子,为进一步理解IRE1α活化提供了新的见...
The overloaded ER Ca2+in TMCO1-deficient cells can cause BiP dissociation from IRE1α, promote the dimerization and stability of the IRE1α protein, and boost IRE1α activation. Intriguingly, attenuation of the over-activated IRE1α-XBP1s signaling by a IRE1α inhibitor can cause a ...
ER Ca2 overload activates the IRE1α signaling and promotes cell survival Background: Maintaining homeostasis of Ca2 stores in the endoplasmic reticulum (ER) is crucial for proper Ca2 signaling and key cellular functions. Altho... S Zhao,H Feng,D Jiang,... - 《Cell & Bioscience》 被引量:...
intracellular Ca2+to the ER. In addition, it is thought that ER stress is affected by ER communication with membrane-less organelles. The roles of the UPR and ER-phagy (autophagy of the ER) for the turnover of the different components in cell homeostasis and their dysregulation in disease c...
ER Ca2 depletion triggers apoptotic signals for endoplasmic reticulum (ER) overload response induced by overexpressed reticulon 3 (RTN3/HAP)Ersheng Kuang a... Kuang E, Wan Q, Li X, Xu H, Liu Q, Qi Y. ER Ca(2+) depletion triggers apoptotic signals for endoplasmic reticulum (ER) overlo...
Maintenance of Ca2+ER homeostasis may play an important role in the cellular antioxidant defense mechanism.10 The increase in the [Ca2+]Cyto level after [Ca2+]ER store depletion, besides affecting the activation of caspase-12, might induce as a secondary effect a mitochondrial Ca2+ overload and...
Strikingly, the final outcome of a PML functional loss at the cellular level is similar to the one observed in cells over- expressing Bcl-2 or lacking of Bax/Bak (albeit through a completely different molecular mechanism): a reduced mitochondrial Ca2 þ overload upon pro-apoptotic stimuli ...
Although Ca2+ uptake by the mitochondria can activate oxidative metabolism and promote cell survival, dysregulated release of ER Ca2+ initiates programmed cell death by several mechanisms including mitochondrial Ca2+ overload, depolarization, ATP loss, generation of reactive oxygen species, and cytochrome...
In proliferating cells with high anabolic demand, mitochondrial fission predominates over mitochondrial fusion, MERCS can help determine mitochondrial morphology and allow efficient transfer of Ca2+ and other metabolites to mitochondria during proliferation. The accumulation of cells that have entered cell ...
6H-K, M). This finding is similar to previous observations in nonmalignant cells (hepatocytes, neurons, and podocytes) that GRP75-silencing attenuates [Ca2+]m overload in conditions of oxidative stress [26, 29, 56, 57]. However, three distinct points should be clarified: (1) CP-induced ...