Results 121 to 130 of about 43,432 (263)
TKI treatment promotes mitochondrial fission and metabolic reprogramming toward oxidative phosphorylation in residual EGFR‐mutant lung cancer cells. Targeting this metabolic vulnerability restores TKI sensitivity and provides a promising strategy to overcome acquired resistance.
Yu Zhao +8 more
wiley +1 more source
Dissection of Mitochondrial Function via Chemical Perturbation and Single‐Cell Profiling
We establish a systematic framework to dissect mitochondrial function at the module level by combining targeted chemical perturbations with scRNA‐seq. This approach reveals shared and module‐specific programs linking mitochondrial activity to mito‐nuclear communication, stress response, and cell cycle, highlighting the tight coupling between ...
Hao Luo +4 more
wiley +1 more source
In hyperuricemia, uric acid inhibits CCDC90B ubiquitination degradation by binding to it. Excessive CCDC90B induces mitochondrial calcium overload, leading to mitochondrial quality control imbalance and ultimately resulting in SLC senescence and decreased testosterone levels.
Jiayu Huang +8 more
wiley +1 more source
Excessive mechanical stress induces nucleus pulposus cell pyroptosis and intervertebral disc degeneration. Itgb1 inhibits MNAT1‐mediated ubiquitination and degradation of Vimentin. Vimentin alleviates excessive mechanical stress‐induced nucleus pulposus cell pyroptosis and intervertebral disc degeneration through PINK1‐Parkin‐dependent mitophagy ...
Xuening Liu +7 more
wiley +1 more source
Targeting m6A Modifications Regulating Ferroptosis Offers Novel Therapy in Diseases
m6A RNA modification regulates ferroptosis by balancing iron metabolism, lipid peroxidation, and antioxidant defenses. Dysregulated m6A signaling disrupts pro‐ and anti‐ferroptotic factors, leading to excess ROS, Fe3+ accumulation, and lipid peroxidation–driven cell death. Targeting m6A‐mediated ferroptotic regulation represents a promising therapeutic
Lida Du +7 more
wiley +1 more source
Proteostasis ensures proper protein folding, modification, and degradation, while its impairment triggers ER stress. Chronic ER stress and maladaptive UPR via the CHOP–ERO1 axis remodel ERMCs, altering calcium signaling and mitochondrial metabolism.
Giorgia Maria Renna +5 more
wiley +1 more source
Proteostasis of organelles in aging and disease
Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi +5 more
wiley +1 more source
Methods to Study Mitochondrial Metabolism and Homeostasis in Fission Yeast
Yeast, EarlyView.
Ferran Gómez‐Armengol +2 more
wiley +1 more source
GCN2 in proteostasis: structural logic, signalling networks and disease
Threats to protein synthesis activate the kinase GCN2, initiating the integrated stress response (ISR). GCN2 is triggered by stalled ribosomes and uncharged tRNAs, which accumulate when amino acids are scarce. The ISR adjusts cellular physiology by promoting redox balance, protein quality control, and mitochondrial optimisation.
JiaYi Zhu, Stefan J. Marciniak
wiley +1 more source
Exercise‐related microRNAs cel‐miR‐249‐3p and cel‐miR‐77‐5p in C. elegans regulate lifespan, fitness, mitochondrial morphology and membrane potential. Although lacking direct mammalian orthologs, H2O2‐induced microRNAs mmu‐miR‐181a‐5p and mmu‐miR‐378a‐3p regulate myogenesis, autophagy, mitochondrial content and respiration in murine myoblasts ...
Qin Xia +7 more
wiley +1 more source

