Results 141 to 150 of about 46,487 (267)

TANC1::HTRA1 fusion in schwannomas

open access: yes
Brain Pathology, EarlyView.
Ilay Caliskan   +3 more
wiley   +1 more source

Proteostasis of organelles in aging and disease

open access: yesThe FEBS Journal, EarlyView.
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

GCN2 in proteostasis: structural logic, signalling networks and disease

open access: yesThe FEBS Journal, EarlyView.
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

Spatiotemporal dynamics of β‐arrestin‐mediated Src activation in 5‐HT7 receptor signaling pathway

open access: yesThe FEBS Journal, EarlyView.
GPCRs induce distinct cellular responses via G protein‐ or β‐arrestin‐mediated signaling pathways. This study revealed that β‐arrestin‐biased 5‐HT7R ligand induces slow, sustained Src activation, contrasting with transient G protein‐mediated activation.
Hyunbin Kim   +8 more
wiley   +1 more source

Biogenesis of TNF‐α‐insights into proteostasis and inflammation

open access: yesThe FEBS Journal, EarlyView.
TNF‐α biogenesis, trafficking, and signalling are tightly and reciprocally coupled to cellular proteostasis systems, including ER chaperones and endoplasmic reticulum‐associated degradation. This bidirectional crosstalk determines whether TNF‐α responses are adaptive or proteotoxic.
Bailasan Haidar   +3 more
wiley   +1 more source

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