Results 321 to 330 of about 24,048,620 (390)

Astrocytic PERK Deficiency Drives Prefrontal Circuit Dysfunction and Depressive‐Like Behaviors

open access: yesAdvanced Science, EarlyView.
Chen et al. show that the endoplasmic reticulum (ER) stress sensor PERK is downregulated in prefrontal cortex (PFC) astrocytes in major depressive disorder and in chronic‐stress mouse models. In young mice, astrocyte‐specific PERK loss reduces the synaptogenic cue thrombospondin‐1 (TSP1), leading to synaptic and circuit deficits and depressive‐like ...
Kai Chen   +8 more
wiley   +1 more source

Nuclear Factor I‐B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription

open access: yesAdvanced Science, EarlyView.
This study identifies the transcription factor Nuclear Factor I‐B (NFIB) as a key suppressor of liver fibrosis. NFIB expression declines during hepatic stellate cell activation, and its overexpression reduces fibrosis in mice models. The mechanism involves NFIB directly repressing chemokine C─C motif ligand 5 (CCL5), thereby alleviating oxidative ...
Qianqian Chen   +14 more
wiley   +1 more source

Homoisoflavanone Delays Colorectal Cancer Progression via DNA Damage‐Induced Mitochondrial Apoptosis and Parthanatos‐Like Cell Death

open access: yesAdvanced Science, EarlyView.
Homoisoflavanone (HIF), a bioactive compound isolated from Polygonatum kingianum, selectively suppresses colorectal cancer progression by inducing DNA damage‐mediated mitochondrial apoptosis and parthanatos‐like cell death. HIF triggers mitochondrial dysfunction, including depolarized membrane potential, elevated ROS, and ATP depletion, while impairing
Hongjie Fan   +12 more
wiley   +1 more source

Development of Endogenous Protein Probes for Characterizing Surface Proteins and Cellular Interactors of Extracellular Vesicles

open access: yesAdvanced Science, EarlyView.
The proximity labeling enzyme APEX2 is displayed on extracellular vesicle (EV) surfaces via genetic fusion with EV‐sorting scaffolds, enabling in situ biotinylation of native surface proteins, adsorbed corona components, and interacting cellular proteins.
Wenyi Zheng   +5 more
wiley   +1 more source

Inhibition of SLC11A1‐Mediated Lysosomal Iron Accumulation in Microglia Promotes Repair Following White Matter Stroke

open access: yesAdvanced Science, EarlyView.
Genetic and pharmacological inhibition of SLC11A1 functioning as an H+/Fe2+ antiporter–mediated lysosomal iron accumulation in microglia promotes lysosomal lumen acidification, increases CTSD expression, enhances lysosomal myelin debris uptake and degradation, and promotes repair following white matter stroke. ABSTRACT White matter stroke (WMS) results
Lingling Qiu   +11 more
wiley   +1 more source

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