Results 181 to 190 of about 1,231,329 (288)

An Enzyme‐Like Catalyzed Nanosheets for Redox Stress Oscillation Therapy Against Bacterial Infections

open access: yesAdvanced Science, EarlyView.
Bacterial biofilms form a physicochemical barrier. Their dense network structure and redox homeostasis confer high resistance to antimicrobial treatments and immune‐mediated killing and clearance. In this study, SnSe nanosheets with enzyme‐like properties and piezoelectric catalysis can oscillate to regulate bacterial redox homeostasis and improve the ...
Min Ge   +9 more
wiley   +1 more source

NIBAN2/FLII/RREB1 Axis Drives Glioma Stem Cell Malignancy via TLR3 Pathway Activation

open access: yesAdvanced Science, EarlyView.
NIBAN2, highly expressed in glioma stem‐like cells (GSCs), assembles with FLII and transcription factor RREB1 to form a nuclear complex. This complex transcriptionally activates stemness‐associated genes (e.g., CD44, NANOG) and metabolic enzymes (e.g., LDHA), thereby sustaining both transcriptional and metabolic stemness programs.
Liang liang Shi   +14 more
wiley   +1 more source

Cortical Somatostatin Neurons Regulate Seizure Susceptibility via MINAR1/Gαs–cAMP Signaling

open access: yesAdvanced Science, EarlyView.
Our study identifies MINAR1 as a novel regulator of cortical interneuron excitability and seizure susceptibility. MINAR1 is preferentially expressed in SST+ interneurons. Genetic ablation of MINAR1 leads to seizure hypersensitivity, reduced SST+ neuron excitability, and impaired Gαs–cAMP signaling, disrupting the E/I balance.
Wei‐Tang Liu   +20 more
wiley   +1 more source

RIPK3 Orchestrates Scar‐Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis

open access: yesAdvanced Science, EarlyView.
Beyond signaling cell death, RIPK3 emerges as a critical metabolic regulator in pulmonary fibrosis. This research reveals that RIPK3 promotes PI3K‐AKT signaling in scar‐associated macrophages to fuel polyamine synthesis, independent of its kinase activity.
Tao Yang   +12 more
wiley   +1 more source

Diabetes Mellitus Facilitates Gallstone Formation Through CXCR2‐NETs–Mediated Liver‐Bile Barrier Damage

open access: yesAdvanced Science, EarlyView.
Diabetes is an independent risk factor for gallstones. It upregulates CXCR2 expression in hepatic neutrophils, stimulating the formation of NETs that disrupt hepatocellular tight junctions and the liver‐bile barrier. NETs enter bile to accelerate gallstone development, while sarcosine inhibits CXCR2 and NETs production, effectively reducing diabetes ...
Chao Shi   +10 more
wiley   +1 more source

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