Results 151 to 160 of about 23,920 (329)

Dual Targeting of Mutant p53 and SNRPD2 via Engineered Exosomes Modulates Alternative Splicing to Suppress Ovarian Cancer

open access: yesAdvanced Science, EarlyView.
Mutant p53 drives oncogenic splicing to promote the progression of ovarian cancer by partnering with the spliceosome factor SNRPD2. Therefore, it is engineered iRGD‐exosomes to co‐deliver siRNAs against both targets. This approach restored tumor‐suppressive mRNA isoforms, effectively enhanced sensitivity to cisplatin, and ultimately blocked tumor ...
Wei Zhao   +14 more
wiley   +1 more source

Label‐Free Molecular Characterization of Protein Aggregates in Differentiated Astrocytes

open access: yesAdvanced Science, EarlyView.
Mid‐infrared photothermal microscopy enables label‐free structural, molecular, and functional imaging of protein aggregates in astrocyte cells. The processes of astrocytes differentiated on a nanomaterial interface are characterized by α‐helical signatures combined with enhanced interfacial thermal resistance properties, while the cell soma of non ...
Panagis D. Samolis   +9 more
wiley   +1 more source

The Microbiota Shapes Central Nervous System Myelination in Early Life

open access: yesAdvanced Science, EarlyView.
Gut microbiota shapes brain development by regulating myelination and glial cell maturation in early life. Using germ‐free (GF) mice and zebrafish, this study reveals sex‐ and age‐dependent effects on myelin growth, integrity, and related gene expression.
Caoimhe M. K. Lynch   +13 more
wiley   +1 more source

Arginine Methylation Antagonizes TEAD3‐Mediated Repression to Promote Osteogenic Differentiation by Disrupting RUNX2‐Sequestrating Condensates

open access: yesAdvanced Science, EarlyView.
In the unmethylated state, TEAD forms stable, repressive condensates that sequester the osteogenic master regulator RUNX2. Arginine methylation of TEAD at R55 acts as a molecular brake, dissolving these condensates to release RUNX2 and activate the osteogenic program.
Lei Cao   +6 more
wiley   +1 more source

Selenoprotein H Functions as a PPARα Coactivator to Link Selenium Homeostasis to Hepatic Lipid Metabolism and Protect against Steatohepatitis

open access: yesAdvanced Science, EarlyView.
Our study identifies selenium deficiency as a hallmark of MASH pathogenesis. Dietary selenium supplementation enhances hepatic fatty acid oxidation (FAO) and attenuates MASH progression by activating the PPARα pathway via selenoprotein H (SELENOH). This selenium‐SELENOH‐PPARα nexus redefines the functional scope of selenoproteins, moving from redox ...
Yuwei Zhang   +11 more
wiley   +1 more source

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