Results 211 to 220 of about 2,313,292 (299)

Secreted Nonstructural Protein 3 is a Pathogenic Determinant of Orbivirus

open access: yesAdvanced Science, EarlyView.
This study uncovers a conserved PIP2‐dependent secretory pathway of orbivirus NS3 that induces vascular leakage. Pharmacological disruption of PIP2‐NS3 interaction significantly reduces viral pathogenicity and provides protective efficacy in murine models, establishing PIP2‐mediated NS3 secretion as both a key virulence determinant and a promising ...
Junyong Guan   +11 more
wiley   +1 more source

RCSB Protein Data Bank: Delivering integrative structures alongside experimental structures and computed structure models. [PDF]

open access: yesNucleic Acids Res
Vallat B   +25 more
europepmc   +1 more source

A Dual‐Functional Biohybrid Nanorobot to Synergistically Eradicate Biofilm and Degrade Antibiotic Resistance Genes

open access: yesAdvanced Science, EarlyView.
A biohybrid nanorobot integrating lytic bacteriophage N4 with Pd nanozymes is developed for targeted eradication of multidrug‐resistant E. coli biofilms. Synergistic bacterial lysis and ROS‐mediated oxidation enable simultaneous biofilm removal and antibiotic resistance genes degradation, maintaining high efficacy in complex wastewater environments ...
Junzheng Zhang   +9 more
wiley   +1 more source

Chromosome-level genome assembly of masu salmon (Oncorhynchus masou masou). [PDF]

open access: yesSci Data
Wu B   +8 more
europepmc   +1 more source

Mechanosensitive Piezo1/Osteocalcin/Irisin Axis Protects Against Disuse‐Induced Muscle Atrophy

open access: yesAdvanced Science, EarlyView.
Mechanical unloading suppresses bone Piezo1 expression, which reduces circulating undercarboxylated osteocalcin (unOCN). unOCN reduction subsequently exacerbates IMM‐induced Fndc5/Irisin decrease and drives severe muscle atrophy. Bone Piezo1 activation or exogenous osteocalcin/Irisin ameliorate muscle atrophy, while muscle‐specific Gprc6a or Fndc5 ...
Zhaolu Wang   +5 more
wiley   +1 more source

A Viscous DES‐AAV‐Foxo1 Delivery System With High Transfection Efficiency for the Treatment of Corneal Endothelial Dysfunction by Restoring Mitochondria‐ER Contacts

open access: yesAdvanced Science, EarlyView.
High glucose triggers corneal endothelial dysfunction by impairing FOXO1‐mediated ITPR1 transcription, leading to disrupted mitochondria‐associated membrane (MAM) integrity and defective ER‐to‐mitochondria Ca2+ transfer. This study develops an innovative viscous DES‐AAV‐Foxo1 delivery system with enhanced transfection efficiency. This non‐invasive gene
Hongran Zhao   +10 more
wiley   +1 more source

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