Results 221 to 230 of about 112,628 (307)

FUCA2 Sustains AKT Signaling and Suppresses Senescence by Antagonizing FUT3‐Mediated ErbB3 Fucosylation in Lung Adenocarcinoma

open access: yesAdvanced Science, EarlyView.
ABSTRACT While targeted therapies have improved outcomes in lung adenocarcinoma (LUAD), many patients still lack targetable mutations. Here, we identified alpha‐L‐fucosidase 2 (FUCA2) as a crucial driver of LUAD by preventing cellular senescence. Mechanistically, through the restriction of fucosyltransferase 3 (FUT3)‐mediated α‐1,3‐fucosylation of ...
Lu Chen   +18 more
wiley   +1 more source

Cyclic Mechanical Loading of Cardiomyocytes via Pressure‐Driven Non‐Planar Membrane Deformation in a Bioreactor System

open access: yesAdvanced Science, EarlyView.
In this research article, Mansoor and coworkers present a novel device that applies controlled mechanical stimuli to cardiomyocytes using pressure‐driven membrane deformation. By exposing cells to physiologically and pathologically relevant loading conditions, the platform reproduces distinct structural, functional and molecular responses associated ...
Haris Mansoor   +11 more
wiley   +1 more source

Sustainable Fabrication of Tailored Bone Substitutes: From High‐Throughput Scaffold Manufacturing, Scaled‐Up HMSC Expansion to Dynamic Cultivation in a Perfusion Bioreactor

open access: yesAdvanced Science, EarlyView.
ABSTRACT The demand for off‐the‐shelf biocompatible bone substitutes has driven the development of numerous independent in vitro technologies to generate products resembling physiological tissues. Due to technical challenges and overly simplified cultivation approaches/niches, the end‐products are often uniformly shaped and inferior to native bone ...
Franziska Braun   +10 more
wiley   +1 more source

Lilrb4a Suppression Reprograms Microglia to Mitigate APOE4‐Associated Amyloid Plaques and Cerebral Amyloid Angiopathy in Association With a PPAR‐Linked Pro‐Clearance State

open access: yesAdvanced Science, EarlyView.
Targeting Lilrb4a in Apolipoprotein E4 (APOE4)‐associated Alzheimer's disease (AD) reprograms microglia toward a beneficial, phagocytic state. Genetic deletion or antisense inhibition of Lilrb4a suppresses p‐SHP2/NF‐κB/STAT1 signaling, restores PPAR‐linked lipid and energy metabolism, and reduces amyloid plaque burden and cerebral amyloid angiopathy ...
Changxu Nie   +12 more
wiley   +1 more source

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