Results 201 to 210 of about 418,423 (300)

CD9+ B Cells Induce T Follicular Helper Cell Apoptosis to Regulate Germinal Center Regression

open access: yesAdvanced Science, EarlyView.
A unique subset of CD9+ B cells regulates germinal center B (GC‐B) cell regression by inducing T follicular helper (Tfh) cell apoptosis through multiple signaling pathways, such as ALCAM‐CD6. FOXP1 plays a key role in GC‐B cell differentiation. These findings clarify mechanisms of GC degeneration and termination and offer potential targets for adenoid ...
Wenjing Liao   +27 more
wiley   +1 more source

An Anti‐Amyloidogenic Approach to Specifically Block Memory Consolidation in Mice for Therapeutic Intervention

open access: yesAdvanced Science, EarlyView.
Functional amyloid conversion of the translation regulator CPEB3 is essential for long‐term memory persistence. This study demonstrates that targeting this molecular switch with the anti‐amyloidogenic peptide QBP1 selectively blocks CPEB3 fibrillation without disrupting phase separation.
Paula López‐García   +13 more
wiley   +1 more source

Physical Origin of Temperature Induced Activation Energy Switching in Electrically Conductive Cement

open access: yesAdvanced Science, EarlyView.
The temperature‐induced Arrhenius activation energy switching phenomenon of electrical conduction in electrically conductive cement originates from structural degradation within the biphasic ionic‐electronic conduction architecture and shows percolation‐governed characteristics: pore network opening dominates the low‐percolation regime with downward ...
Jiacheng Zhang   +7 more
wiley   +1 more source

An Adipocyte MKK3–p38β Axis Preserves Insulin Responsiveness in Mice and Is Reciprocally Altered in Human Obesity

open access: yesAdvanced Science, EarlyView.
The adipocyte MKK3–p38β axis emerges as an adaptive stress‐response pathway during obesity. Human visceral adipose tissue analyses, adipocyte‐specific mouse models, and primary adipocytes show that the MKK3–p38β axis supports insulin responsiveness by restraining p70S6K‐dependent inhibitory IRS1 feedback and preserving AKT–GLUT4 signaling. This pathway
Edgar Bernardo   +20 more
wiley   +1 more source

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