Results 181 to 190 of about 939,121 (301)
RNF213 is characterized as a dual‐functional antiviral effector. It directly mediates the degradation of the influenza A virus nucleoprotein (NP) while simultaneously activating the MDA5‐mediated innate immune signaling pathway. This coordinated response establishes a powerful host defense system against viral infection. ABSTRACT Influenza A virus (IAV)
Haoning Li +5 more
wiley +1 more source
Identification of Pathogenic Bacteria from Public Libraries via Proteomics Analysis. [PDF]
Jung RH +4 more
europepmc +1 more source
RETREG1‐Mediated Reticulophagy is Essential for Dendritic Cell Maturation and Function in Sepsis
Reticulophagy regulator 1 (RETREG1) maintains dendritic cell (DC) maturation and function in early sepsis. Mechanistically, activating transcription factor 6 (ATF6) acts as a direct transcription factor regulating RETREG1 expression in response to sepsis‐induced endoplasmic reticulum (ER) stress.
Ren‐Qi Yao +28 more
wiley +1 more source
Prediction of health information-seeking behavior components based on health anxiety among users of public libraries. [PDF]
Musarezaie N +3 more
europepmc +1 more source
LMO7 Suppresses Tumor‐Associated Macrophage Phagocytosis of Tumor Cells Through Degradation of LRP1
LMO7 in tumor‐associated macrophages suppresses phagocytosis of tumor cells and limits cytotoxic T lymphocytes infiltration, fostering tumor progression. Mechanistically, LMO7 mediates the ubiquitination and degradation of the phagocytic receptor LRP1, impairing its ability to engulf tumor cells and driving macrophages toward an antitumor phenotype ...
Mengkai Li +12 more
wiley +1 more source
"Our Doors Are Open to Everybody": Public Libraries as Common Ground for Public Health. [PDF]
Morgan AU +4 more
europepmc +1 more source
This study identifies B4GALNT4 as a key driver of prostate cancer (PCa). It shows that B4GALNT4 glycosylates PDK1 protein at the N531 site, which stabilizes the PDK1 and constitutively activates the PI3K‐AKT pathway. This mechanism promotes tumor cell proliferation, migration, and invasion. The findings establish the B4GALNT4‐PDK1 glycosylation axis as
Shaoqin Jiang +12 more
wiley +1 more source
CDK4/6 inhibition promotes CD8+ T cell expansion through tumor‐macrophage crosstalk by activating HIF‐1α and enhancing MIF‐CD44/CD74 signaling. This reprograms TAMs to boost MHC‐I antigen presentation, and CDK4/6 inhibitor‐trained M1 TAM supernatant therapy synergizes with low‐dose PD‐1 blockade to restore antitumor immunity.
Lin He +17 more
wiley +1 more source

