Results 211 to 220 of about 14,115 (284)

NIBAN2/FLII/RREB1 Axis Drives Glioma Stem Cell Malignancy via TLR3 Pathway Activation

open access: yesAdvanced Science, EarlyView.
NIBAN2, highly expressed in glioma stem‐like cells (GSCs), assembles with FLII and transcription factor RREB1 to form a nuclear complex. This complex transcriptionally activates stemness‐associated genes (e.g., CD44, NANOG) and metabolic enzymes (e.g., LDHA), thereby sustaining both transcriptional and metabolic stemness programs.
Liang liang Shi   +14 more
wiley   +1 more source

CD3ɛ Nanobody‐Engineered Extracellular Vesicles Driving In Vivo Generation of TCE‐secreting CAR‐Ts for Solid Tumor Therapy With Memory Response and Minimal Immunogenicity

open access: yesAdvanced Science, EarlyView.
HEK‐293T‐derived CD3ε Nb‐engineered EVs to generate dual‐targeting CAR‐T cells directly in vivo. These EVs selectively deliver CAR.BiTE transgenes into T cells and reprogramed to HLA‐G/PD‐L1‐targeting effector cells with enhanced memory and persistence.
Shi‐Wei Huang   +27 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

PD‐L1‐Binding Antigen Presenters: Redirecting Vaccine‐Induced Antibodies for Cancer Immunotherapy

open access: yesAdvanced Science, EarlyView.
The PBAP‐gE complex anchors gE antigen to PD‐L1 on tumor cells. Vaccine‐induced anti‐gE antibodies simultaneously engage FcγRIIIa on NK cells and tumor‐bound PBAP‐gE, triggering NK cell activation and antibody‐dependent cellular cytotoxicity, thereby selectively eliminating PD‐L1–expressing tumor cells.
Huixin Gao   +24 more
wiley   +1 more source

miR‐135a‐5p Is a Promising Target to Prevent the Glomerulosclerosis Associated with Podocyte Developmental Toxicity in Offspring Induced by Prenatal Dexamethasone Exposure

open access: yesAdvanced Science, EarlyView.
Prenatal dexamethasone exposure (PDE) programs persistent podocyte developmental injury and adult glomerulosclerosis. Mechanistically, glucocorticoid receptor (GR) binds the miR‐135a‐5p promoter and recruits the histone acetyltransferase p300, increasing promoter histone acetylation and sustaining miR‐135a‐5p expression. Elevated miR‐135a‐5p suppresses
Xiaoqi Zhao   +8 more
wiley   +1 more source

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