Results 191 to 200 of about 468,211 (255)

Cortical Somatostatin Neurons Regulate Seizure Susceptibility via MINAR1/Gαs–cAMP Signaling

open access: yesAdvanced Science, EarlyView.
Our study identifies MINAR1 as a novel regulator of cortical interneuron excitability and seizure susceptibility. MINAR1 is preferentially expressed in SST+ interneurons. Genetic ablation of MINAR1 leads to seizure hypersensitivity, reduced SST+ neuron excitability, and impaired Gαs–cAMP signaling, disrupting the E/I balance.
Wei‐Tang Liu   +20 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

Oral Celastrol Nanomedicine Targeting Intestinal Antigen‐Presenting Cells to Effectively Mitigate Autoimmune Uveitis via Gut‐Retina Axis

open access: yesAdvanced Science, EarlyView.
Oral nanoCEL exhibits effective intestinal targeting of antigen‐presenting cells and restores the Th17/Treg balance in lymph nodes and spleen, ultimately protecting the blood‐retinal barrier by inhibiting peripheral immune cell infiltration and suppressing retinal glial cell activation.
Jinrun Chen   +13 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

Don Alcibíades Santa Cruz

open access: yesAtenea (Concepción), 1944
openaire   +1 more source

Cellular Identity Crisis: RD3 Loss Fuels Plasticity and Immune Silence in Progressive Neuroblastoma

open access: yesAdvanced Science, EarlyView.
Researchers discovered that therapy‐induced loss of RD3 protein in neuroblastoma triggers a dangerous shift: cancer cells become more stem‐like, invasive, and resistant to treatment while evading immune detection. RD3 loss suppresses antigen presentation and boosts immune checkpoints, creating an immune‐silent environment.
Poorvi Subramanian   +7 more
wiley   +1 more source

Microglial GPR35 Ameliorates Epileptogenesis and Neuroinflammation via PDGFA Domain 2 Signaling

open access: yesAdvanced Science, EarlyView.
Activation of microglial G protein–coupled receptor 35 (GPR35) by L‐kynurenic acid (L‐Kyna) initiates a platelet‐derived growth factor A (PDGFA)–dependent phosphoinositide 3‐kinase–protein kinase B (PI3K–AKT) signaling cascade that dampens hippocampal neuroinflammation, thereby restraining epileptogenesis, lowering seizure susceptibility, and ...
Qi Wang   +17 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

The UCSC Genome Browser database: 2026 update. [PDF]

open access: yesNucleic Acids Res
Casper J   +21 more
europepmc   +1 more source

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