Results 181 to 190 of about 26,469 (297)

Astrocytic Phenotypic Switching in Posterior Piriform Cortex Orchestrates Bone Cancer Pain–Depression Comorbidity via Purinergic–Noradrenergic Signaling

open access: yesAdvanced Science, EarlyView.
Bone cancer pain and depression share a common origin: astrocytic A2‐to‐A1 transition in the posterior piriform cortex. This phenotypic shift disrupts the ATP–adenosine–A2AR–norepinephrine axis, simultaneously driving nociceptive and affective dysfunction.
Jiang‐Ping Liu   +14 more
wiley   +1 more source

TME/NIR Dual‐Responsive Zinc‐Based Targeted Nanoagonist for Multimodal Amplification of STING‐Mediated Cancer Immunotherapy

open access: yesAdvanced Science, EarlyView.
A multifunctional nanoagonist (cDZ@IP) enables nano‐metabolite–driven multimodal activation of the STING pathway and enhanced immune recognition, achieving potent antitumor immunity and suppressing tumor growth and metastasis. This strategy highlights the rational design of therapeutic metabolites and establishes a new paradigm bridging nanomedicine ...
Kepeng Hu   +17 more
wiley   +1 more source

Nonclinical Considerations for Support of Pregnancy and Lactation in Clinical Trials. [PDF]

open access: yesBirth Defects Res
Stanislaus D   +18 more
europepmc   +1 more source

Disruption of the SNRPF–DDX24–E2F4 Feedback Loop Uncouples Splicing and Transcriptional Regulation to Suppress Ovarian Cancer Progression

open access: yesAdvanced Science, EarlyView.
This study identifies SNRPF as a critical oncogenic driver in ovarian cancer. By regulating a self‐sustaining SNRPF–DDX24–E2F4 feedback loop through intron retention and nonsense‐mediated decay, SNRPF couples RNA splicing with transcriptional regulation to promote tumor progression.
Yingwei Li   +4 more
wiley   +1 more source

Early Detection and Inhibition of Post‐Surgical Cancer Recurrence by Synthetic Extracellular Vesicles

open access: yesAdvanced Science, EarlyView.
An implantable hydrogel is designed to hold gene transfection agents engineered to turn early recurrent tumor cells into generators of synthetic EVs. These synthetic EVs can express engineered miR‐26a (E‐miR‐26a) for highly sensitive detection and PD‐1 (a PD‐L1‐blocking agent) for therapeutic intervention, thereby enabling early detection and ...
Junli Zhang   +7 more
wiley   +1 more source

Brain and Liver Dual‐Targeting Oridonin Nanoparticles to Enhance Aβ Clearance for Alzheimer's Disease Therapy

open access: yesAdvanced Science, EarlyView.
We developed a nanoparticle named OAF, which simultaneously targeted to both the brain and liver via the transferrin receptor 1 (TfR1) receptor, promoting lipoprotein receptor‐related protein 1 (LRP1) expression to enhance amyloid‐beta (Aβ) clearance. In AD mice model, OAF significantly reduced Aβ deposition and cognitive impairment, while a mitigating
Wenshuai Gong   +8 more
wiley   +1 more source

Dual Cytoplasmic and Chloroplastic Mechanisms Fine‐Tune Chloroplast Division through ARC3 Protein Stability

open access: yesAdvanced Science, EarlyView.
ARC3 levels are controlled by cytosolic and chloroplast proteolytic systems. PUB52 mediates ARC3 precursor ubiquitination and degradation in the cytosol, while CLPC1 promotes ARC3 degradation in chloroplasts, where ARC2 protects ARC3 from excessive breakdown. Disrupting these components causes chloroplast division defects, placing them upstream of ARC3.
Yang Yuan   +5 more
wiley   +1 more source

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

BIN1 and ALDH1B1 Deficiency in Colonic Smooth Muscle Drives Mitochondrial Dysfunction and Fibrosis in Slow‐Transit Constipation

open access: yesAdvanced Science, EarlyView.
Slow‐transit constipation (STC) is a disabling motility disorder with unclear smooth‐muscle mechanisms. Spatial proteomic analysis of STC patient colon reveals both the central pathogenic role of smooth muscle cells (SMCs) in STC and novel regulators of intestinal motility, BIN1 and ALDH1B1.
Jianbo Liu   +10 more
wiley   +1 more source

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