Results 121 to 130 of about 97,183 (266)

The E3 Ligase RNF115 Aggravates Pathological Cardiac Hypertrophy via Ubiquitin‐Mediated Degradation of SPTBN1

open access: yesAdvanced Science, EarlyView.
In response to hypertrophic stimuli, increased c‑JUN phosphorylation upregulates RNF115, leading to SPTBN1 ubiquitination and degradation. which promotes F‑actin depolymerization and YAP activation, driving cardiac hypertrophy. The RNF115 inhibitor DTD effectively suppresses SPTBN1 ubiquitination and cardiac hypertrophy.
Yan Zu   +12 more
wiley   +1 more source

Single‐Cell Reveal GALNT7‐Dependent Ferroptosis Suppression as a Mechanism of Immunotherapy Resistance in Non‐Small Cell Lung Cancer

open access: yesAdvanced Science, EarlyView.
Integrated clinical and mechanistic analyses identify GALNT7 as a ferroptosis‐suppressive regulator associated with immunotherapy resistance in non‐small cell lung cancer. GALNT7 depletion promotes lipid peroxidation, mitochondrial dysfunction, and ferroptosis, enhances CD8+ T‐cell activation and IFN‐γ production, and sensitizes tumors to PD‐1 blockade,
Jiadi Gan   +11 more
wiley   +1 more source

Membrane Fusion‐Mediated Cytosolic Delivery of Threose Nucleic Acids via Homotypic Nanoparticles Overcomes Drug Resistance in Triple‐Negative Breast Cancer

open access: yesAdvanced Science, EarlyView.
This study introduces a biomimetic “nanofusion” platform that integrates the biostability of threose nucleic acids (TNA) with homotypic cell‐membrane cloaking to combat drug‐resistant TNBC. By leveraging a non‐canonical membrane‐fusion pathway for direct cytosolic delivery, the platform bypasses endosomal sequestration. To achieve potent AKT2 silencing
Wei Zheng   +7 more
wiley   +1 more source

Single‐Cell RNA Editing Identifies T Cell ADAR1 as a Key Regulator of Immune Exhaustion and Anti‐PD‐1 Resistance in Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
Single‐cell RNA editing analysis identifies ADAR1 as a regulator of dysfunctional T cell states in colorectal cancer. Elevated ADAR1 activity promotes T cell exhaustion and impairs antitumor immunity partly through TGF‐β‐SMAD signaling, contributing to anti‐PD‐1 resistance and highlighting T cell ADAR1 as a potential therapeutic target and biomarker ...
Da Kang   +10 more
wiley   +1 more source

Cholesterol Laundry of Cell Membrane and Fatty Liver by Detergent Liposomes to Improve Anti‐Cancer Drug Responsiveness of Patient Liver Tissues

open access: yesAdvanced Science, EarlyView.
Cholesterol‐enriched plasma membranes in hepatocellular carcinoma impede drug penetration. Cholesterol (+)‐liposomes act as membrane‐specific detergents, extracting cholesterol and reducing barrier function without cytotoxicity. Following endocytosis, cholesterol transfers from endosomes to liposomes and is metabolized in the ER.
Chansik Kim   +9 more
wiley   +1 more source

Engineered Au@CeO2 Hybrid Nanoparticles With Microenvironment Dependent Self‐Adjustability for Integration of Tumor‐Specific Photothermal‐Chemodynamic Therapy and Inflammation Prevention

open access: yesAdvanced Science, EarlyView.
An intelligent Au@CeO2 Hybrid Nanoparticles (ACEF) with microenvironment‐dependent self‐adjustability was engineered to not only perform efficient and tumor‐specific photothermal‐chemodynamic therapy for precise tumor elimination, but also serve as a ROS scavenger in healthy tissues around the tumor to avoid the unexpected oxidative damage and ...
Wenyun Mu   +8 more
wiley   +1 more source

Targeting Lipopolysaccharide Transport Induces Membrane Lipid Remodeling and Sensitizes Acinetobacter baumannii to Colistin Treatment

open access: yesAdvanced Science, EarlyView.
This study identifies C4 as a lead inhibitor of the Lpt system. Notably, C4 potentiates colistin activity by disrupting LPS transport and remodeling phospholipid homeostasis, revealing a functional interplay between the Lpt and Mla systems. These findings establish a mechanistic link between Lpt inhibition and membrane lipid remodeling, positioning Lpt–
Jianya Luo   +6 more
wiley   +1 more source

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