Results 191 to 200 of about 9,299,804 (276)

A Spatiotemporal Single‐Cell Atlas Uncovers Dysregulated ECM Dynamics and Septal Remodeling Arrest in Human Ventricular Septal Defects

open access: yesAdvanced Science, EarlyView.
Integrating single‐cell and spatial transcriptomics reveals human ventricular septal defect (VSD) as a disease of microenvironmental insufficiency and structural remodeling arrest. Attenuated endothelial‐fibroblast crosstalk, alongside downregulated THBS1/TGF‐β1 and MMP2 signaling networks, impairs the endothelial‐to‐mesenchymal transition (EndoMT) and
Xiaoyuan Zhang   +9 more
wiley   +1 more source

USP4‐Dependent CHAF1B Stabilization Regulates Distinct SETDB1 Ubiquitin States Linked to AKT T308 Signaling and Lipogenic Remodeling in HCC

open access: yesAdvanced Science, EarlyView.
USP4 stabilizes CHAF1B by limiting K48‐linked ubiquitination. Stabilized CHAF1B supports UHRF1‐associated K63‐linked SETDB1 ubiquitination and cytoplasmic redistribution, whereas CHAF1B loss favors VHL‐dependent K11‐associated degradative ubiquitination and proteasomal loss of SETDB1.
Saiyan Bian   +9 more
wiley   +1 more source

Soil pH Amelioration Synergizes Carbon Accrual with Yield Gains Under Organic Substitution

open access: yesAdvanced Science, EarlyView.
Soil pH shifts towards neutrality in both acidic and alkaline soils under organic substitution. A global synthesis links pH amelioration to soil organic carbon accrual through enhanced microbial biomass after accounting for added organic carbon and its interaction with pH. This pH amelioration‐shared soil organic carbon accrual accounts for 5.1–8.6% of
Xunzhuo Dong   +7 more
wiley   +1 more source

PLOD1 Catalytic Activity Stabilizes ENO1 by Limiting FBXW7‐dependent Degradation to Promote Glycolysis and TMZ Resistance in Glioblastoma

open access: yesAdvanced Science, EarlyView.
PLOD1 interacts with ENO1 and limits its FBXW7‐dependent ubiquitination and proteasomal degradation through a mechanism requiring PLOD1 catalytic activity. ENO1 stabilization sustains glycolysis, promoting glioblastoma cell proliferation, migration, and temozolomide resistance.
Fen Xue   +4 more
wiley   +1 more source

Alkylating Agent–Induced FANCL Impairment Damages Pulmonary Arterial, Venous, and Microvascular Endothelial Cells and Predisposes to PAH/PVOD

open access: yesAdvanced Science, EarlyView.
This study establishes a novel cisplatin‐induced rat model of PAH/PVOD and identifies a conserved mechanistic axis—FANCL impairment, DNA damage accumulation, and endothelial dysfunction—triggered by cisplatin or mitomycin C across pulmonary arteries, veins, and microvessels.
Shiyun Liu   +20 more
wiley   +1 more source

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