Results 181 to 190 of about 169,468 (266)

Ubiquitination of ACSL4 by Parkin Suppresses Ferroptosis and Rescues Glucocorticoid‐Induced Bone Loss

open access: yesAdvanced Science, EarlyView.
GCs reduce Parkin, leading to ACSL4 accumulation and PUFA‐phospholipid‐driven ferroptosis in BMSCs, which impairs osteogenesis and promotes adipogenesis, causing GIOP. Parkin restoration (via OE‐Parkin or Parkin‐LNP@DSS6) ubiquitinates and degrades ACSL4, inhibiting ferroptosis, rescuing bone formation, and rescues GIOP bone loss.
Li‐jiang Han   +16 more
wiley   +1 more source

WDR72 Promotes Neuroblastoma Stemness and Progression by Sequestering TRIM31‐Mediated Degradation of CBX8

open access: yesAdvanced Science, EarlyView.
This study unveiled that METTL14 mediates m6A modification of WDR72 mRNA to stabilize and enhance WDR72 expression, which disrupts TRIM31‐mediated ubiquitination of CBX8 protein and retards its degradation, finally the elevated CBX8 contributes to tumor stemness.
Huijuan Zeng   +13 more
wiley   +1 more source

LRG1 Drives Pathological Angiogenesis by Disrupting Neutrophil Mitochondrial Homeostasis in Bladder Cancer

open access: yesAdvanced Science, EarlyView.
In bladder cancer, LRG1 binds to ANXA2 to trigger mitochondrial ROS‐dependent NETosis. This pathogenic cascade actively uncouples endothelial‐mural cell interactions, driving profound vascular destabilization. Consequently, targeting the LRG1‐ANXA2 axis attenuates the neutrophil burden and induces structural vascular normalization, offering a powerful ...
Dongshan Chen   +8 more
wiley   +1 more source

Biological effects of 5G-modulated 700 MHz RF-EMF exposure on neuronal and glial cell models under isothermal conditions. [PDF]

open access: yesSci Rep
Puginier E   +10 more
europepmc   +1 more source

A Programmable Calcification Nanoplatform for Loco‐Regional Calcification‐Immune Hepatocellular Carcinoma Therapy

open access: yesAdvanced Science, EarlyView.
An in situ‐grown BP‐CaO2 nanoplatform supplies coordinated Ca2+, endogenous phosphate, and oxidative stress to convert tumor calcification from a passive endpoint into an active immune‐remodeling process. Widespread hydroxyapatite deposition is visualized by CT, while multi‐omics reveals MCOLN2 as a calcium‐responsive mediator linking biomineralization
Long Liu   +11 more
wiley   +1 more source

QRICH1 Disrupts Endoplasmic Reticulum Homeostasis and Amplifies NF‐κB Signaling in Periodontal Ligament Stem Cells to Exacerbate Diabetic Periodontitis

open access: yesAdvanced Science, EarlyView.
QRICH1 has been established as a key factor contributing to impaired osteogenic potential and accelerated apoptosis of PDLSCs in diabetic periodontitis. QRICH1 not only significantly enhances UPR‐associated apoptotic signaling but also amplifies NF‐κB‐mediated inflammatory responses. Its inhibition restores osteogenic capacity and reduces alveolar bone
Han Li   +9 more
wiley   +1 more source

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