Results 181 to 190 of about 231,680 (303)

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

NCOA4 Accelerates Abdominal Aortic Aneurysm Formation by Regulating Macrophage Activation and Ferroptosis via STAT1–CH25H Axis

open access: yesAdvanced Science, EarlyView.
Under pathological stimulation, NCOA4 in macrophages interacts with STAT1 to promote CH25H transcription. The subsequent increase in 25‐HC production activates macrophages, triggers inflammatory responses and ferroptosis, and accelerates the progression of AAA.
Zhinan Wu   +9 more
wiley   +1 more source

Mitochondrial stress in advanced fibrosis and cirrhosis associated with chronic hepatitis B, chronic hepatitis C, or nonalcoholic steatohepatitis

open access: yesHepatology, EarlyView., 2022
Adaptive mitochondrial mechanisms allow mitochondrial resilience and prevent the worsening of fibrosis, while deregulation of these mechanisms promotes the progression from no/minimal‐mild (F0‐F2) fibrosis to advanced fibrosis and cirrhosis (F3‐F4). Abstract Background and Aims Hepatitis B virus (HBV) infection causes oxidative stress (OS) and alters ...
Dimitri Loureiro   +17 more
wiley   +1 more source

Ubiquitin and a charged loop regulate the ubiquitin E3 ligase activity of Ark2C. [PDF]

open access: yesNat Commun, 2022
Paluda A   +4 more
europepmc   +1 more source

Functional characterization of an E3 ubiquitin ligase involved in plant response to abiotic stress

open access: yes, 2010
Protein ubiquitination is a post-translational modification that targets protein substrates for 26S proteasome-mediated degradation. It is based on the covalent attachment of the 76-amino acid eukaryotic molecule, ubiquitin, to substrate proteins ...
Guerra, Davide
core  

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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