Results 91 to 100 of about 1,442,074 (300)

β‐Catenin/c‐Myc Axis Modulates Autophagy Response to Different Ammonia Concentrations

open access: yesAdvanced Biology, Volume 9, Issue 3, March 2025.
Ammonia, detoxified by the liver into urea and glutamine, impacts autophagy differently at varying levels. Low ammonia activates autophagy via c‐Myc and β‐catenin, while high levels suppress it. Using Huh7 cells and Spf‐ash mice, c‐Myc's role in cytoprotective autophagy is revealed, offering insights into hyperammonemia and potential therapeutic ...
S. Sergio   +11 more
wiley   +1 more source

Microglial Deubiquitinase OTUD7B Stabilizes STAT3 to Promote Neuroinflammation and Cognitive Decline in Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
. ABSTRACT Neuroinflammation driven by microglial activation is a defining feature of Alzheimer's disease (AD), yet the molecular mechanisms sustaining this proinflammatory state remain unclear. Here, we identify the deubiquitinase OTUD7B as a critical regulator of microglial activation and AD pathology.
Luyao Li   +15 more
wiley   +1 more source

Proteasome subunit PSMC3 variants cause neurosensory syndrome combining deafness and cataract due to proteotoxic stress

open access: yesEMBO Molecular Medicine, 2020
The ubiquitin–proteasome system degrades ubiquitin‐modified proteins to maintain protein homeostasis and to control signalling. Whole‐genome sequencing of patients with severe deafness and early‐onset cataracts as part of a neurological, sensorial and ...
Ariane Kröll‐Hermi   +28 more
doaj   +1 more source

Loss of E3 Ubiquitin Ligase RINES via CpG Methylation Relieves Suppression of STAT3 and MYC, Facilitating Multiple Tumorigeneses

open access: yesAdvanced Science, EarlyView.
Dysregulated protein modifications drive tumorigenesis. RINES, an E3 ubiquitin ligase, represses tumor cell proliferation and metastasis by facilitating RING domain‐dependent, ubiquitin–proteasome‐mediated degradation of STAT3 and MYC, which consequently restrains cancer stemness and oncogenic progression.
Lili Li   +8 more
wiley   +1 more source

Early Retinal UCHL1 Dysregulation Coupled With Synaptic Loss Reflects Alzheimer's Disease Severity

open access: yesAdvanced Science, EarlyView.
This study identifies synapse‐enriched deubiquitinase UCHL1 as an early Aβ‐responsive regulator of retinal synaptopathy in Alzheimer's disease. Retinal UCHL1 loss accompanies excitatory synapse degeneration, p75NTR activation, and neuroinflammation, and predicts Braak stage and cognitive decline. Aβ42 fibrils trigger synaptic and UCHL1 depletion before
Altan Rentsendorj   +25 more
wiley   +1 more source

Antagonism of proteasome inhibitor-induced heme oxygenase-1 expression by PINK1 mutation.

open access: yesPLoS ONE, 2017
PTEN-induced putative kinase 1 (PINK1) is an integral protein in the mitochondrial membrane and maintains mitochondrial fidelity. Pathogenic mutations in PINK1 have been identified as a cause of early-onset autosomal recessive familial Parkinson's ...
Xiang-Jun Sheng   +7 more
doaj   +1 more source

TED1 Promotes the Assembly of SCFD3‐D14‐D53 to Reinforce Strigolactone Signaling in Rice

open access: yesAdvanced Science, EarlyView.
This study identifies TED1 as a positive regulator of strigolactones (SL) signaling in rice. The ted1 mutants display dwarfism and increased tillering with significantly reduced SLs sensitivity. Through its longer C‐terminal region, TED1 interacts with D53 and D14 to promote the assembly of SCFD3‐D14‐D53, thereby facilitating the efficient ...
Sheng Luo   +22 more
wiley   +1 more source

Discovery of novel proteasome inhibitors using a high-content cell-based screening system.

open access: yesPLoS ONE, 2009
The regulated degradation of damaged or misfolded proteins, as well as down-regulation of key signaling proteins, within eukaryotic and bacterial cells is catalyzed primarily by large, ATP-dependent multimeric proteolytic complexes, termed proteasomes ...
Irena Lavelin   +6 more
doaj   +1 more source

Limited Proteolysis: DisRUPting Proteasomal Inhibition [PDF]

open access: yesCurrent Biology, 2014
The 26S proteasome is a protease complex that completely degrades substrate proteins marked with a chain of ubiquitins, but is also able to perform endoproteolytic cleavage. A new study now demonstrates that regulated ubiquitin-proteasome-dependent processing ameliorates proteasomal inhibition.
openaire   +2 more sources

Emodin potentiates the antiproliferative effect of interferon alpha/beta by activation of JAK/STAT pathway signaling through inhibition of the 26S proteasome

open access: yes, 2016
The 26S proteasome is a negative regulator of type I interferon (IFN-alpha/beta) signaling. Inhibition of the 26S proteasome by small molecules may be a new strategy to enhance the efficacy of type I IFNs and reduce their side effects.
He, YJ   +11 more
core  

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