Results 241 to 250 of about 355,945 (323)

Macrophage TRIM21 Inhibition Ameliorates Murine Acute Pancreatitis via PHB2‐Mediated Mitochondrial Stabilization

open access: yesAdvanced Science, EarlyView.
Macrophage‐derived TRIM21 drives the progression of AP via ubiquitin‐proteasome‐mediated degradation of PHB2, leading to impaired PHB2‐mediated mitophagy. Therefore, accumulation of cytosolic mtDNA hyperactivates the cGAS‐STING signaling axis, thereby amplifying inflammatory cascades.
Yansong Xu   +7 more
wiley   +1 more source

In-situ cross-linking mass spectrometry reveals compartment-specific proteasomal interactions and structural heterogeneity. [PDF]

open access: yesNat Commun
Zhao L   +10 more
europepmc   +1 more source

Potent and Selective IGF‐IIR‐Recruiting Bifunctional Molecules for Targeted Lysosomal Degradation of Extracellular and Membrane Proteins

open access: yesAdvanced Science, EarlyView.
Lysosome‐targeting chimeras (LYTACs) enable degradation of extracellular and membrane proteins via lysosomal trafficking. We report a novel IGF‐II mutant (Del1–7, Y27L) that selectively engages IGF‐IIR while avoiding IGF‐IR and IR‐A. mutIGF‐II–based LYTACs enhance target internalization and degradation and support a genetically encodable, all‐protein ...
Yuan Zhao   +16 more
wiley   +1 more source

Chaperone‐Mediated Autophagic Degradation of USP9X in Macrophages Exacerbates Postmyocardial Infarction Inflammation and Cardiac Dysfunction

open access: yesAdvanced Science, EarlyView.
This study demonstrates that inflammatory stimuli induce the acetylation‐triggered, chaperone‐mediated autophagic degradation of ubiquitin‐specific peptidase 9 X‐linked (USP9X) in macrophages. USP9X acts as a macrophage “inflammation switch” after myocardial infarction (MI). USP9X loss destabilizes tumor necrosis factor receptor‐associated factor (TRAF)
Biqing Wang   +7 more
wiley   +1 more source

Proteasome inhibition as a potential therapeutic target in thymic cancer. [PDF]

open access: yesCell Death Dis
Okada S   +20 more
europepmc   +1 more source

Targeted Mitochondrial ECSIT Overexpression Attenuates MASH by Increasing OTUD3 Expression

open access: yesAdvanced Science, EarlyView.
Mitochondrial ECSIT expression is reduced during MASH pathogenesis. Overexpression of mitochondrial ECSIT mitigates steatohepatitis and maintains hepatic metabolic homeostasis. Mechanistically, ECSIT enhances intramitochondrial OTUD3 expression to stabilize SIRT3 through deubiquitination, thus preserving mitochondrial function and impeding disease ...
Yuqing Jiang   +11 more
wiley   +1 more source

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