Results 251 to 260 of about 405,626 (326)
Using iPSC‐derived motoneurons and postmortem tissue from FUS‐ALS patients, it is demonstrated that increased mitochondrial transcription leads to elevated cytosolic double‐stranded RNA (dsRNA) levels. This aberrant accumulation activates a RIG‐I–dependent innate immune response leading to neurodegeneration, which is amenable for FDA‐ and EMA‐approved ...
Marcel Naumann +26 more
wiley +1 more source
Abstract 1042 Liquid-liquid phase separation induced by interactions between the picornavirus 3C(D) main protease and genomic RNA control elements [PDF]
David D. Boehr +3 more
openalex +1 more source
Nuclear ribonucleoprotein RALY downregulates foot-and-mouth disease virus replication but antagonized by viral 3C protease. [PDF]
Wu J +8 more
europepmc +1 more source
Liver stiffness promotes intrahepatic cholesterol accumulation by repressing LXRα through YAP/TAZ activation. Stiff matrices impair cholesterol efflux in hepatocytes, while YAP/TAZ deletion restores LXRα activity and prevents cholesterol‐induced fibrosis.
Na Young Lee +9 more
wiley +1 more source
Enterovirus D68 3C protease antagonizes type I interferon signaling by cleaving signal transducer and activator of transcription 1. [PDF]
Li X +8 more
europepmc +1 more source
Chronic Hypoxia Disrupts Spermatogenesis Through ASXL2–EZH2–Mediated Microtubule Destabilization
This study reveals the mechanism by which chronic hypoxia impairs spermatogenesis via the ASXL2–EZH2 axis, hindering the transition of spermatids from round to elongated forms. Key findings reveal that under hypoxic conditions, downregulated ASXL2 expression reduces EZH2 binding to the CEP162 promoter, leading to decreased H3K27me3 modification and ...
Jun Yin +11 more
wiley +1 more source
Seneca Valley virus 3C protease cleaves OPTN (optineurin) to Impair selective autophagy and type I interferon signaling. [PDF]
Song J +5 more
europepmc +1 more source
CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis
Ferroptosis is driven by mitochondrial permeability transition pore (mPTP) opening, which induces mitochondrial swelling and releases oxidized mitochondrial DNA. The released mtDNA activates cGAS–STING signaling, promotes ferritinophagy, and amplifies ferroptotic cell death. Disruption of mtDNA repair sensitizes tumors to ferroptosis in vivo, revealing
Hong Zhou +5 more
wiley +1 more source

