Results 191 to 200 of about 70,372 (263)

A multiplex interactome of Ebola virus proteins reveals TM9SF2 as a cell‐surface attachment factor that promotes viral entry

open access: yesiMetaOmics, EarlyView.
This study generates a comprehensive Ebola virus (EBOV)‐human protein–protein interactome, comprising 1728 core high‐confidence interactions. Further interactome analysis revealed the potential association of EBOV glycoprotein (GP) with the host factor TM9SF2. Subsequent mechanistic investigations confirmed that TM9SF2 functions as an attachment factor
Limin Shang   +16 more
wiley   +1 more source

Hyperoside alleviates endometrial stromal cell senescence in unexplained recurrent spontaneous abortion via DHX9‐mediated R‐loop resolution

open access: yesiMeta, EarlyView.
This study suggests that the food‐derived flavonoid hyperoside may act as a natural DExH‐box helicase 9 (DHX9) modulator, directly targeting Thr419 of DHX9 to help resolve pathological R‐loop accumulation. Consequently, it suppresses cyclic GMP‐AMP synthase‐stimulator of interferon genes (cGAS‐STING)‐driven endometrial stromal senescence and restores ...
Yuepeng Jiang   +18 more
wiley   +1 more source

Polydatin Alleviates APAP‐Induced Hepatotoxicity by Targeting C/EBPβ to Suppress the NLRP3 Inflammasome Signaling Pathway

open access: yesiNew Medicine, EarlyView.
PD alleviates APAP‐induced ALI by inhibiting the NLRP3 inflammasome signaling pathway. C/EBPβ is identified as a direct target via multimethod validation. PD promotes the deacetylation of C/EBPβ via Sirt1. The Sirt1/C/EBPβ/NLRP3 signaling axis is defined for PD's hepatoprotective effect.
Tian‐Yu Yang   +6 more
wiley   +1 more source

Methodological validation of a cryo-TEM-based detection method for empty capsid ratio in recombinant adeno-associated virus. [PDF]

open access: yesBiochem Biophys Rep
Xu L   +11 more
europepmc   +1 more source

Sel1l preserves condylar cartilage matrix homeostasis by regulating PERK signaling

open access: yesInterdisciplinary Medicine, EarlyView.
Our study revealed that the expression of Sel1l was downregulated in OA cartilage and that Sel1l deficiency induced cartilage catabolism. Mechanistically, Sel1l depletion aberrantly activated PERK signaling and resulted in ER stress. PERK inhibition rescued the phenotype of Sel1l‐deficient chondrocytes and alleviated TMJOA pathogenesis.
Xinqi Huang   +3 more
wiley   +1 more source

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