Results 131 to 140 of about 293,887 (293)
Wedelolactone (WED), a natural TLR2 agonist, promotes neutrophil differentiation and enhances bactericidal function, offering a potential therapeutic strategy for neutropenia. Using a multi‐omics approach, this study reveals that WED activates the TLR2/MEK/ERK pathway, upregulating key transcription factors (PU.1, CEBPβ) to drive neutrophil development.
Long Wang +16 more
wiley +1 more source
Seasonal cold adaptation is vital for insect survival, yet the molecular mechanisms linking diapause to mitochondrial resilience remain largely unresolved. We identify ascaroside C9 (asc‐C9) as a key endocrine signal that enhances diapause survival during cold stress by activating the AKHR–PGC1α–UCP4 axis, thereby driving cold‐induced lipolysis and ...
Jiao Zhou +14 more
wiley +1 more source
In silico Molecular Docking and ADME/Tox Study on Benzoxazole Derivatives Against Inosine 5’-Monophosphate Dehydrogenase [PDF]
Pratibha Teotia +2 more
openalex +1 more source
Citation: 'docking' in the IUPAC Compendium of Chemical Terminology, 5th ed.; International Union of Pure and Applied Chemistry; 2025. Online version 5.0.0, 2025. 10.1351/goldbook.11437 • License: The IUPAC Gold Book is licensed under Creative Commons Attribution-ShareAlike CC BY-SA 4.0 International for individual terms.
openaire +1 more source
Cinnamic‐hydroxamic‐acid derivatives (CHADs) are identified as novel inhibitors of the bacterial nucleoid‐associated protein HU, exhibiting potent antibacterial, anti‐biofilm (both inhibition and eradication), and DNA relaxation (anti‐supercoiling) activities. Moreover, CHADs demonstrate strong synergistic effects with multiple antibiotics.
Huan Chen +22 more
wiley +1 more source
This study reveals that the E3 ubiquitin ligase TRIM56 exacerbates neuronal ferroptosis and brain damage by mediating K48‐linked ubiquitination and degradation of KLF4, leading to suppression of the xCT/GSH/GPX4 axis. Targeting TRIM56 alleviates cerebral ischemia‐reperfusion injury in vivo and in vitro, highlighting its therapeutic potential.
Qiangping Wang +15 more
wiley +1 more source
This study shows that lower NAM levels in PE‐derived pEVs correlate with disease severity. NAM‐deficient pEVs reduce Th1 and Th17 inhibition, leading to PE‐like symptoms. NAM in pEVs inhibits Th1 via SIRT1 and Th17 via macrophages. Reduced NAM in PE‐EVs is due to decreased HRS expression in trophoblasts, resulting from elevated HSP27.
Haiyi Fei +10 more
wiley +1 more source

