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Thus, mtDNA release acts as a molecular bridge coupling cellular stress to chronic neuroinflammation

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either TLR4 or NOX4 knockdown significantly improved left ventricular remodelling and reduced myocyte death

Upon transfection into 293 T Lenti-X cells of either full-length spike or Spike-C3 expression plasmids, both constructs showed comparable expression levels on the cell surface (Fig

These inhibitors bind to the dimerization domain of G3BP1/2, specifically disrupting the co-condensation of RNA, G3BP and SG network (Freibaum et al, 2024)