Shafagh A. Waters

The paper shows how SARS-CoV-2 variants, particularly Omicron, evolved proteolytic controls at the Spike furin cleavage site to enhance transmission while reducing lower respiratory tract pathogenicity.

The paper identifies a prophage-encoded sRNA, HnrS, that counteracts xenogenic silencing by repressing Hha, enabling virulence gene expression in E. coli.

This paper shows that SARS-CoV-2 Omicron lineages replicate using a specific ACE2 pool that does not complex with TMPRSS2, unlike pre-Omicron variants.

The paper validates repurposed drugs against SARS-CoV-2 using stem cell-derived cardiomyocyte and nasal epithelium models, confirming fluvoxamine's antiviral efficacy in combination with other drugs.

The paper identifies the RSX interactome in marsupials and shows functional coherence with the Xist interactome in XCI.

The paper characterizes the functional and structural defects of the R352Q CFTR mutation using patient-derived organoids and molecular dynamics simulations, showing residual function restored by potentiators but not correctors.

The paper functionally and structurally characterizes an ultra-rare CFTR mutation, showing it responds to specific potentiators and correctors, with altered lasso motif interactions affecting channel gating.

The paper shows non-linear sequence similarity between Xist and Rsx repeat domains, suggesting shared functional roles through similar protein-binding motif enrichments.