SasF enzyme is essential for S. aureus resistance to skin fatty acids and is required for skin colonization and infection, highlighting its role in virulence.
- Open access
Moving in bioRxiv, Journal of bacteriology, Applied and environmental microbiology, Communications Biology, Gastroenterology, Virulence, Cell Reports and Cellular & molecular immunology.
Rebuilt
Nothing in this topic has moved yet this week.
Newest first · last 60 days
SasF enzyme is essential for S. aureus resistance to skin fatty acids and is required for skin colonization and infection, highlighting its role in virulence.
Milk-grown Staphylococcus aureus exhibits extreme resistance to reactive oxygen species, antimicrobial tolerance, and accelerated killing in a larval infection model compared to serum-grown bacteria.
Lacticaseibacillus rhamnosus GG enhances gefitinib efficacy and reduces gastrointestinal and hepatic toxicity without changing systemic drug levels in mice.
A rapid sphingomyelin-dependent entry pathway in S. aureus alters intracellular fate, influencing bacterial replication and host cell death within minutes of contact.
TrbA binds and locks KorB, a DNA-sliding clamp, to repress transcription on multi-drug resistance plasmids, revealing a conserved clamp-locking mechanism involving multiple partners.
C. difficile assembles a unique divisome complex in three phases, with PBP1 replacing FtsW-FtsI in septal peptidoglycan synthesis, highlighting a distinct bacterial division mechanism.
Loss of YqeK in Staphylococcus aureus causes a 1,000-fold increase in Ap 4 N levels and impairs stress resistance and virulence gene expression.
Polyunsaturated fatty acids effectively kill glycolytic Staphylococcus aureus strains, including persisters and small colony variants, by inducing lipid peroxidation.
MbcS, a refunctionalized acyl-CoA synthetase in Staphylococcus aureus, provides a significant fitness advantage during intra-species competition under nutrient-limited conditions.
Candida albicans reprograms Staphylococcus aureus glycolytic pathways, increasing its virulence by 2- to 3-fold in glucose-rich environments.
The G2019S mutation in LRRK2 enhances NADPH oxidase-2 activity in neutrophils, improving bacterial infection control in mice by 2- to 3-fold.
Journals this month
Topics moving, week to 23 Oct 2026