Publications by authors named "F Alonzo"

The ccessory ene egulatory (Agr) system is required for virulence factor gene expression and pathogenesis of . The Agr system is activated in response to the accumulation of a cyclic autoinducing peptide (AIP), which is matured and secreted by the bacterium. The precursor of AIP, AgrD, consists of the AIP flanked by an N-terminal [Formula: see text]-helical Leader and a charged C-terminal tail.

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Article Synopsis
  • Mammalian AIM-2-like receptor (ALR) proteins are critical for the immune response, as they bind to nucleic acids and trigger the production of interferons or inflammasomes.
  • The ALR gene region in mice is highly variable and undergoes rapid evolution, with the IFI207 gene emerging through gene conversion or recombination events and varying significantly among species.
  • IFI207 enhances the immune response against murine leukemia virus infection and stabilizes STING protein, illustrating the ongoing evolution between hosts and pathogens, which leads to new gene functions that play vital roles in immunity.
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Unlabelled: Pathogenic bacteria rely on secreted virulence factors to cause disease in susceptible hosts. However, in Gram-positive bacteria, the mechanisms underlying secreted protein activation and regulation post-membrane translocation remain largely unknown. Using proteomics, we identified several proteins that are dependent on the secreted chaperone PrsA2.

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Incorporation of host-derived exogenous fatty acids (eFAs), particularly unsaturated fatty acids (UFAs), by could affect the bacterial membrane fluidity and susceptibility to antimicrobials. In this work, we found that glycerol ester hydrolase (Geh) is the primary lipase hydrolyzing cholesteryl esters and, to a lesser extent, triglycerides and that human serum albumin (HSA) could serve as a buffer of eFAs, where low levels of HSA facilitate the utilization of eFAs but high levels of HSA inhibit it. The fact that the type II fatty acid synthesis (FASII) inhibitor, AFN-1252, leads to an increase in UFA content even in the absence of eFA suggests that membrane property modulation is part of its mechanism of action.

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