FIGURE 1 Schematic representation of exploitation of host cell signaling by bacterial pathogens via effector-mediated post-translational modifications. Effector proteins secreted by invading pathogenic bacteria have been shown to harbor diverse enzymatic activities, subverting host cellular pathways. For instance, Shigellaeffector OspC3 targets host caspase-4/11 for ADP-riboxanation, which blocks the cleavage of GSDMD by caspase-4/11 (Li et al., 2021).Salmonella kinase SteC remodels the host F-actin cytoskeleton by phosphorylating FMNL1 (Poh et al., 2008), whereas enteropathogenicEscherichia coli effector kinases NleH1 and NleH2 target Ser775 of host microvillus protein Eps8 for phosphorylation, thus inhibiting its bundling activity and driving its dispersal from the attaching and effacing (AE) lesion during infection (Pollock et al., 2022). In addition, Lpg0080 (also named as Ceg3) and Lpg0081 from Legionella pneumophila coordinately modulate host mitochondrial ADP/ATP exchange via reversible ADP-ribosylation of ANTs (Kubori et al., 2022; Fu et al., 2022). Due to space limitation, only a few representative effectors and their associated pathways are shown in the figure.