ArticleScientific reports2025
Phosphorylation of the β
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Actinobacillus pleuropneumoniae, the causative agent of porcine pleuropneumonia, produces various virulence factors, including the exotoxin ApxI, which contributes to disease pathogenesis. ApxI induces cytotoxicity through porcine lymphocyte function-associated antigen-1 (LFA-1; CD11a/CD18) while concurrently attenuating Akt activity. This study aimed to investigate the regulatory role of porcine CD18, focusing on the tyrosine 735 residue in its cytoplasmic tail, and to examine the involvement of Akt in ApxI-induced cytotoxicity. Through transfection experiments, we demonstrated that the expression of porcine CD18 alone in ApxI-insensitive human embryonic kidney 293 cells conferred susceptibility to ApxI, while cotransfection of porcine CD11a with porcine CD18 resulted in the highest ApxI sensitivity, accompanied by reduced Akt activity. Substituting the wild-type CD18 with a CD18 harboring a tyrosine 735-to-proline (CD18
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