Differential Proteomic Analysis Reveals Protein Networks and Pathways that May Contribute to Helicobacter pylori FKBP-Type PPIase-Associated Gastric Diseases.
Previously, we identified two PPIase enzymes in <i>Staphylococcus aureus</i> (PpiB and PrsA) that are involved in the regulation of virulence determinants and have shown that PpiB contributes to <i>S. aureus</i> virulence in a murine abscess model of infection.
We discovered that FKBP7 was upregulated in human prostate cancers and its expression correlated with the recurrence observed in patients receiving docetaxel.
Our results provided insight on the protein interaction networks and signaling pathways that may contribute to PPIase-FKBP-associated gastric diseases and may lead to a better understanding of the mechanisms indicating the oncogenic effects of H. pylori PPIase-FKBP.
Our findings provide evidence that PPIase CypA promoted macrophages polarization toward pro-inflammatory M1 phenotype via transcriptional activating NF-κB, thus leading to aggravated arthritis.