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.
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.
We discovered that FKBP7 was upregulated in human prostate cancers and its expression correlated with the recurrence observed in patients receiving docetaxel.