FPR2 (Formyl Peptide Receptor 2)

The observed discrepancies in LL-37 function across studies highlight its complex, context-dependent role in tumor biology. Further research is needed to elucidate the mechanistic basis of LL-37 signaling and its potential as a therapeutic target in CRC.

Herein, we analyze the LAT1/SLC7A5-mediated uptake of several essential AAs in FPR2-stimulated CaLu-6 and HCC1937 cells and prove: (i) the redox regulation of both LAT1/SLC7A5 and 4F2hc/SLC3A2/CD98, which form a heterodimer on the plasma membrane; (ii) the redox activation of the mTOR pathway and, in turn, of S6K1 and 4E-BP1, which stimulate protein synthesis; (iii) c-Myc and miR-126 regulation, which control LAT1/SLC7A5 synthesis at the transcriptional and post-transcriptional level, respectively. These findings provide new approaches for the development of novel therapeutic strategies for the treatment of human cancers.

We detail the quantitative expression profiles of these molecules on various subsets of leukocytes and provide validation data for these mAbs. The implications of these expression profiles are discussed for the potential therapeutic targeting of immune-mediated diseases and cancer.

We identified distinct PPI networks and the hub proteins specific to papillary and nonpapillary urothelial carcinomas. However, these findings are limited by the use of transcriptomic data and require experimental validation to confirm the functional relevance of the identified targets.

In addition, the complex cFPR2/HP2-20 exhibited a marked increase in the number of H-bonds, hydrophobic interactions and electrostatic charges compared to the complex cFPR2/WRW4. In conclusion, these results showed that CCoV replication is related to FPR2, suggesting it as an interesting target to develop new drugs to fight CoVs infection.

Notably, high mucosal FPR2/ALX levels were associated with poor response to anti-tumor necrosis factor-α (TNF-α) agent infliximab, and were predictive of disease status (AUC = 0.9143)...We showed that oral administration of QC1 or QC7 significantly reduced disease active index (DAI) in wild-type mice, whereas the therapeutic effects were markedly impaired in Fpr2-silenced mice. We conclude that FPR2/ALX may serve as a potential biomarker and therapeutic target for IBD.

Single-cell RNA sequencing analysis demonstrated a decrease in SPHK1 and FCGR2B, while VSIG4 and FPR2 progressively increased during macrophage differentiation. These findings provide a potential framework for targeted therapy.

Furthermore, FPR2 inhibition substantially attenuates cisplatin-induced inflammatory factor release and hair cell death. These findings identify FPR2 as a novel mediator of cisplatin-induced ototoxicity, suggesting its potential as a therapeutic target for preventing hearing loss in cancer patients.

The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 38: 3297‑3308, 2017; DOI: 10.3892/or.2017.6034].

The optimal gastric cancer tissue staining protocol for the VENTANA FGFR2b (FPR2-D) Mouse Monoclonal Antibody was referenced to develop an assay for other solid tumor types. This investigation shows the importance of parameter screening approaches when evaluating FGFR2b across tumor types in immunohistochemistry to ensure optimal staining performance.

Immunotherapy, as well as Palbociclib and Perifosine, were predicted to be more effective for low-risk patients. Conversely, high-risk patients were more likely to benefit from Axitinib, Imatinib, Nilotinib, and Temsirolimus. This study identified 5 signature genes as potential biomarkers and therapeutic targets for THCA. These findings provide novel insights into the prognosis and targeted therapy of THCA, offering a foundation for furture clinical applications.

They mediate synergy with chemokines by the interaction with cognate G protein-coupled receptors (GPCRs), formyl peptide receptor 2 (FPR2) and (CC and CXC) chemokine receptors. In conclusion, SAA1 enforces the action of many chemokines and assists in local leukocyte recruitment, in particular, when the concentrations of specifically-induced chemokines are still low.