mProX™ Human FPR3 Stable Cell Line

Hu T, Chen X. "Role of neutrophil extracellular trap and immune infiltration in atherosclerotic ." Medicine, 2023.
The instability of atherosclerotic plaques has been linked to an increased risk of acute coronary syndrome. Recent research has highlighted the important role of neutrophil extracellular traps (NETs) in the formation and development of these plaques. To address the need for early detection and prevention of plaque erosion or disruption, a study was conducted to identify novel diagnostic biomarkers for unstable plaques. By analyzing gene expression and performing pathway and network analyses, the study identified 8 differential NET-related genes involved in immune responses and smooth muscle contractility, and 4 of these genes were found to be capable of distinguishing unstable plaques. Furthermore, an understanding of immune cell infiltration and regulatory factors such as miRNAs and transcription factors may aid in the identification and prevention of plaque rupture. The 4 identified diagnostic genes (AQP9, C5AR1, FPR3, and SIGLEC9) and associated immune cell subsets provide promising candidates for early recognition and prevention of atherosclerotic plaque complications.
Pubmed: 37747003   DOI: 10.1097/MD.0000000000034918

Hashemi Karoii D, et al. "Altered G-Protein Transduction Protein Gene Expression in the Testis of Infertile ." DNA and cell biology, 2023.
Recent studies have revealed that the G-protein-coupled receptor (GPCR) superfamily plays a critical role in maintaining ion-water homeostasis in sperm and Sertoli cells, as well as in the development of germ cells, the formation of the blood barrier, and the maturation of sperm. Microarray and bioinformatics analysis of 3513 sperm and Sertoli cell genes revealed changes in the expression of GPCR, guanyl-nucleotide exchange factor, membrane traffic protein, and small GTPase genes in three human cases of non-obstructive azoospermia (NOA). Upregulation of GOLGA8IP, OR2AT4, PHKA1, A2M, OR56A1, SEMA3G, LRRC17, APP, ARHGAP33, RABGEF1, NPY2R, GHRHR, LTB4R2, GRIK5, OR6K6, NAPG, OR6C65, VPS35, FPR3, and ARL4A, and downregulation of MARS, SIRPG, OGFR, GPR150, LRRK1, and NGEF were observed. Sertoli cells in NOA cases also showed an increase in expression of GBP3, GBP3, TNF, TGFB3, and CLTC, and a decrease in expression of PAQR4, RRAGD, RAC2, SERPINB8, IRPB1, MRGPRF, RASA2, SIRPG, RGS2, RAP2A, RAB2B, ARL17, SERINC4, XIAP, DENND4C, ANKRA2, CSTA, STX18, and SNAP23. An integrated analysis of Enrich Shiny Gene Ontology (GO), STRING, and Cytoscape was used to identify potential molecular interactions and key pathways. Functional enrichment analysis showed significant changes in biological processes such as the regulation of protein metabolic processes and small GTPase-mediated signal transduction, as well as changes in molecular functions related to GPCR activity, guanyl ribonucleotide binding, GTPase activity, and nucleoside-triphosphatase activity. Similar findings were observed in Sertoli cells. The identified gene mutations could potentially be used to develop new receptor-selective GPCR antagonists or agonists,
Pubmed: 37610843   DOI: 10.1089/dna.2023.0189