mProX™ Human CCR5 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Expression of functional CCR5 in CEM-GFP reporter cells.
CCR5 expression was assessed via FACS in untreated CEM-GFP cells (a), retrovirus-transduced and briefly hygromycin-selected cells (b), and cells isolated using magnetic beads (c). Subsequently, CEM-GFP (d-f) or bead-isolated CEM-GFP/CCR5+ cells (g-i) underwent mock treatment (d and g) or were exposed to HIV-1 CXCR4-tropic strain NL4-3 (e and h) or HIV-1 CCR5-tropic strain JR-CSF (f and i), with HIV-1 infection detected by FACS on day 5 post-infection.
Ref: Brockman, Mark A., et al. "Use of a novel GFP reporter cell line to examine replication capacity of CXCR4-and CCR5-tropic HIV-1 by flow cytometry." Journal of virological methods 131.2 (2006): 134-142.
Pubmed: 16182382
DOI: 10.1016/j.jviromet.2005.08.003
Research Highlights
Tang Q, et al. "Identification of two immune subtypes and four hub immune-related genes in ." Medicine, 2023.
The immune classification of ovarian cancer (OV) is becoming increasingly significant for its use in immunotherapy. However, the current research on immune subtypes of OV is limited. Therefore, there is an urgent need to investigate and identify the immune subtypes and key immune-related genes (IRGs) for further treatment. A total of 379 OV samples were obtained from the UCSC online database. Single sample gene set enrichment analysis was utilized to identify immune subtypes, while gene set variation analysis was used to explore the hallmarks and Kyoto Encyclopedia of Genes and Genomes pathways of these subtypes. Two immune subtypes (Immunity_H and Immunity_L) were identified, with the Immunity_H group showing longer overall survival compared to the Immunity_L group. The Immunity_H group also had higher stromal score, immune score, and estimated score, while the tumor purity had an inverse relationship. Furthermore, the gene set variation analysis revealed a positive correlation between improved immune response and pathways related to classical signaling pathways (PI3K/AKT/MTOR, P53, TNFA/NFkB signaling pathways) and immune responses (T/B cell receptor signaling pathways and primary immunodeficiency). Additionally, through weighted gene co-expression network construction and Cytoscape, four hub IRGs (CCR5, IL10RA, ITGAL, and PTPRC) were identified. The mutations of these four hub IRGs were further explored, and PTPRC was found to have a nearly 7% amplification rate. Moreover, eight immune-checkpoint genes showed higher expression in the Immunity_H group compared to the Immunity_L group, except for CD276. The correlation between PD-1/PD-L1 and the four hub IRGs was investigated, and gene set enrichment analysis was conducted to uncover the underlying mechanisms of PTPRC in OV. Ultimately, western blotting revealed that PTPRC can regulate the expression of immune checkpoint PD-L1 through the JAK-STAT signaling pathway. In conclusion, through multiple analyses, two immune subtypes and four key IRGs were identified in OV.
Pubmed:
37800814
DOI:
10.1097/MD.0000000000035246
Costa RM, et al. "Role Of The C-C Motif Chemokine Ligand 5 (CCL5) And Its Receptor, C-C Motif ." bioRxiv : the preprint server for biology, 2023.
Aldosterone, a mineralocorticoid steroid hormone, is known to contribute to the development of cardiovascular diseases through increased sterile vascular inflammation. While the functions of C-C Motif Chemokine Ligand 5 (CCL5) and its receptor, C-C Motif Chemokine Receptor 5 (CCR5), are well understood in infectious diseases, their roles in aldosterone-induced vascular injury and hypertension have yet to be elucidated. In this study, wild-type (CCR5 (+/+) ) and CCR5 knockout (CCR5 (-/-) ) mice were treated with aldosterone and monitored for vascular damage, blood pressure, and renal injury. It was found that CCR5 plays a significant role in aldosterone-induced vascular injury, hypertension, and renal damage. Mice lacking CCR5 were protected from these effects, and it was determined that CCL5 activates NADPH oxidase 1 (Nox1) and subsequent reactive oxygen species (ROS) formation, leading to endothelial dysfunction and inflammation. This study highlights the potential of targeting CCR5/CCL5 in treating conditions with excess aldosterone.
Pubmed:
37790434
DOI:
10.1101/2023.09.22.558020