mProX™ Human CXCR4 Stable Cell Line

Lyu F, et al. "Maternal CXCR4 deletion results in placental defects and pregnancy loss mediated ." JCI insight, 2023.
The study investigates the role of CXCR4, a key regulator of NK cell and dendritic cell development, in pregnancy. While its importance in early placental development and immune tolerance at the maternal-fetal interface is established, its specific function in pregnancy remains unclear. The research reveals that deletion of CXCR4 in adult mice, but not in the uterus, results in increased pregnancy loss and decreased litter size. These mice exhibited abnormal decidual NK cell aggregates and infiltration into trophoblast areas, as well as decreased expression of the NK cell granule effector granzyme B, indicating NK cell dysfunction. This was associated with placental vascular abnormalities and increased expression of inflammatory genes. Rescue of reproductive deficits was observed through transplanting wild type CXCR4+ bone marrow cells into CXCR4-deficient mice, which normalized NK cell function and placental vascular development. In conclusion, this study highlights the important role of maternal CXCR4 expression in immune cell function, placental development, and pregnancy maintenance.
Pubmed: 37815869   DOI: 10.1172/jci.insight.172216

Xu X, et al. "Sequence-directed concentration of G protein-coupled receptors in COPII vesicles.." iScience, 2023.
The largest superfamily of plasma membrane signaling proteins, G protein-coupled receptors (GPCRs), remains largely unexplored in terms of their recruitment to COPII vesicles for forward delivery after synthesis in the endoplasmic reticulum (ER). In this study, it has been demonstrated that certain GPCRs, such as the Angiotensin II type 2 receptor (AT2R) and CXCR4, are highly concentrated at ER exit sites (ERES) before COPII budding. Furthermore, it has been found that specific di-acidic and 9-residue motifs are responsible for directing the concentration of these receptors, and also control their ER-Golgi traffic. It has also been observed that the AT2R interacts with the Sar1 GTPase, and that different GPCRs exhibit varying rates of ER-Golgi transport via COPII, independent of their concentration at ERES. These findings highlight the active capture of GPCRs by COPII through specific motifs and interactions with COPII components, which in turn, play a crucial role in their export dynamics and provide valuable insights into the targeting and forward trafficking of nascent GPCRs.
Pubmed: 37810244   DOI: 10.1016/j.isci.2023.107969