The GPR75 Knockout A2780 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population originating from the A2780 human ovarian carcinoma line, specifically engineered to disrupt the GPR75 gene. This loss-of-function model impairs GPR75 receptor expression across the heterogeneous cell pool, enabling rigorous investigation of GPR75-dependent signaling without the confounding influence of endogenous receptor activity.
The A2780 host cell line is an epithelial ovarian cancer model derived from an untreated female patient with ovarian endometrioid adenocarcinoma. It displays typical epithelial morphology and is widely employed in ovarian cancer research, including studies of tumor metabolism, chemosensitivity, and oncogenic signal transduction. Its stable growth characteristics and well-documented genomic profile make it a dependable platform for generating gene-edited derivatives.
GPR75 functions as a receptor for fibroblast growth factor 21 (FGF21) and couples to the G??s protein, stimulating adenylyl cyclase to elevate intracellular cAMP levels. This activates protein kinase A (PKA), which phosphorylates the transcription factor CREB, driving the expression of metabolic genes such as UCP1. Additionally, GPR75 interacts with ??-arrestin, likely modulating receptor desensitization or scaffolding of alternative effectors. CRISPR-mediated disruption of GPR75 thus uncouples the FGF21?CGPR75?CG??s?CcAMP?CPKA?CCREB signaling axis, blocking downstream transcriptional programs that regulate energy homeostasis and glucose metabolism.
In the A2780 ovarian carcinoma context, ablation of GPR75-mediated signaling may uncover unique roles for metabolic regulation in cancer cell adaptation. Although A2780 cells are not classic models of metabolic disease, their epithelial origin and malignant phenotype permit the dissection of how GPR75 influences nutrient sensing, energy balance, and stress responses in a tumor setting. This polyclonal knockout population therefore provides a null background to differentiate GPR75-specific contributions from other FGF receptor pathways, and to explore potential crosstalk between metabolic and oncogenic networks.
This knockout cell product supports diverse experimental workflows: cAMP accumulation assays and PKA kinase activity measurements quantify proximal signaling; western blotting for phospho-CREB confirms pathway activation; RT-qPCR analysis of metabolic targets (e.g., UCP1, PGC1??) assesses transcriptional output; and immunofluorescence or flow cytometry verifies receptor loss. Metabolic profiling via Seahorse analysis, cell proliferation assays, and drug sensitivity testing facilitate translational studies. Applications span FGF21?CGPR75 signaling dissection, obesity and type 2 diabetes target validation, and ovarian cancer metabolism research. For additional details, please contact Ascent Research.
