In Stock Cell Lines
Homo sapiens (Human)
Kidney
Adherent
The GPR75 Knockout HEK293 Cell Line is a CRISPR/Cas9-edited knockout cell line enabling loss-of-function studies of the orphan GPCR GPR75, which regulates energy homeostasis and insulin sensitivity via G??s/G??q coupling, cAMP/PKA, and MAPK/ERK pathways, involving downstream effectors such as PKA, CREB, and AKT. This model leverages the HEK293 background for robust GPCR signaling analysis. Knockout of GPR75 eliminates receptor-specific signaling, facilitating drug target validation, insulin resistance modeling, and investigation of metabolic disease mechanisms. Researchers can perform cAMP accumulation, calcium flux, and phospho-ERK assays to dissect GPR75-dependent pathways.
CARD16 Knockout A2780 Polyclonal Cells
Cat. No. ARG29002
CYP1B1 Knockout Jurkat Polyclonal Cells
Cat. No. ARG13288
BLOC1S5 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24346
HMOX2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG38122
HBP1 Knockout huh-7 Polyclonal Cells
Cat. No. ARG28270
INS-1
Cat. No. ARC0355
The GPR75 Knockout HEK293 Cell Line is a CRISPR/Cas9-edited knockout cell line engineered for targeted disruption of the human GPR75 gene. This loss-of-function model provides a defined genetic background to investigate the physiological roles of GPR75, an orphan G protein-coupled receptor implicated in energy homeostasis and insulin sensitivity. By eliminating GPR75 expression in HEK293 cells, researchers can examine receptor-specific signaling consequences and validate GPR75 as a potential therapeutic target for metabolic disorders.
HEK293 cells are a widely used human embryonic kidney epithelial cell line originally transformed with adenovirus type 5. These cells exhibit robust proliferation, ease of transfection, and reliable expression of exogenous genes, making them a preferred host for GPCR functional studies. Their epithelial origin and capacity to support downstream signaling cascades render them suitable for dissecting G protein-coupled receptor pathways, including those mediated by G??s and G??q proteins. The combination of HEK293??s experimental tractability and the knockout of GPR75 creates a powerful system for signaling analysis.
GPR75 encodes an orphan GPCR that, upon activation, couples primarily to G??s and/or G??q heterotrimeric G proteins, stimulating adenylate cyclase to increase intracellular cAMP levels and phospholipase C to mobilize calcium. Downstream effectors include protein kinase A (PKA), cAMP response element-binding protein (CREB), extracellular signal-regulated kinases 1 and 2 (ERK1/2), and AKT. GPR75 signaling is modulated by receptor activity-modifying proteins (RAMP1, RAMP2, RAMP3) and the calcitonin receptor-like receptor (CALCRL). Known upstream regulators encompass CCL5 (RANTES), insulin, and amylin (IAPP). Through these molecular interactions, GPR75 integrates signals that influence insulin sensitivity and metabolic balance.
In the HEK293 background, deletion of GPR75 ablates receptor-specific signaling, enabling direct interrogation of GPR75-dependent pathways. This knockout cell line allows researchers to distinguish GPR75-mediated effects from those of other endogenous GPCRs and to reconstitute signaling via exogenous receptor expression for structure-function studies. The model is particularly relevant for investigating how GPR75 contributes to cAMP/PKA and MAPK/ERK signaling cascades that govern metabolic regulation, thereby providing mechanistic insights into obesity and type 2 diabetes pathogenesis.
Applications of the GPR75 Knockout HEK293 Cell Line include obesity and metabolic disease research, GPCR signaling dissection, drug target validation, and insulin resistance modeling. Researchers can employ this cell line in a range of assays such as cAMP accumulation measurements, phospho-ERK analysis, calcium flux assays, and insulin sensitivity testing. Additionally, the knockout background facilitates CRISPR-based screening and synthetic pathway reconstruction. For further information, please contact Ascent Research.
