CellOnco™ CHO-K1-Tg(Human GPR91 Receptor) Division-Arrested Cell, Single Clone (CAT#: ITS-0624-HMM557)

Creative Biolabs offers CHO-K1-Tg(Human GPR91 Receptor) Division-Arrested Cell which GPR91 receptor stably expressed in CHO-K1 cells.

CHO-K1-Tg(Human GPR91 Receptor) Division-Arrested Cell was engineered to express the receptor human GPR91 (GenBank Accession umber: NM_033050.3). This cell line can be used to study GPR91 receptor function, signaling pathways, and potential therapeutic interventions. Dividing-arrest cells are cells that are normally kept under specific culture conditions or treated with agents that prevent cell division from being held in a non-dividing state. This can be achieved through methods such as serum starvation, chemical inhibitors of cell cycle progression, or genetic modification.

Well-characterized stable cell lines;
for cell-based high-throughput screening;
Low-cost evaluation of stable cell lines or limited quantities of compounds.

GPR91 receptor function, signaling pathways, and potential therapeutic interventions.

GPCR

GPR91

Citric Acid Cycle Intermediates

Human

CHO-K1

Expression vector containing full-length human GPR91 cDNA (GenBank Accession umber: NM_033050.3) with FLAG tag sequence at N- terminus.

GenBank Accession umber: NM_033050.3

GPR91, also known as SUCNR1, is a G Protein-Coupled Receptor with 339 amino acids. It has been characterized as a receptor for Succinate, a citric acid cycle intermediate. Succinate plays a key role in energy metabolism. Local interstitial accumulation of Succinate has recently been reported to serve as an indicator of ischemic or diabetic organ damage in the brain, liver, and kidney. In diabetes patients, the accumulation of Succinate is detectable in the plasma, and more significantly in the renal tubular fluid and urine. It is therefore considered a potential new biomarker of local tissue damage. It has also been shown that Succinate increases blood pressure in animals. The Succinate-induced hypertensive effect involves the renin-angiotensin system that is shown to be absent in GPR91-deficient mice. There is a possible role for GPR91 in renovascular hypertension, a disease closely linked to atherosclerosis, diabetes and renal failure. In a recombinant system overexpressing GPR91, Succinate was shown to not only stimulate calcium mobilization and inositol phosphate (IP) accumulation through the stimulation of Gαq pathway but also to activate the Erk1/2 MAPK pathway and inhibit forskolin- stimulated cAMP accumulation through Gαi pathway.