Short Decsription
Creative Biolabs offers HEK293T-Tg(Human Gαqi5//Human CX3CR1 Receptor) Division-Arrested Cell which CX3CR1 receptor stably expressed in HEK293T cells which overexpress Gαqi5.
Description
HEK293T-Tg(Human Gαqi5//Human CX3CR1 Receptor) Division-Arrested Cell was engineered to express the receptor human CX3CR1 (NM_001337) and Gαqi5 gene. This cell line can be used to study CX3CR1 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.
Features
Well-characterized stable cell lines;
for cell-based high-throughput screening;
Low-cost evaluation of stable cell lines or limited quantities of compounds.
Applications
CX3CR1 receptor function, signaling pathways, and potential therapeutic interventions.
Protein Target
GPCR
Receptor Name
CX3CR1
Receptor Family
Chemokine
Species
Human
Parental Cell Line
HEK293T Gαqi5
Transfection
Expression vector containing full-length human CX3CR1 cDNA (GenBank Accession Number NM_001337) with FLAG tag sequence at N-terminus
Gene
NM_001337
Background
CX3CR1, (CX3C-chemokine receptor 1, fractalkine receptor or GPR13) is a receptor for the CX3C chemokine fractalkine. CX3CR1 is expressed in cytotoxic effector lymphocytes, including natural killer cells, cytotoxic T lymphocytes and macrophages. Soluble fractalkine causes migration of these cells, whereas the membrane-bound form captures and enhances the subsequent migration in response to secondary stimulation with other chemokines. Furthermore, stimulation through membrane-bound fractalkine activates natural killer cells, leading to increased cytotoxicity and interferon-gamma production. Fractalkine is involved in the pathogenesis of various clinical disease states or processes, such as atherosclerosis, glomerulonephritis, cardiac allograft rejection and rheumatoid arthritis. In addition, polymorphisms in CX3CR1, which reduce its binding activity to fractalkine, have been reported to increase the risk of HIV disease and to reduce the risk of coronary artery disease.

For Research Use Only | Not For Clinical Use

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