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M00228
293/EP1 Stable Cell Line
2 vials
Product Name 293/EP1 Stable Cell Line
Full Name
Human Recombinant EP1 Prostanoid Receptor Stable Cell Line
Documents
Document-EXAMPLE: 10023_20090630012808.JPG (JPG)
TECHNICAL MANUAL: 10024_20090630013059.PDF (PDF)
Document-MSDS: 10397_20090813070023.PDF (PDF)
Figures
Reference
Species
Human
Description
Prostaglandins are known to affect the nervous system and can modulate synaptic transmission and neurotransmitter release, the sleep/wake cycle, fever, pain, and the immune system. Prostaglandin E2 receptor, EP1 subtype (EP1/PTGER1) is a receptor for prostaglandin E2 (PGE2). The members of the EP receptor family, EP1, EP2, EP3, and EP4, elicit their actions by altering cyclic adenosine monophosphate (cAMP) or intracellular calcium concentrations. EP1 activates phospholipase C and phosphatidylinositol turnover and stimulates the release of intracellular calcium via a Gi/Gq-coupled mechanism. EP2 and EP4 both signal through a Gs-coupled mechanism that stimulates adenylyl cyclase and increases intracellular levels of cAMP. EP1 appears to mediate the effects of PGE2 in promoting the formation of precancerous lesions in animal models of colon cancer. In addition, EP1 has an inhibitory effect on stress-induced aggressive and risk-taking behaviors in mice.
Freeze Medium
45% culture medium, 45% FBS, 10% DMSO
Culture Medium
DMEM, 10% FBS, 200 μg/ml Zeocin, 250 μg/ml G418
Storage
Liquid nitrogen immediately upon delivery
Application
Functional assay for EP1 receptor
Application Examples
Figure 1. PGE2-induced concentration-dependent stimulation of intracellular calcium mobilization in 293/EP1 and 293 cells. The cells were loaded with Calcium-4 prior to stimulation with an EP1 receptor agonist, PGE2. The intracellular calcium change was measured by FlexStation. The relative fluorescent units (RFU) were plotted against the log of the cumulative doses (10-fold dilution) of PGE2 (Mean ± SD, n = 2). The EC50 of PGE2 on EP1 in 293 cells was 0.22 nM. The S/B of PGE2 on EP1 in 293 cells was 34.
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