Figure 1: Substance P-induced concentration-dependent stimulation of intracellular calcium mobilization in CHO-K1/NK1 cells. The cells were loaded with Calcium-4 prior to stimulation with NK1 receptor agonist, Substance P. The intracellular calcium change was measured by FLIPR. The relative fluorescent units (RFU) were normalized and plotted against the log of the cumulative doses (5-fold dilution) of Substance P (Mean ± SD, n = 3). The EC50 of Substance P on NK1/CHO-K1 cells was 67 nM.
Note:
1. EC50 value is calculated with four parameter logistic equation:
Y=Bottom + (Top-Bottom)/ (1+10^ ((LogEC50-X)*HillSlope))
X is the logarithm of concentration.
Y is the response and starts at Bottom and goes to Top with a sigmoid shape.
CHO-K1/NK1 Stable Cell Line
Tachykinins are peptides sharing the common C-terminal amino acid sequence Phe-X-Gly-Leu-Met-NH2. This neuropeptide family is composed of substance P, neurokinin A, and neurokinin B, which are widely distributed in mammalian central and peripheral nervous systems. It plays a role as both a neurotransmitter and a neuromodulator. Their actions are mediated by binding with three distinct receptors, namely, NK1, NK2, and NK3. NK1 has high affinity with substance P. In the CNS, NK1 has been implicated to play a role in regulating neuronal survival and degeneration. In the cardiovascular system, NK1 mediates endothelium-dependent vasodilatation and plasma protein extravasations. In the gastrointestinal system, NK1 receptors mediate intestinal motility, secretion, and vascular functions. SP-NK1 receptor communication is also involved in glioma development and progression. NK1 receptor antagonists may have several therapeutic applications in diseases mediated by tachykinins, such as pulmonary disorders, gut disorders, and the pathophysiology of depression.
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