https://www.selleckchem.com/products/pt2399.html
001, n = 6). When the pipette solution contained ADPR (300 μM) and the TRPM2 antagonists flufenamic acid (FFA) (100 μM), N-(p-amylcinnamoyl) anthranilic acid (ACA) (50 μM) and 8-bromo-cADP-Ribose (8-Br-cADPR) (50 μM), the membrane potential shifted in a hyperpolarizing direction. ADPR did not significantly change the resting membrane potential and action potential firing rate of stellate cells from TRPM2-/- mice. In conclusion, the results obtained using these molecular, immunohistochemical and electrophysiological approaches reveal the
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