citations: 11
Alomone Labs Nifedipine blocks L-type Ca2+currents inXenopusoocytes. - A. Time course of L-type channel (CaV1.2+?2?1+?1a) activity before and during applications of 0.10.512 and 10 ?MNifedipine(#N-120) as indicated and upon wash. Holding potential was -80 mV and currents were elicited every 10 seconds by 100 ms ramp to +50 mV. B. Superimposed current traces of L-type channels (CaV1.2+?2?1+?1a) before and during applications of 0.1 1 and 10 ?M Nifedipine as indicated. Holding potential was -100 mV and currents were elicited every 10 seconds by 100 ms steps to +10 mV.
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citations: 2
Alomone Labs Capsaicin induces Ca2+influx via activation of TRPV1 channels expressed in C6 cells. - Cells were loaded with Fluo-3 AM and stimulated withCapsaicin(#C-125). Changes in intracellular Ca2+were detected via changes in Fluo-3 emission following application. The left panel shows normalized fluorescence before and after application at 20 seconds of 0-10 M Capsaicin (as indicated). The right panel shows normalized fluorescence plotted against Capsaicin concentrations.
Peptide (C)KAEEDEILNRSPRNRK corresponding to amino acid residues 572-587 of rat Canx (AccessionP35565). Intracellular C-terminus.
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Alomone Labs Diazepam inhibits specific binding of Flunitrazepam to rat brain GABA(A) receptors. - Percent inhibition of the specific binding of 1 nM [3H]Flunitrazepam to membranes from whole rat brain (except cerebellum) was plotted against concentrations ofDiazepam(#D-215) (green circles) and of Diazepam standard (black squares) and used to calculate IC50and Ki values for Diazepam (IC50? 36 nM and Ki ? 29 nM).
Alomone Labs Curcumin activates TRPA1 channels expressed in HEK-293 cells. - Dose-response curve for the activation of human TRPA1 expressing HEK-293 cells loaded with Calcium 5 dye for changes in intracellular Ca2+measurements. Calcium signal was apparent with 100 MCurcumin(#C-230).
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Alomone Labs Lidocaine inhibits NaV1.2 channels expressed inXenopusoocytes. - A. Currents were elicited by a double test pulse protocol applied every 10 sec which is schematically described on the top panel. For the first pulse the holding potential was -120 mV while the second pulse was preceded by 100 ms at -80 mV. On the bottom; superimposed example current responses to the voltage stimulation before (black) and during application of 0.5 mM Lidocaine (#L-105) (green). B. Time course of NaV1.2 current amplitude changes as a result of Lidocaine application for each of the two test pulses (demonstrating the dependency of the inhibition on the voltage driven conformation of the channel).
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Alomone Labs SB 203580 inhibits the phosphorylation of Elk1 and Atf2 via p38 in 3T3-L1 cells. - Cells were grown to 70% confluence and serum starved for 3 h. The cells were then incubated for 2 h with various concentrations ofSB 203580(#S-370) and stimulated with 5 MAnisomycin(#A-520). Cell proteins were resolved by SDS-PAGE and probed with anti-phospho-p38 MAPK antip38 MAPK anti-phospho-Elk1 and anti-phospho-Atf2 as indicated. The phosphorylation of Elk1 and Atf2 decreased in a dose-dependent manner.
Alomone LabsQO-40enhances KCNQ2/KCNQ3heteromeric channels expressed inXenopusoocytes. - A. Time course of KCNQ2/KCNQ3 current enhancement by 40 and 100 MQO-40(#Q-265). Currents were elicited by application of voltage step from a holding potential of -100 mV to -60 mV (800 msec). B. Superimposed example traces of current responses before and during perfusion of 40 and 100 M QO-40 as indicated.
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