charybdotoxin  (Alomone Labs)


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    Alomone Labs charybdotoxin
    External Ca 2+ dependence and sensitivity to K + channel blocker <t>charybdotoxin</t> of EGF Ca 2+ transients. A/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in 3 mM extracellular Ca 2+ (n = 24) or in 0 mM Ca 2+/ 1 mM EGTA (n = 28) in the extracellular medium. B/Fluorescence intensity signaling of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when 3 mM Ca 2+ was present (n = 24). The averaged population signal is shown as a thick black trace. C/Fluorescence intensity of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when Ca 2+ was removed and 1 mM EGTA was added to the extracellular medium (n = 28). The averaged population signal is shown as a thick black trace. D/Average of all cell signals during 2 nM EGF application, synchronized at the time of the first fluorescence peak and averaged for 150 sec, when 3 mM Ca 2+ was present (black line, n = 24) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 28). E/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in 3 mM extracellular Ca 2+ (n = 13) or in 0 mM Ca 2+/ 1 mM EGTA (n = 11) in the extracellular medium. F/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when 3 mM Ca 2+ was present (n = 13). The averaged population signal is shown as a thick black trace. G/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (n = 11). The averaged population signal is shown as a thick black trace. H/Average of all cell signals during 20 pM EGF application, synchronized at the time the first fluorescence peak and for 150 sec, when 3 mM Ca 2+ was present (black line, n = 13) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 11). I/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in the absence (0, n = 24/27) or in the presence (100, n = 16/19) of 100 nM charybdotoxin (chx) in the extracellular medium. J/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in the absence (0, n = 16/22) or in the presence (100, n = 6/22) of 100 nM charybdotoxin (chx) in the extracellular medium.
    Charybdotoxin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/charybdotoxin/product/Alomone Labs
    Average 93 stars, based on 40 article reviews
    Price from $9.99 to $1999.99
    charybdotoxin - by Bioz Stars, 2022-08
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    Images

    1) Product Images from "Physiological Epidermal Growth Factor Concentrations Activate High Affinity Receptors to Elicit Calcium Oscillations"

    Article Title: Physiological Epidermal Growth Factor Concentrations Activate High Affinity Receptors to Elicit Calcium Oscillations

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0106803

    External Ca 2+ dependence and sensitivity to K + channel blocker charybdotoxin of EGF Ca 2+ transients. A/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in 3 mM extracellular Ca 2+ (n = 24) or in 0 mM Ca 2+/ 1 mM EGTA (n = 28) in the extracellular medium. B/Fluorescence intensity signaling of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when 3 mM Ca 2+ was present (n = 24). The averaged population signal is shown as a thick black trace. C/Fluorescence intensity of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when Ca 2+ was removed and 1 mM EGTA was added to the extracellular medium (n = 28). The averaged population signal is shown as a thick black trace. D/Average of all cell signals during 2 nM EGF application, synchronized at the time of the first fluorescence peak and averaged for 150 sec, when 3 mM Ca 2+ was present (black line, n = 24) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 28). E/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in 3 mM extracellular Ca 2+ (n = 13) or in 0 mM Ca 2+/ 1 mM EGTA (n = 11) in the extracellular medium. F/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when 3 mM Ca 2+ was present (n = 13). The averaged population signal is shown as a thick black trace. G/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (n = 11). The averaged population signal is shown as a thick black trace. H/Average of all cell signals during 20 pM EGF application, synchronized at the time the first fluorescence peak and for 150 sec, when 3 mM Ca 2+ was present (black line, n = 13) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 11). I/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in the absence (0, n = 24/27) or in the presence (100, n = 16/19) of 100 nM charybdotoxin (chx) in the extracellular medium. J/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in the absence (0, n = 16/22) or in the presence (100, n = 6/22) of 100 nM charybdotoxin (chx) in the extracellular medium.
    Figure Legend Snippet: External Ca 2+ dependence and sensitivity to K + channel blocker charybdotoxin of EGF Ca 2+ transients. A/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in 3 mM extracellular Ca 2+ (n = 24) or in 0 mM Ca 2+/ 1 mM EGTA (n = 28) in the extracellular medium. B/Fluorescence intensity signaling of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when 3 mM Ca 2+ was present (n = 24). The averaged population signal is shown as a thick black trace. C/Fluorescence intensity of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when Ca 2+ was removed and 1 mM EGTA was added to the extracellular medium (n = 28). The averaged population signal is shown as a thick black trace. D/Average of all cell signals during 2 nM EGF application, synchronized at the time of the first fluorescence peak and averaged for 150 sec, when 3 mM Ca 2+ was present (black line, n = 24) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 28). E/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in 3 mM extracellular Ca 2+ (n = 13) or in 0 mM Ca 2+/ 1 mM EGTA (n = 11) in the extracellular medium. F/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when 3 mM Ca 2+ was present (n = 13). The averaged population signal is shown as a thick black trace. G/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (n = 11). The averaged population signal is shown as a thick black trace. H/Average of all cell signals during 20 pM EGF application, synchronized at the time the first fluorescence peak and for 150 sec, when 3 mM Ca 2+ was present (black line, n = 13) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 11). I/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in the absence (0, n = 24/27) or in the presence (100, n = 16/19) of 100 nM charybdotoxin (chx) in the extracellular medium. J/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in the absence (0, n = 16/22) or in the presence (100, n = 6/22) of 100 nM charybdotoxin (chx) in the extracellular medium.

    Techniques Used: Fluorescence, Size-exclusion Chromatography

    2) Product Images from "HIV-1 gp120 and chemokines activate ion channels in primary macrophages through CCR5 and CXCR4 stimulation"

    Article Title: HIV-1 gp120 and chemokines activate ion channels in primary macrophages through CCR5 and CXCR4 stimulation

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi:

    Potassium and chloride currents evoked by gp120 in MDM. The ionic nature of currents elicited in MDM by gp120 from JRFL ( A ) and IIIB ( B ) was determined from the reversal potential (right) and with channel inhibitors (left). At peak activation, the outward JRFL current reversed direction at ≈−78 mV ( A , top right) whereas the peak inward currents elicited by JRFL ( A , bottom right) and IIIB ( B , right) reversed at ≈5 mV (squares). In low Cl − bath solution, the current voltage relationship of the inward current elicited by both Envs shifted to ≈+40 mV (circles). Charybdotoxin (100 nM) blocked the JRFL-evoked outward current, and NPPB (10 μM) blocked the inward currents activated by both Envs ( A and B , left).
    Figure Legend Snippet: Potassium and chloride currents evoked by gp120 in MDM. The ionic nature of currents elicited in MDM by gp120 from JRFL ( A ) and IIIB ( B ) was determined from the reversal potential (right) and with channel inhibitors (left). At peak activation, the outward JRFL current reversed direction at ≈−78 mV ( A , top right) whereas the peak inward currents elicited by JRFL ( A , bottom right) and IIIB ( B , right) reversed at ≈5 mV (squares). In low Cl − bath solution, the current voltage relationship of the inward current elicited by both Envs shifted to ≈+40 mV (circles). Charybdotoxin (100 nM) blocked the JRFL-evoked outward current, and NPPB (10 μM) blocked the inward currents activated by both Envs ( A and B , left).

    Techniques Used: Activation Assay

    3) Product Images from "Characterisation of K+ Channels in Human Fetoplacental Vascular Smooth Muscle Cells"

    Article Title: Characterisation of K+ Channels in Human Fetoplacental Vascular Smooth Muscle Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057451

    Characterisation of Ca 2+ -activated K + channel isoforms in CPASMCs. Representative example of the inhibition of outward currents by the BK Ca and IK Ca blocker charybdotoxin (ChTx; n = 4; N = 2; 100 nM; A ), but not the specific IK Ca inhibitor TRAM-34 (n = 3, N = 2; 10µM; B ). The specific BK Ca blocker iberiotoxin (IbTx; 100 nM; C ) inhibited outward currents at depolarised potentials. Mean current-voltage relationships measured at the end of the 500 ms voltage step ranging from -70 mV to +80 mV were obtained in the absence (•) and presence (○) of IbTx ( D ; *P
    Figure Legend Snippet: Characterisation of Ca 2+ -activated K + channel isoforms in CPASMCs. Representative example of the inhibition of outward currents by the BK Ca and IK Ca blocker charybdotoxin (ChTx; n = 4; N = 2; 100 nM; A ), but not the specific IK Ca inhibitor TRAM-34 (n = 3, N = 2; 10µM; B ). The specific BK Ca blocker iberiotoxin (IbTx; 100 nM; C ) inhibited outward currents at depolarised potentials. Mean current-voltage relationships measured at the end of the 500 ms voltage step ranging from -70 mV to +80 mV were obtained in the absence (•) and presence (○) of IbTx ( D ; *P

    Techniques Used: Inhibition, Mass Spectrometry

    4) Product Images from "Duration differences of corticostriatal responses in striatal projection neurons depend on calcium activated potassium currents"

    Article Title: Duration differences of corticostriatal responses in striatal projection neurons depend on calcium activated potassium currents

    Journal: Frontiers in Systems Neuroscience

    doi: 10.3389/fnsys.2013.00063

    Ca 2+ -activated K + -currents control the propagation of autoregenerative potentials in iSPNs. (A) Green trace shows a control suprathreshold corticostriatal response in an iSPN. Addition of 100 nM apamin discloses an autoregenerative and propagated action potential whose main ionic component is Ca 2+ (purple trace; Bargas et al., 1991 ). Subsequent addition of 20 nM ChTx in the continuous presence of apamin further prolongs the duration of the regenerative event without increasing its amplitude, illustrating its all-or-none properties (black trace). (B) Green trace is a spontaneous regenerative event that sometimes appears in control suprathreshold responses in iSPNs (alternating with the initial burst of spikes). Addition of 2.5 μM NS 309 hindered the propagation of this event to the somatic area and accelerated the repolarization (orange trace). Clearly, fast spikes inactivate when calcium autoregenerative potentials propagate.
    Figure Legend Snippet: Ca 2+ -activated K + -currents control the propagation of autoregenerative potentials in iSPNs. (A) Green trace shows a control suprathreshold corticostriatal response in an iSPN. Addition of 100 nM apamin discloses an autoregenerative and propagated action potential whose main ionic component is Ca 2+ (purple trace; Bargas et al., 1991 ). Subsequent addition of 20 nM ChTx in the continuous presence of apamin further prolongs the duration of the regenerative event without increasing its amplitude, illustrating its all-or-none properties (black trace). (B) Green trace is a spontaneous regenerative event that sometimes appears in control suprathreshold responses in iSPNs (alternating with the initial burst of spikes). Addition of 2.5 μM NS 309 hindered the propagation of this event to the somatic area and accelerated the repolarization (orange trace). Clearly, fast spikes inactivate when calcium autoregenerative potentials propagate.

    Techniques Used:

    Blockade of BK and SK channels depolarize and prolong corticostriatal responses in striatal projection neurons. (A) Three superimposed records from a dSPN were obtained without changing stimulus strength: they show a corticostriatal response in control conditions (red trace), the same response in the presence of the blocker of BK-channels, 20 nM charybdotoxin (ChTx, blue trace), and finally, the same response in the presence of both ChTx and the blocker of SK channels, 100 nM apamin (ChTx + apamin, black trace). Each blocker depolarized and prolonged the response, and also increased the number of action potentials that were fired. Digital subtractions at bottom illustrate the hyperpolarizing influence that Ca 2+ -activated K + -currents exerted over the corticostriatal responses and that were suppressed by the blockade of ChTx (blue) and apamin (black). Note that the hyperpolarizing influence of Ca 2+ -activated K + -currents rise slowly and last hundreds of milliseconds thus contributing to restrain the build up of the corticostriatal response. (B) Intensity-response (I-R) graphs obtained by plotting average half width (duration at 50% of the peak amplitude of the response) as a function of threshold intensity including: minimal, subthreshold (0.5×), threshold (1.0×) and suprathreshold responses (2.0×). A sigmoid function was fitted. Curves with the action of each blocker are plotted individually as well as the administration of both blockers together. Shadowed colored areas denote 95% confidence intervals, symbols depict average values of the samples for each stimulus strength ± s.e.m. (C) Tukey box plots illustrate the distributions of measurements for suprathreshold responses (half width at 2× threshold strength), in control, in the presence of each blocker, and in the presence of both blockers. Differences are significant: * P
    Figure Legend Snippet: Blockade of BK and SK channels depolarize and prolong corticostriatal responses in striatal projection neurons. (A) Three superimposed records from a dSPN were obtained without changing stimulus strength: they show a corticostriatal response in control conditions (red trace), the same response in the presence of the blocker of BK-channels, 20 nM charybdotoxin (ChTx, blue trace), and finally, the same response in the presence of both ChTx and the blocker of SK channels, 100 nM apamin (ChTx + apamin, black trace). Each blocker depolarized and prolonged the response, and also increased the number of action potentials that were fired. Digital subtractions at bottom illustrate the hyperpolarizing influence that Ca 2+ -activated K + -currents exerted over the corticostriatal responses and that were suppressed by the blockade of ChTx (blue) and apamin (black). Note that the hyperpolarizing influence of Ca 2+ -activated K + -currents rise slowly and last hundreds of milliseconds thus contributing to restrain the build up of the corticostriatal response. (B) Intensity-response (I-R) graphs obtained by plotting average half width (duration at 50% of the peak amplitude of the response) as a function of threshold intensity including: minimal, subthreshold (0.5×), threshold (1.0×) and suprathreshold responses (2.0×). A sigmoid function was fitted. Curves with the action of each blocker are plotted individually as well as the administration of both blockers together. Shadowed colored areas denote 95% confidence intervals, symbols depict average values of the samples for each stimulus strength ± s.e.m. (C) Tukey box plots illustrate the distributions of measurements for suprathreshold responses (half width at 2× threshold strength), in control, in the presence of each blocker, and in the presence of both blockers. Differences are significant: * P

    Techniques Used:

    Influence of Ca 2+ -activated K + -currents on subthreshold corticostriatal responses. (A) Subthreshold synaptic potentials recorded after cortical stimulation in a dSPN in control conditions (red), after addition of 100 nM apamin (purple) and after addition of 20 nM ChTx in the continuous presence of apamin (black). (B) The same experiment was performed on an iSPN (control condition is in green). Note that Ca 2+ -activated K + -currents appear to exert more influence on subthreshold synaptic events of iSPNs. (C) Subthreshold synaptic potentials recorded after cortical stimulation in a dSPN in control conditions (red), after addition of 2.5 μM NS 309 (orange), an enhancer of SK-channels, and after addition of 2.5 μM NS 1619, an enhancer of BK-channels, in the continuous presence of NS 309 (black). (D) The same experiment performed on an iSPN (control condition is in green). Enhancers of Ca 2+ -activated K + -currents also indicate more influence of these currents in subthreshold synaptic events of iSPNs.
    Figure Legend Snippet: Influence of Ca 2+ -activated K + -currents on subthreshold corticostriatal responses. (A) Subthreshold synaptic potentials recorded after cortical stimulation in a dSPN in control conditions (red), after addition of 100 nM apamin (purple) and after addition of 20 nM ChTx in the continuous presence of apamin (black). (B) The same experiment was performed on an iSPN (control condition is in green). Note that Ca 2+ -activated K + -currents appear to exert more influence on subthreshold synaptic events of iSPNs. (C) Subthreshold synaptic potentials recorded after cortical stimulation in a dSPN in control conditions (red), after addition of 2.5 μM NS 309 (orange), an enhancer of SK-channels, and after addition of 2.5 μM NS 1619, an enhancer of BK-channels, in the continuous presence of NS 309 (black). (D) The same experiment performed on an iSPN (control condition is in green). Enhancers of Ca 2+ -activated K + -currents also indicate more influence of these currents in subthreshold synaptic events of iSPNs.

    Techniques Used:

    5) Product Images from "Inhibition of T cell proliferation by selective block of Ca2+-activated K+ channels"

    Article Title: Inhibition of T cell proliferation by selective block of Ca2+-activated K+ channels

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi:

    ( A ) Effect of clotrimazole and ketoconazole on T cell proliferation. Cells were incubated for 5 days in culture medium with PPD and the IK channel blockers (10 μM clotrimazole or 10 μM ketoconazole), which were added 30 min before the addition of PPD. [ 3 H]Thymidine (1 mCi) incorporation was then measured in triplicate wells. The bars represents 12 independent experiments ± SE; control = 26 ± 12 × 10 3 cpm per well; clotrimazole = 12 ± 6 × 10 3 cpm per well; ketoconazole = 20 ± 10 × 10 3 cpm per well. ∗, P ≤ 0.008 vs. control. ( B ) Effect of nitrendipine, clotrimazole, and charybdotoxin on T cell proliferation. Cells were incubated for 5 days in culture medium with Candida albicans and the IK channel blockers (10 μM nitrendipine, 100 nM charybdotoxin, or 10 μM clotrimazole), which were added 30 min before the addition of Candida albicans. [ 3 H]Thymidine (1 mCi) incorporation was then measured in triplicate wells. The bars represents 9 independent experiments ± SE for control, and 3 independent experiments in the presence of nitrendipine, clotrimazole, and charybdotoxin, respectively. ∗, P ≤ 0.05 vs. control; ∗∗, P ≤ 0.01 vs. control.
    Figure Legend Snippet: ( A ) Effect of clotrimazole and ketoconazole on T cell proliferation. Cells were incubated for 5 days in culture medium with PPD and the IK channel blockers (10 μM clotrimazole or 10 μM ketoconazole), which were added 30 min before the addition of PPD. [ 3 H]Thymidine (1 mCi) incorporation was then measured in triplicate wells. The bars represents 12 independent experiments ± SE; control = 26 ± 12 × 10 3 cpm per well; clotrimazole = 12 ± 6 × 10 3 cpm per well; ketoconazole = 20 ± 10 × 10 3 cpm per well. ∗, P ≤ 0.008 vs. control. ( B ) Effect of nitrendipine, clotrimazole, and charybdotoxin on T cell proliferation. Cells were incubated for 5 days in culture medium with Candida albicans and the IK channel blockers (10 μM nitrendipine, 100 nM charybdotoxin, or 10 μM clotrimazole), which were added 30 min before the addition of Candida albicans. [ 3 H]Thymidine (1 mCi) incorporation was then measured in triplicate wells. The bars represents 9 independent experiments ± SE for control, and 3 independent experiments in the presence of nitrendipine, clotrimazole, and charybdotoxin, respectively. ∗, P ≤ 0.05 vs. control; ∗∗, P ≤ 0.01 vs. control.

    Techniques Used: Incubation

    Time course of whole-cell currents from a T cell activated by purified protein derivative (PPD) at −80 mV measured from voltage ramps (±100 mV every 5 s, 200-ms duration) under control conditions (extracellular K + solution in the bath) and during the application of the indicated compounds. The concentrations used were ketoconazole (Keto), 1 μM; nitrendipine (Nitr), 1 μM; charybdotoxin (ChTx), 200 nM; and clotrimazole (CLT), 1 μM. Free Ca 2+ in the pipette solutions was 1 μM.
    Figure Legend Snippet: Time course of whole-cell currents from a T cell activated by purified protein derivative (PPD) at −80 mV measured from voltage ramps (±100 mV every 5 s, 200-ms duration) under control conditions (extracellular K + solution in the bath) and during the application of the indicated compounds. The concentrations used were ketoconazole (Keto), 1 μM; nitrendipine (Nitr), 1 μM; charybdotoxin (ChTx), 200 nM; and clotrimazole (CLT), 1 μM. Free Ca 2+ in the pipette solutions was 1 μM.

    Techniques Used: Purification, Mass Spectrometry, Transferring

    ( Upper ) Dose–response relations of nitrendipine, clotrimazole, and charybdotoxin on T cell proliferation. Cells were incubated for 5 days in culture medium with PPD. The IK channel blockers, in the concentrations indicated, were added 30 min before the addition of antigen. [ 3 H]Thymidine (1 mCi) incorporation was then measured in triplicate wells. The bars represents nine independent experiments ± SE for control, and three independent experiments in the presence of nitrendipine, clotrimazole, or charybdotoxin, respectively. ∗, P ≤ 0.05 vs. control. Six other experiments using Candida albicans or tetanus toxin as the antigen challenge gave similar results. ( Lower ) Donor variability of the clotrimazole effect on T cell proliferation. PHA, phytohemagglutinin. Cells from three different donors were incubated for 5 days in culture medium with mitogen (ConA or PHA) or antigen (tetanus toxin or PPD) and 10 μM clotrimazole, which was added 30 min before the addition of Candida albicans . [ 3 H]Thymidine (1 mCi) incorporation was then measured in triplicate wells. The bars represents three independent experiments ± SE.
    Figure Legend Snippet: ( Upper ) Dose–response relations of nitrendipine, clotrimazole, and charybdotoxin on T cell proliferation. Cells were incubated for 5 days in culture medium with PPD. The IK channel blockers, in the concentrations indicated, were added 30 min before the addition of antigen. [ 3 H]Thymidine (1 mCi) incorporation was then measured in triplicate wells. The bars represents nine independent experiments ± SE for control, and three independent experiments in the presence of nitrendipine, clotrimazole, or charybdotoxin, respectively. ∗, P ≤ 0.05 vs. control. Six other experiments using Candida albicans or tetanus toxin as the antigen challenge gave similar results. ( Lower ) Donor variability of the clotrimazole effect on T cell proliferation. PHA, phytohemagglutinin. Cells from three different donors were incubated for 5 days in culture medium with mitogen (ConA or PHA) or antigen (tetanus toxin or PPD) and 10 μM clotrimazole, which was added 30 min before the addition of Candida albicans . [ 3 H]Thymidine (1 mCi) incorporation was then measured in triplicate wells. The bars represents three independent experiments ± SE.

    Techniques Used: Incubation

    6) Product Images from "Potent Suppression of Kv1.3 Potassium Channel and IL-2 Secretion by Diphenyl Phosphine Oxide-1 in Human T Cells"

    Article Title: Potent Suppression of Kv1.3 Potassium Channel and IL-2 Secretion by Diphenyl Phosphine Oxide-1 in Human T Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0064629

    Inhibitory effect of DPO-1 and potassium channel blockers on IL-2 production in activated Jurkat cells. Jurkat cells were activated with PHA (5 µg/mL) and PMA (80 nM) for 24 h. DPO-1 (3 and 10 µM), MgTX (10 nM) and ChTX (100 nM) were added simultaneously. *** P
    Figure Legend Snippet: Inhibitory effect of DPO-1 and potassium channel blockers on IL-2 production in activated Jurkat cells. Jurkat cells were activated with PHA (5 µg/mL) and PMA (80 nM) for 24 h. DPO-1 (3 and 10 µM), MgTX (10 nM) and ChTX (100 nM) were added simultaneously. *** P

    Techniques Used:

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    • chlorotoxin chtx  (Alomone Labs)
    93
    Alomone Labs chlorotoxin chtx
    Effect of SOL, SOL plus acetylcholine (ACh), SOL plus iberiotoxin (Iber), SOL plus apamin (Apa), SOL plus tolbutamide (TLB), SOL plus <t>chlorotoxin</t> <t>(ChTx),</t> SOL plus Lino, or SOL plus TRH on the amplitude of I K(M) . In these experiments, we bathed GH 3 cells in high-K + , Ca 2+ -free solution and the recording electrode was filled with K + -enriched (145 mM) solution. Current amplitude was measured at the end of the depolarizing step from −50 to −10 mV. Each bar represents the mean ± SEM ( n = 7). * Significantly different from controls ( p
    Chlorotoxin Chtx, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/chlorotoxin chtx/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    chlorotoxin chtx - by Bioz Stars, 2022-08
    93/100 stars
    		  Buy from Supplier
    charybdotoxin chtx  (Alomone Labs)
    93
    Alomone Labs charybdotoxin chtx
    K+ channel blockers inhibit GrB production by activated CD8+ T cells. Freshly isolated CD8+ T cells were pretreated with a Kv1.3 channel blocker, ShK at various concentrations (A) or with ShK (10 nM), MgTX (30 nM), <t>ChTX</t> (50 nM) and TRAM-34 (500 nM) (B) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone. The levels of GrB were measured in cell supernatants by ELISA at 6 h (A) and indicated times (B and C). Data are mean of triplicate ± SD of one representative of three independent and reproducible experiments. Values that are significantly different from that of non-blocker vehicle treated control are indicated as follows: *, p
    Charybdotoxin Chtx, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/charybdotoxin chtx/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    charybdotoxin chtx - by Bioz Stars, 2022-08
    93/100 stars
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    Image Search Results


    Effect of SOL, SOL plus acetylcholine (ACh), SOL plus iberiotoxin (Iber), SOL plus apamin (Apa), SOL plus tolbutamide (TLB), SOL plus chlorotoxin (ChTx), SOL plus Lino, or SOL plus TRH on the amplitude of I K(M) . In these experiments, we bathed GH 3 cells in high-K + , Ca 2+ -free solution and the recording electrode was filled with K + -enriched (145 mM) solution. Current amplitude was measured at the end of the depolarizing step from −50 to −10 mV. Each bar represents the mean ± SEM ( n = 7). * Significantly different from controls ( p

    Journal: International Journal of Molecular Sciences

    Article Title: The Effectiveness in Activating M-Type K+ Current Produced by Solifenacin ([(3R)-1-azabicyclo[2.2.2]octan-3-yl] (1S)-1-phenyl-3,4-dihydro-1H-isoquinoline-2-carboxylate): Independent of Its Antimuscarinic Action

    doi: 10.3390/ijms222212399

    Figure Lengend Snippet: Effect of SOL, SOL plus acetylcholine (ACh), SOL plus iberiotoxin (Iber), SOL plus apamin (Apa), SOL plus tolbutamide (TLB), SOL plus chlorotoxin (ChTx), SOL plus Lino, or SOL plus TRH on the amplitude of I K(M) . In these experiments, we bathed GH 3 cells in high-K + , Ca 2+ -free solution and the recording electrode was filled with K + -enriched (145 mM) solution. Current amplitude was measured at the end of the depolarizing step from −50 to −10 mV. Each bar represents the mean ± SEM ( n = 7). * Significantly different from controls ( p

    Article Snippet: Chlorotoxin (ChTx) was kindly provided by Professor Dr. Woei-Jer Chuang (Department of Biochemistry, National Cheng Kung University Medical College, Tainan, Taiwan).

    Techniques:

    K+ channel blockers inhibit GrB production by activated CD8+ T cells. Freshly isolated CD8+ T cells were pretreated with a Kv1.3 channel blocker, ShK at various concentrations (A) or with ShK (10 nM), MgTX (30 nM), ChTX (50 nM) and TRAM-34 (500 nM) (B) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone. The levels of GrB were measured in cell supernatants by ELISA at 6 h (A) and indicated times (B and C). Data are mean of triplicate ± SD of one representative of three independent and reproducible experiments. Values that are significantly different from that of non-blocker vehicle treated control are indicated as follows: *, p

    Journal: PLoS ONE

    Article Title: Blockade of Kv1.3 Potassium Channels Inhibits Differentiation and Granzyme B Secretion of Human CD8+ T Effector Memory Lymphocytes

    doi: 10.1371/journal.pone.0054267

    Figure Lengend Snippet: K+ channel blockers inhibit GrB production by activated CD8+ T cells. Freshly isolated CD8+ T cells were pretreated with a Kv1.3 channel blocker, ShK at various concentrations (A) or with ShK (10 nM), MgTX (30 nM), ChTX (50 nM) and TRAM-34 (500 nM) (B) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone. The levels of GrB were measured in cell supernatants by ELISA at 6 h (A) and indicated times (B and C). Data are mean of triplicate ± SD of one representative of three independent and reproducible experiments. Values that are significantly different from that of non-blocker vehicle treated control are indicated as follows: *, p

    Article Snippet: Charybdotoxin (ChTx) and margatoxin (MgTx) were purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Isolation, Enzyme-linked Immunosorbent Assay

    Kv1.3 blockade suppresses proliferation and differentiation of anti-CD3 stimulated CD8+ T cells. ( A) Freshly isolated CD8+ T cells were pretreated with Kv channel blockers, ShK (10 nM), MgTx (30 nM) and ChTx (50 nM), for 3 hours, then stimulated with anti-CD3 alone or anti-CD3/CD28. After 4 days of culture, proliferation was measured by [3H] thymidine uptake. Data show the mean ± SD of three experiments. Significant differences are marked as follows: (*, p

    Journal: PLoS ONE

    Article Title: Blockade of Kv1.3 Potassium Channels Inhibits Differentiation and Granzyme B Secretion of Human CD8+ T Effector Memory Lymphocytes

    doi: 10.1371/journal.pone.0054267

    Figure Lengend Snippet: Kv1.3 blockade suppresses proliferation and differentiation of anti-CD3 stimulated CD8+ T cells. ( A) Freshly isolated CD8+ T cells were pretreated with Kv channel blockers, ShK (10 nM), MgTx (30 nM) and ChTx (50 nM), for 3 hours, then stimulated with anti-CD3 alone or anti-CD3/CD28. After 4 days of culture, proliferation was measured by [3H] thymidine uptake. Data show the mean ± SD of three experiments. Significant differences are marked as follows: (*, p

    Article Snippet: Charybdotoxin (ChTx) and margatoxin (MgTx) were purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Isolation

    K+ channel blockers do not affect CD107a expression on activated CD8+ T cells. (A) Freshly isolated CD8+ T cells were stimulated with anti-CD3/CD28 or anti-CD3 for 24 hours. Cells were then stained with a CD107a-specific mAb, or an IgG1 isotype control (filled histogram) at the indicated times. (B). CD8+ T cells were pretreated with ShK (10 nM), MgTX (30 nM), ChTX (50 nM) and TRAM-34 (500 nM) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone for 6 hours. Surface expression levels of CD107a were then analyzed by flow cytometry. FACS plots shown are representative data from three separate experiments.

    Journal: PLoS ONE

    Article Title: Blockade of Kv1.3 Potassium Channels Inhibits Differentiation and Granzyme B Secretion of Human CD8+ T Effector Memory Lymphocytes

    doi: 10.1371/journal.pone.0054267

    Figure Lengend Snippet: K+ channel blockers do not affect CD107a expression on activated CD8+ T cells. (A) Freshly isolated CD8+ T cells were stimulated with anti-CD3/CD28 or anti-CD3 for 24 hours. Cells were then stained with a CD107a-specific mAb, or an IgG1 isotype control (filled histogram) at the indicated times. (B). CD8+ T cells were pretreated with ShK (10 nM), MgTX (30 nM), ChTX (50 nM) and TRAM-34 (500 nM) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone for 6 hours. Surface expression levels of CD107a were then analyzed by flow cytometry. FACS plots shown are representative data from three separate experiments.

    Article Snippet: Charybdotoxin (ChTx) and margatoxin (MgTx) were purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Expressing, Isolation, Staining, Flow Cytometry, Cytometry, FACS

    External Ca 2+ dependence and sensitivity to K + channel blocker charybdotoxin of EGF Ca 2+ transients. A/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in 3 mM extracellular Ca 2+ (n = 24) or in 0 mM Ca 2+/ 1 mM EGTA (n = 28) in the extracellular medium. B/Fluorescence intensity signaling of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when 3 mM Ca 2+ was present (n = 24). The averaged population signal is shown as a thick black trace. C/Fluorescence intensity of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when Ca 2+ was removed and 1 mM EGTA was added to the extracellular medium (n = 28). The averaged population signal is shown as a thick black trace. D/Average of all cell signals during 2 nM EGF application, synchronized at the time of the first fluorescence peak and averaged for 150 sec, when 3 mM Ca 2+ was present (black line, n = 24) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 28). E/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in 3 mM extracellular Ca 2+ (n = 13) or in 0 mM Ca 2+/ 1 mM EGTA (n = 11) in the extracellular medium. F/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when 3 mM Ca 2+ was present (n = 13). The averaged population signal is shown as a thick black trace. G/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (n = 11). The averaged population signal is shown as a thick black trace. H/Average of all cell signals during 20 pM EGF application, synchronized at the time the first fluorescence peak and for 150 sec, when 3 mM Ca 2+ was present (black line, n = 13) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 11). I/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in the absence (0, n = 24/27) or in the presence (100, n = 16/19) of 100 nM charybdotoxin (chx) in the extracellular medium. J/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in the absence (0, n = 16/22) or in the presence (100, n = 6/22) of 100 nM charybdotoxin (chx) in the extracellular medium.

    Journal: PLoS ONE

    Article Title: Physiological Epidermal Growth Factor Concentrations Activate High Affinity Receptors to Elicit Calcium Oscillations

    doi: 10.1371/journal.pone.0106803

    Figure Lengend Snippet: External Ca 2+ dependence and sensitivity to K + channel blocker charybdotoxin of EGF Ca 2+ transients. A/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in 3 mM extracellular Ca 2+ (n = 24) or in 0 mM Ca 2+/ 1 mM EGTA (n = 28) in the extracellular medium. B/Fluorescence intensity signaling of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when 3 mM Ca 2+ was present (n = 24). The averaged population signal is shown as a thick black trace. C/Fluorescence intensity of individual cells (each represented by a different color) during the application of 2 nM EGF (white bar) when Ca 2+ was removed and 1 mM EGTA was added to the extracellular medium (n = 28). The averaged population signal is shown as a thick black trace. D/Average of all cell signals during 2 nM EGF application, synchronized at the time of the first fluorescence peak and averaged for 150 sec, when 3 mM Ca 2+ was present (black line, n = 24) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 28). E/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in 3 mM extracellular Ca 2+ (n = 13) or in 0 mM Ca 2+/ 1 mM EGTA (n = 11) in the extracellular medium. F/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when 3 mM Ca 2+ was present (n = 13). The averaged population signal is shown as a thick black trace. G/Fluorescence intensity of individual cells (each represented by a different color) during the application of 20 pM EGF (white bar) when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (n = 11). The averaged population signal is shown as a thick black trace. H/Average of all cell signals during 20 pM EGF application, synchronized at the time the first fluorescence peak and for 150 sec, when 3 mM Ca 2+ was present (black line, n = 13) or when Ca 2+ was removed from and 1 mM EGTA was added to the extracellular medium (red line, n = 11). I/Proportion of cells responding (grey bar) or not responding (white bar) to 2 nM EGF in the absence (0, n = 24/27) or in the presence (100, n = 16/19) of 100 nM charybdotoxin (chx) in the extracellular medium. J/Proportion of cells responding (grey bar) or not responding (white bar) to 20 pM EGF in the absence (0, n = 16/22) or in the presence (100, n = 6/22) of 100 nM charybdotoxin (chx) in the extracellular medium.

    Article Snippet: Charybdotoxin (Alomone labs), a blocker of Ca2+ -activated K+ channels KCa1.1 , KCa3.1 and voltage-dependent Kv1.3 channels was added to cells at a concentration of 100 nM, 20 min before starting the time-lapse recording.

    Techniques: Fluorescence, Size-exclusion Chromatography

    Potassium and chloride currents evoked by gp120 in MDM. The ionic nature of currents elicited in MDM by gp120 from JRFL ( A ) and IIIB ( B ) was determined from the reversal potential (right) and with channel inhibitors (left). At peak activation, the outward JRFL current reversed direction at ≈−78 mV ( A , top right) whereas the peak inward currents elicited by JRFL ( A , bottom right) and IIIB ( B , right) reversed at ≈5 mV (squares). In low Cl − bath solution, the current voltage relationship of the inward current elicited by both Envs shifted to ≈+40 mV (circles). Charybdotoxin (100 nM) blocked the JRFL-evoked outward current, and NPPB (10 μM) blocked the inward currents activated by both Envs ( A and B , left).

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: HIV-1 gp120 and chemokines activate ion channels in primary macrophages through CCR5 and CXCR4 stimulation

    doi:

    Figure Lengend Snippet: Potassium and chloride currents evoked by gp120 in MDM. The ionic nature of currents elicited in MDM by gp120 from JRFL ( A ) and IIIB ( B ) was determined from the reversal potential (right) and with channel inhibitors (left). At peak activation, the outward JRFL current reversed direction at ≈−78 mV ( A , top right) whereas the peak inward currents elicited by JRFL ( A , bottom right) and IIIB ( B , right) reversed at ≈5 mV (squares). In low Cl − bath solution, the current voltage relationship of the inward current elicited by both Envs shifted to ≈+40 mV (circles). Charybdotoxin (100 nM) blocked the JRFL-evoked outward current, and NPPB (10 μM) blocked the inward currents activated by both Envs ( A and B , left).

    Article Snippet: The pharmacological inhibitors NPPB, IAA, niflumic acid, and DIDS were obtained from Calbiochem, and charybdotoxin was obtained from Alomone Laboratories (Jerusalem).

    Techniques: Activation Assay