The Experts below are selected from a list of 7380 Experts worldwide ranked by ideXlab platform
Won Sun Park - One of the best experts on this subject based on the ideXlab platform.
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the Calmodulin Inhibitor cgs 9343b inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Toxicology and Applied Pharmacology, 2015Co-Authors: Da Hye Hong, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Hye Won Kim, Won Sun ParkAbstract:Abstract We investigated the effects of the Calmodulin Inhibitor CGS 9343B on voltage-dependent K + (Kv) channels using whole-cell patch clamp technique in freshly isolated rabbit coronary arterial smooth muscle cells. CGS 9343B inhibited Kv currents in a concentration-dependent manner, with a half-maximal Inhibitory concentration (IC 50 ) value of 0.81 μM. The decay rate of Kv channel inactivation was accelerated by CGS 9343B. The rate constants of association and dissociation for CGS 9343B were 2.77 ± 0.04 μM − 1 s − 1 and 2.55 ± 1.50 s − 1 , respectively. CGS 9343B did not affect the steady-state activation curve, but shifted the inactivation curve toward to a more negative potential. Train pulses (1 or 2 Hz) application progressively increased the CGS 9343B-induced Kv channel inhibition. In addition, the inactivation recovery time constant was increased in the presence of CGS 9343B, suggesting that CGS 9343B-induced inhibition of Kv channel was use-dependent. Another Calmodulin Inhibitor, W-13, did not affect Kv currents, and did not change the Inhibitory effect of CGS 9343B on Kv current. Our results demonstrated that CGS 9343B inhibited Kv currents in a state-, time-, and use-dependent manner, independent of Calmodulin inhibition.
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the Calmodulin Inhibitor and antipsychotic drug trifluoperazine inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Biochemical and Biophysical Research Communications, 2014Co-Authors: Da Hye Hong, Youn Kyoung Son, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Won Sun ParkAbstract:Abstract We investigated the effect of the Calmodulin Inhibitor and antipsychotic drug trifluoperazine on voltage-dependent K + (Kv) channels. Kv currents were recorded by whole-cell configuration of patch clamp in freshly isolated rabbit coronary arterial smooth muscle cells. The amplitudes of Kv currents were reduced by trifluoperazine in a concentration-dependent manner, with an apparent IC 50 value of 1.58 ± 0.48 μM. The rate constants of association and dissociation by trifluoperazine were 3.73 ± 0.33 μM −1 s −1 and 5.84 ± 1.41 s −1 , respectively. Application of trifluoperazine caused a positive shift in the activation curve but had no significant effect on the inactivation curve. Furthermore, trifluoperazine provoked use-dependent inhibition of the Kv current under train pulses (1 or 2 Hz). These findings suggest that trifluoperazine interacts with Kv current in a closed state and inhibits Kv current in the open state in a time- and use-dependent manner, regardless of its function as a Calmodulin Inhibitor and antipsychotic drug.
Da Hye Hong - One of the best experts on this subject based on the ideXlab platform.
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the Calmodulin Inhibitor cgs 9343b inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Toxicology and Applied Pharmacology, 2015Co-Authors: Da Hye Hong, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Hye Won Kim, Won Sun ParkAbstract:Abstract We investigated the effects of the Calmodulin Inhibitor CGS 9343B on voltage-dependent K + (Kv) channels using whole-cell patch clamp technique in freshly isolated rabbit coronary arterial smooth muscle cells. CGS 9343B inhibited Kv currents in a concentration-dependent manner, with a half-maximal Inhibitory concentration (IC 50 ) value of 0.81 μM. The decay rate of Kv channel inactivation was accelerated by CGS 9343B. The rate constants of association and dissociation for CGS 9343B were 2.77 ± 0.04 μM − 1 s − 1 and 2.55 ± 1.50 s − 1 , respectively. CGS 9343B did not affect the steady-state activation curve, but shifted the inactivation curve toward to a more negative potential. Train pulses (1 or 2 Hz) application progressively increased the CGS 9343B-induced Kv channel inhibition. In addition, the inactivation recovery time constant was increased in the presence of CGS 9343B, suggesting that CGS 9343B-induced inhibition of Kv channel was use-dependent. Another Calmodulin Inhibitor, W-13, did not affect Kv currents, and did not change the Inhibitory effect of CGS 9343B on Kv current. Our results demonstrated that CGS 9343B inhibited Kv currents in a state-, time-, and use-dependent manner, independent of Calmodulin inhibition.
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the Calmodulin Inhibitor and antipsychotic drug trifluoperazine inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Biochemical and Biophysical Research Communications, 2014Co-Authors: Da Hye Hong, Youn Kyoung Son, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Won Sun ParkAbstract:Abstract We investigated the effect of the Calmodulin Inhibitor and antipsychotic drug trifluoperazine on voltage-dependent K + (Kv) channels. Kv currents were recorded by whole-cell configuration of patch clamp in freshly isolated rabbit coronary arterial smooth muscle cells. The amplitudes of Kv currents were reduced by trifluoperazine in a concentration-dependent manner, with an apparent IC 50 value of 1.58 ± 0.48 μM. The rate constants of association and dissociation by trifluoperazine were 3.73 ± 0.33 μM −1 s −1 and 5.84 ± 1.41 s −1 , respectively. Application of trifluoperazine caused a positive shift in the activation curve but had no significant effect on the inactivation curve. Furthermore, trifluoperazine provoked use-dependent inhibition of the Kv current under train pulses (1 or 2 Hz). These findings suggest that trifluoperazine interacts with Kv current in a closed state and inhibits Kv current in the open state in a time- and use-dependent manner, regardless of its function as a Calmodulin Inhibitor and antipsychotic drug.
Ilwhan Choi - One of the best experts on this subject based on the ideXlab platform.
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the Calmodulin Inhibitor cgs 9343b inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Toxicology and Applied Pharmacology, 2015Co-Authors: Da Hye Hong, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Hye Won Kim, Won Sun ParkAbstract:Abstract We investigated the effects of the Calmodulin Inhibitor CGS 9343B on voltage-dependent K + (Kv) channels using whole-cell patch clamp technique in freshly isolated rabbit coronary arterial smooth muscle cells. CGS 9343B inhibited Kv currents in a concentration-dependent manner, with a half-maximal Inhibitory concentration (IC 50 ) value of 0.81 μM. The decay rate of Kv channel inactivation was accelerated by CGS 9343B. The rate constants of association and dissociation for CGS 9343B were 2.77 ± 0.04 μM − 1 s − 1 and 2.55 ± 1.50 s − 1 , respectively. CGS 9343B did not affect the steady-state activation curve, but shifted the inactivation curve toward to a more negative potential. Train pulses (1 or 2 Hz) application progressively increased the CGS 9343B-induced Kv channel inhibition. In addition, the inactivation recovery time constant was increased in the presence of CGS 9343B, suggesting that CGS 9343B-induced inhibition of Kv channel was use-dependent. Another Calmodulin Inhibitor, W-13, did not affect Kv currents, and did not change the Inhibitory effect of CGS 9343B on Kv current. Our results demonstrated that CGS 9343B inhibited Kv currents in a state-, time-, and use-dependent manner, independent of Calmodulin inhibition.
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the Calmodulin Inhibitor and antipsychotic drug trifluoperazine inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Biochemical and Biophysical Research Communications, 2014Co-Authors: Da Hye Hong, Youn Kyoung Son, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Won Sun ParkAbstract:Abstract We investigated the effect of the Calmodulin Inhibitor and antipsychotic drug trifluoperazine on voltage-dependent K + (Kv) channels. Kv currents were recorded by whole-cell configuration of patch clamp in freshly isolated rabbit coronary arterial smooth muscle cells. The amplitudes of Kv currents were reduced by trifluoperazine in a concentration-dependent manner, with an apparent IC 50 value of 1.58 ± 0.48 μM. The rate constants of association and dissociation by trifluoperazine were 3.73 ± 0.33 μM −1 s −1 and 5.84 ± 1.41 s −1 , respectively. Application of trifluoperazine caused a positive shift in the activation curve but had no significant effect on the inactivation curve. Furthermore, trifluoperazine provoked use-dependent inhibition of the Kv current under train pulses (1 or 2 Hz). These findings suggest that trifluoperazine interacts with Kv current in a closed state and inhibits Kv current in the open state in a time- and use-dependent manner, regardless of its function as a Calmodulin Inhibitor and antipsychotic drug.
Han Sol Kim - One of the best experts on this subject based on the ideXlab platform.
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the Calmodulin Inhibitor cgs 9343b inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Toxicology and Applied Pharmacology, 2015Co-Authors: Da Hye Hong, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Hye Won Kim, Won Sun ParkAbstract:Abstract We investigated the effects of the Calmodulin Inhibitor CGS 9343B on voltage-dependent K + (Kv) channels using whole-cell patch clamp technique in freshly isolated rabbit coronary arterial smooth muscle cells. CGS 9343B inhibited Kv currents in a concentration-dependent manner, with a half-maximal Inhibitory concentration (IC 50 ) value of 0.81 μM. The decay rate of Kv channel inactivation was accelerated by CGS 9343B. The rate constants of association and dissociation for CGS 9343B were 2.77 ± 0.04 μM − 1 s − 1 and 2.55 ± 1.50 s − 1 , respectively. CGS 9343B did not affect the steady-state activation curve, but shifted the inactivation curve toward to a more negative potential. Train pulses (1 or 2 Hz) application progressively increased the CGS 9343B-induced Kv channel inhibition. In addition, the inactivation recovery time constant was increased in the presence of CGS 9343B, suggesting that CGS 9343B-induced inhibition of Kv channel was use-dependent. Another Calmodulin Inhibitor, W-13, did not affect Kv currents, and did not change the Inhibitory effect of CGS 9343B on Kv current. Our results demonstrated that CGS 9343B inhibited Kv currents in a state-, time-, and use-dependent manner, independent of Calmodulin inhibition.
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the Calmodulin Inhibitor and antipsychotic drug trifluoperazine inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Biochemical and Biophysical Research Communications, 2014Co-Authors: Da Hye Hong, Youn Kyoung Son, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Won Sun ParkAbstract:Abstract We investigated the effect of the Calmodulin Inhibitor and antipsychotic drug trifluoperazine on voltage-dependent K + (Kv) channels. Kv currents were recorded by whole-cell configuration of patch clamp in freshly isolated rabbit coronary arterial smooth muscle cells. The amplitudes of Kv currents were reduced by trifluoperazine in a concentration-dependent manner, with an apparent IC 50 value of 1.58 ± 0.48 μM. The rate constants of association and dissociation by trifluoperazine were 3.73 ± 0.33 μM −1 s −1 and 5.84 ± 1.41 s −1 , respectively. Application of trifluoperazine caused a positive shift in the activation curve but had no significant effect on the inactivation curve. Furthermore, trifluoperazine provoked use-dependent inhibition of the Kv current under train pulses (1 or 2 Hz). These findings suggest that trifluoperazine interacts with Kv current in a closed state and inhibits Kv current in the open state in a time- and use-dependent manner, regardless of its function as a Calmodulin Inhibitor and antipsychotic drug.
Yeongmin Park - One of the best experts on this subject based on the ideXlab platform.
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the Calmodulin Inhibitor cgs 9343b inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Toxicology and Applied Pharmacology, 2015Co-Authors: Da Hye Hong, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Hye Won Kim, Won Sun ParkAbstract:Abstract We investigated the effects of the Calmodulin Inhibitor CGS 9343B on voltage-dependent K + (Kv) channels using whole-cell patch clamp technique in freshly isolated rabbit coronary arterial smooth muscle cells. CGS 9343B inhibited Kv currents in a concentration-dependent manner, with a half-maximal Inhibitory concentration (IC 50 ) value of 0.81 μM. The decay rate of Kv channel inactivation was accelerated by CGS 9343B. The rate constants of association and dissociation for CGS 9343B were 2.77 ± 0.04 μM − 1 s − 1 and 2.55 ± 1.50 s − 1 , respectively. CGS 9343B did not affect the steady-state activation curve, but shifted the inactivation curve toward to a more negative potential. Train pulses (1 or 2 Hz) application progressively increased the CGS 9343B-induced Kv channel inhibition. In addition, the inactivation recovery time constant was increased in the presence of CGS 9343B, suggesting that CGS 9343B-induced inhibition of Kv channel was use-dependent. Another Calmodulin Inhibitor, W-13, did not affect Kv currents, and did not change the Inhibitory effect of CGS 9343B on Kv current. Our results demonstrated that CGS 9343B inhibited Kv currents in a state-, time-, and use-dependent manner, independent of Calmodulin inhibition.
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the Calmodulin Inhibitor and antipsychotic drug trifluoperazine inhibits voltage dependent k channels in rabbit coronary arterial smooth muscle cells
Biochemical and Biophysical Research Communications, 2014Co-Authors: Da Hye Hong, Youn Kyoung Son, In Duk Jung, Yeongmin Park, Wonkyo Jung, Han Sol Kim, Ilwhan Choi, Won Sun ParkAbstract:Abstract We investigated the effect of the Calmodulin Inhibitor and antipsychotic drug trifluoperazine on voltage-dependent K + (Kv) channels. Kv currents were recorded by whole-cell configuration of patch clamp in freshly isolated rabbit coronary arterial smooth muscle cells. The amplitudes of Kv currents were reduced by trifluoperazine in a concentration-dependent manner, with an apparent IC 50 value of 1.58 ± 0.48 μM. The rate constants of association and dissociation by trifluoperazine were 3.73 ± 0.33 μM −1 s −1 and 5.84 ± 1.41 s −1 , respectively. Application of trifluoperazine caused a positive shift in the activation curve but had no significant effect on the inactivation curve. Furthermore, trifluoperazine provoked use-dependent inhibition of the Kv current under train pulses (1 or 2 Hz). These findings suggest that trifluoperazine interacts with Kv current in a closed state and inhibits Kv current in the open state in a time- and use-dependent manner, regardless of its function as a Calmodulin Inhibitor and antipsychotic drug.
