scholarly journals Expression and function of calcium-activated potassium channels in human glioma cells

Glia ◽  
2006 ◽  
Vol 54 (3) ◽  
pp. 223-233 ◽  
Author(s):  
Amy K. Weaver ◽  
Valerie C. Bomben ◽  
Harald Sontheimer
Keyword(s):  
Potassium Channels ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
And Function

scholarly journals Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells

2021 ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying

Abstract Background: Vigabatrin (VGB) is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors; however, its effect on ionic channels in glioma cells remains largely unclear. Methods: With the aid of patch-clamp technology, we investigated the effects of VGB on various ionic currents in the glioblastoma multiforme cell line 13-06-MG. Results: In cell-attached configuration, VGB concentration-dependently reduced the activity of intermediate-conductance Ca2+-activated K+ (IKCa) channels, while DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) counteracted the VGB-induced inhibition of IKCa channels. However, the activity of neither large-conductance Ca2+-activated (BKCa) nor inwardly rectifying K+ (KIR) channels were affected by the presence of VGB in human 13-06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl2 effectively suppressed BKCa and KIR channels. Conclusions: The inhibitory effect of VGB on IKCa channels demonstrated in the current study could be an important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.

Potassium channels in human glioma cells

1989 ◽  
Vol 414 (S1) ◽  
pp. S137-S138 ◽  
Author(s):  
T. Brismar ◽  
V. P. Collins
Keyword(s):  
Potassium Channels ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells

scholarly journals Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells

2020 ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying

Abstract Background: Vigabatrin (VGB) is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors; however, its effect on ionic channels in glioma cells remains largely unclear. Methods: With the aid of patch-clamp technology, we investigated the effects of VGB on various ionic currents in the glioblastoma multiforme cell line 13-06-MG. Results: In cell-attached configuration, VGB concentration-dependently reduced the activity of intermediate-conductance Ca2+-activated K+ (IKCa) channels, while DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) counteracted the VGB-induced inhibition of IKCa channels. However, the activity of neither large-conductance Ca2+-activated (BKCa) nor inwardly rectifying K+ (KIR) channels were affected by the presence of VGB in human 13-06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl2 effectively suppressed BKCa and KIR channels. Conclusions: The inhibitory effect of VGB on IKCa channels demonstrated in the current study could be an important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.

scholarly journals Depressive effectiveness of vigabatrin (γ-vinyl-GABA), an antiepileptic drug, in intermediate-conductance calcium-activated potassium channels in human glioma cells

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying

Abstract Background Vigabatrin (VGB) is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors; however, its effect on ionic channels in glioma cells remains largely unclear. Methods With the aid of patch-clamp technology, we investigated the effects of VGB on various ionic currents in the glioblastoma multiforme cell line 13–06-MG. Results In cell-attached configuration, VGB concentration-dependently reduced the activity of intermediate-conductance Ca2+-activated K+ (IKCa) channels, while DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) counteracted the VGB-induced inhibition of IKCa channels. However, the activity of neither large-conductance Ca2+-activated (BKCa) nor inwardly rectifying K+ (KIR) channels were affected by the presence of VGB in human 13–06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl2 effectively suppressed BKCa and KIR channels. Conclusions The inhibitory effect of VGB on IKCa channels demonstrated in the current study could be an important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.

scholarly journals Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells

2021 ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying

Abstract Background: Vigabatrin (VGB) is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors; however, its effect on ionic channels in glioma cells remains largely unclear. Methods: With the aid of patch-clamp technology, we investigated the effects of VGB on various ionic currents in the glioblastoma multiforme cell line 13-06-MG. Results: In cell-attached configuration, VGB concentration-dependently reduced the activity of intermediate-conductance Ca2+-activated K+ (IKCa) channels, while DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) counteracted the VGB-induced inhibition of IKCa channels. However, the activity of neither large-conductance Ca2+-activated (BKCa) nor inwardly rectifying K+ (KIR) channels were affected by the presence of VGB in human 13-06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl2 effectively suppressed BKCa and KIR channels. Conclusions: The inhibitory effect of VGB on IKCa channels demonstrated in the current study could be an important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.

Mutant IκBα Suppresses Hypoxia-Induced VEGF Expression Through Downregulation of HIF-1α and COX-2 in Human Glioma Cells

2005 ◽  
Vol 15 (3) ◽  
pp. 139-149 ◽  
Author(s):  
Yoshihira Kimba ◽  
Tatsuya Abe ◽  
Jian Liang Wu ◽  
Ryo Inoue ◽  
Minoru Fukiki ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Vegf Expression ◽  
Cox 2

scholarly journals Differential expression and role of p21cip/waf1 and p27kip1 in TNF-α-induced inhibition of proliferation in human glioma cells

2007 ◽  
Vol 6 (1) ◽  
pp. 42 ◽  
Author(s):  
Pabbisetty Kumar ◽  
Anjali Shiras ◽  
Gowry Das ◽  
Jayashree C Jagtap ◽  
Vandna Prasad ◽  
...  
Keyword(s):  
Differential Expression ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Inhibition Of Proliferation ◽  
Tnf Α
Sign in / Sign up

Export Citation Format

Share Document