ArticleAmerican journal of physiology. Cell physiology2012
Differential role of IK and BK potassium channels as mediators of intrinsic and extrinsic apoptotic cell death.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
- Innovative Therapeutic Strategies Targeting the Network Architecture of Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- Piezo1, the new actor in cell volume regulation.Pflugers Archiv : European journal of physiology · 2024Review
- Hypoxia, Ion Channels and Glioblastoma Malignancy.Biomolecules · 2023Review
- CaInternational journal of molecular sciences · 2023Review
- CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development.Cancers · 2022Review
- Cancer as a Channelopathy-Appreciation of Complimentary Pathways Provides a Different Perspective for Developing Treatments.Cancers · 2022Review
- Intermediate conductance CaFrontiers in insect science · 2022Article
- The Interplay between Dysregulated Ion Transport and Mitochondrial Architecture as a Dangerous Liaison in Cancer.International journal of molecular sciences · 2021Review
- Roles of Microglial Ion Channel in Neurodegenerative Diseases.Journal of clinical medicine · 2021Review
- Depressive effectiveness of vigabatrin (γ-vinyl-GABA), an antiepileptic drug, in intermediate-conductance calcium-activated potassium channels in human glioma cells.BMC pharmacology & toxicology · 2021Article
- KCancers · 2019Article
- Cancer-Associated Intermediate Conductance CaCancers · 2019Review
- BK channels blockage inhibits hypoxia-induced migration and chemoresistance to cisplatin in human glioblastoma cells.Journal of cellular physiology · 2018Article
- Structure, Gating and Basic Functions of the Ca2+-activated K Channel of Intermediate Conductance.Current neuropharmacology · 2018Review
- KCa3.1 Channels and Glioblastoma: In Vitro Studies.Current neuropharmacology · 2018Review
- Intermediate-Conductance-Ca2-Activated K Channel IKCa1 Is Upregulated and Promotes Cell Proliferation in Cervical CancerMedical science monitor basic research · 2017Article
- Impact of intracellular ion channels on cancer development and progression.European biophysics journal : EBJ · 2016Review
- A malignant cellular network in gliomas: potential clinical implications.Neuro-oncology · 2016Review
- Article
- Activation of K(+) channel by 1-EBIO rescues the head and neck squamous cell carcinoma cells from Ca(2+) ionophore-induced cell death.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
An important event during apoptosis is regulated cell condensation known as apoptotic volume decrease (AVD). Ion channels have emerged as essential regulators of this process mediating the release of K(+) and Cl(-), which together with osmotically obliged water, results in the condensation of cell volume. Using a Grade IV human glioblastoma cell line, we examined the contribution of calcium-activated K(+) channels (K(Ca) channels) to AVD after the addition of either staurosporine (Stsp) or TNF-α-related apoptosis-inducing ligand (TRAIL) to activate the intrinsic or extrinsic pathway of apoptosis, respectively. We show that AVD can be inhibited in both pathways by high extracellular K(+) or the removal of calcium. However, BAPTA-AM was only able to inhibit Stsp-initiated AVD, whereas TRAIL-induced AVD was unaffected. Specific K(Ca) channel inhibitors revealed that Stsp-induced AVD was dependent on K(+) efflux through intermediate-conductance calcium-activated potassium (IK) channels, while TRAIL-induced AVD was mediated by large-conductance calcium-activated potassium (BK) channels. Fura-2 imaging demonstrated that Stsp induced a rapid and modest rise in calcium that was sustained over the course of AVD, while TRAIL produced no detectable rise in global intracellular calcium. Inhibition of IK channels with clotrimazole or 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (TRAM-34) blocked downstream caspase-3 activation after Stsp addition, while paxilline, a specific BK channel inhibitor, had no effect. Treatment with ionomycin also induced an IK-dependent cell volume decrease. Together these results show that calcium is both necessary and sufficient to achieve volume decrease and that the two major pathways of apoptosis use unique calcium signaling to efflux K(+) through different K(Ca) channels.
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