Biochimica et biophysica acta, 2016-08, Vol.1857 (8), p.1247-1257
2016
Details
- Autor(en) / Beteiligte
- Titel
- What do we not know about mitochondrial potassium channels?
- Ist Teil von
- Biochimica et biophysica acta, 2016-08, Vol.1857 (8), p.1247-1257
- Ort / Verlag
- Netherlands: Elsevier B.V
- Erscheinungsjahr
- 2016
- Link zum Volltext
- Quelle
- Elsevier ScienceDirect Journals Complete
- Beschreibungen/Notizen
- In this review, we summarize our knowledge about mitochondrial potassium channels, with a special focus on unanswered questions in this field. The following potassium channels have been well described in the inner mitochondrial membrane: ATP-regulated potassium channel, Ca2+-activated potassium channel, the voltage-gated Kv1.3 potassium channel, and the two-pore domain TASK-3 potassium channel. The primary functional roles of these channels include regulation of mitochondrial respiration and the alteration of membrane potential. Additionally, they modulate the mitochondrial matrix volume and the synthesis of reactive oxygen species by mitochondria. Mitochondrial potassium channels are believed to contribute to cytoprotection and cell death. In this paper, we discuss fundamental issues concerning mitochondrial potassium channels: their molecular identity, channel pharmacology and functional properties. Attention will be given to the current problems present in our understanding of the nature of mitochondrial potassium channels. This article is part of a Special Issue entitled ‘EBEC 2016: 19th European Bioenergetics Conference, Riva del Garda, Italy, July 2–6, 2016’, edited by Prof. Paolo Bernardi. •Mitochondrial potassium channels contribute to cytoprotection and cell death.•Molecular identity, pharmacology and properties of these channels are discussed.•Unanswered questions and problems in this research field are emphasized.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0005-2728, 0006-3002eISSN: 1879-2650, 1878-2434DOI: 10.1016/j.bbabio.2016.03.007Titel-ID: cdi_crossref_primary_10_1016_j_bbabio_2016_03_007
- Format
- –
- Schlagworte
- Animals, ATP, Epithelial Cells - cytology, Epithelial Cells - drug effects, Epithelial Cells - metabolism, Gene Expression, Humans, Ion Transport, Mitochondria, Mitochondria - drug effects, Mitochondria - metabolism, Myocytes, Cardiac - cytology, Myocytes, Cardiac - drug effects, Myocytes, Cardiac - metabolism, Neurons - cytology, Neurons - drug effects, Neurons - metabolism, Organ Specificity, Plants - drug effects, Plants - metabolism, Potassium channel, Potassium Channel Blockers - pharmacology, Potassium channel opener, Potassium Channels, Calcium-Activated - antagonists & inhibitors, Potassium Channels, Calcium-Activated - genetics, Potassium Channels, Calcium-Activated - metabolism, Potassium Channels, Inwardly Rectifying - antagonists & inhibitors, Potassium Channels, Inwardly Rectifying - genetics, Potassium Channels, Inwardly Rectifying - metabolism, Potassium Channels, Tandem Pore Domain - antagonists & inhibitors, Potassium Channels, Tandem Pore Domain - genetics, Potassium Channels, Tandem Pore Domain - metabolism, Potassium Channels, Voltage-Gated - antagonists & inhibitors, Potassium Channels, Voltage-Gated - genetics, Potassium Channels, Voltage-Gated - metabolism, Saccharomyces cerevisiae - drug effects, Saccharomyces cerevisiae - metabolism, T-Lymphocytes - cytology, T-Lymphocytes - drug effects, T-Lymphocytes - metabolism, Trypanosomatina - drug effects, Trypanosomatina - metabolism