International Union of Basic and Clinical Pharmacology. C. Nomenclature and Properties of Calcium-Activated and Sodium-Activated Potassium Channels

Kaczmarek, Leonard K.; Aldrich, Richard W.; Chandy, K. George; Grissmer, Stephan; Wei, Aguan; Wulff, Heike

doi:10.1124/pr.116.012864

Cited by 83 publications

(75 citation statements)

References 180 publications

(162 reference statements)

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“…The gene encoding the mitochondrial ATP-sensitive K + (K ATP ) channel is unknown, and so here we use the term ‘mitoK ATP ’. For other K + channels, where possible the International Union of Basic and Clinical Pharmacology (IUPHAR) nomenclature is used [43] (see the Abbreviations list); however, there are many alternative names commonly found in the literature, described here.…”

Section: Mitochondrial K+ Homeostasis and Discovery Of Mitochondrial mentioning

confidence: 99%

“…Kcnn1 , Kcnn2 , and Kcnn3 , respectively, code for the SK potassium channels with IUPHAR names K Ca 2.1, K Ca 2.2, and K Ca 2.3 [174], while the Kcnn4 gene encodes an IK potassium (IK) channel termed K Ca 3.1 [43]. The K Ca 3.1 channel has not been implicated in IR protection; however, it does have a role in post-ischemic cardiac remodeling [175,176] and Kcnn4 − / − mice exhibit more damage in ischemic stroke [177].…”

Section: Mitochondrial Kca2x and Kca31 Channels: Composition Pharmmentioning

confidence: 99%

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The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection

Smith

Nehrke

Brookes

2017

Biochemical Journal

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Mitochondria play an important role in tissue ischemia and reperfusion (IR) injury, with energetic failure and the opening of the mitochondrial permeability transition pore being the major causes of IR-induced cell death. Thus, mitochondria are an appropriate focus for strategies to protect against IR injury. Two widely studied paradigms of IR protection, particularly in the field of cardiac IR, are ischemic preconditioning (IPC) and volatile anesthetic preconditioning (APC). While the molecular mechanisms recruited by these protective paradigms are not fully elucidated, a commonality is the involvement of mitochondrial K+ channel opening. In the case of IPC, research has focused on a mitochondrial ATP-sensitive K+ channel (mitoKATP), but, despite recent progress, the molecular identity of this channel remains a subject of contention. In the case of APC, early research suggested the existence of a mitochondrial large-conductance K+ (BK, big conductance of potassium) channel encoded by the Kcnma1 gene, although more recent work has shown that the channel that underlies APC is in fact encoded by Kcnt2. In this review, we discuss both the pharmacologic and genetic evidence for the existence and identity of mitochondrial K+ channels, and the role of these channels both in IR protection and in regulating normal mitochondrial function.

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Section: Mitochondrial K+ Homeostasis and Discovery Of Mitochondrial mentioning

confidence: 99%

Section: Mitochondrial Kca2x and Kca31 Channels: Composition Pharmmentioning

confidence: 99%

The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection

Smith

Nehrke

Brookes

2017

Biochemical Journal

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“…Since then, several studies have reported a similar “Gárdos effect” in various types of neurons (2). We now know that this effect is mediated by a family of Ca 2+ -activated K + channels (3). These channels were historically cataloged as intermediate- or small-conductance Ca 2+ -activated K + (SK) channels to distinguish them from the well-studied large-conductance Ca 2+ -activated K + (BK) channels (4–8).…”

Section: Introductionmentioning

confidence: 99%

Activation mechanism of a human SK-calmodulin channel complex elucidated by cryo-EM structures

Lee

MacKinnon

2018

Science

139

220

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Small-conductance Ca2+-activated K+ (SK) channels mediate neuron excitability and are associated with synaptic transmission and plasticity. They also regulate immune responses and the size of blood cells. Activation of SK channels requires calmodulin (CaM), but how CaM binds and opens SK channels has been unclear. Here we report cryo-electron microscopy (cryo-EM) structures of a human SK4-CaM channel complex in closed and activated states at 3.4- and 3.5-angstrom resolution, respectively. Four CaM molecules bind to one channel tetramer. Each lobe of CaM serves a distinct function: The C-lobe binds to the channel constitutively, whereas the N-lobe interacts with the S4–S5 linker in a Ca2+-dependent manner. The S4–S5 linker, which contains two distinct helices, undergoes conformational changes upon CaM binding to open the channel pore. These structures reveal the gating mechanism of SK channels and provide a basis for understanding SK channel pharmacology.

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“…Among K v 7 channels, Kv7.4 is abundantly expressed in the VSM [3]. Among Ca 2+ -activated K + channels, big conductance Ca 2+ -sensitive K + (BK Ca ) or K Ca 1.1 (also named BK, Maxi K, or Slo1) channels are more important in VSM cells [119, 120]. The effects of H 2 S on K + channels have been described below in sections 7.1.1, 7.1.2, and 7.1.3.…”

Section: Major Types Of Ion Channels In Vsm and Endothelial Cellsmentioning

confidence: 99%

Regulation of vascular tone homeostasis by NO and H2S: Implications in hypertension

Gheibi

Jeddi

Kashfi

et al. 2018

Biochemical Pharmacology

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Nitric oxide (NO) and hydrogen sulfide (HS) are two gasotransmitters that are produced in the vasculature and contribute to the regulation of vascular tone. NO and HS are synthesized in both vascular smooth muscle and endothelial cells; NO functions primarily through the sGC/cGMP pathway, and HS mainly through activation of the ATP-dependent potassium channels; both leading to relaxation of vascular smooth muscle cells. A deficit in the NO/HS homeostasis is involved in the pathogenesis of various cardiovascular diseases, especially hypertension. It is now becoming increasingly clear that there are important interactions between NO and HS and that have a profound impact on vascular tone and this may provide insights into the new therapeutic interventions. The aim of this review is to provide a better understanding of individual and interactive roles of NO and HS in vascular biology. Overall, available data indicate that both NO and HS contribute to vascular (patho)physiology and in regulating blood pressure. In addition, boosting NO and HS using various dietary sources or donors could be a hopeful therapeutic strategy in the management of hypertension.

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International Union of Basic and Clinical Pharmacology. C. Nomenclature and Properties of Calcium-Activated and Sodium-Activated Potassium Channels

Cited by 83 publications

References 180 publications

The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection

The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection

Activation mechanism of a human SK-calmodulin channel complex elucidated by cryo-EM structures

Regulation of vascular tone homeostasis by NO and H2S: Implications in hypertension

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