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Potassium channels and their role in glioma: A mini review.
Liu, J, Qu, C, Han, C, Chen, MM, An, LJ, Zou, W
Molecular membrane biology. 2019;(1):76-85
Abstract
K+ channels regulate a multitude of biological processes and play important roles in a variety of diseases by controlling potassium flow across cell membranes. They are widely expressed in the central and peripheral nervous system. As a malignant tumor derived from nerve epithelium, glioma has the characteristics of high incidence, high recurrence rate, high mortality rate, and low cure rate. Since glioma cells show invasive growth, current surgical methods cannot completely remove tumors. Adjuvant chemotherapy is still needed after surgery. Because the blood-brain barrier and other factors lead to a lower effective concentration of chemotherapeutic drugs in the tumor, the recurrence rate of residual lesions is extremely high. Therefore, new therapeutic methods are needed. Numerous studies have shown that different K+ channel subtypes are differentially expressed in glioma cells and are involved in the regulation of the cell cycle of glioma cells to arrest them at different stages of the cell cycle. Increasing evidence suggests that K+ channels express in glioma cells and regulate glioma cell behaviors such as cell cycle, proliferation and apoptosis. This review article aims to summarize the current knowledge on the function of K+ channels in glioma, suggests K+ channels participating in the development of glioma.
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Beneficial Effects of High Potassium: Contribution of Renal Basolateral K+ Channels.
Staruschenko, A
Hypertension (Dallas, Tex. : 1979). 2018;(6):1015-1022
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3.
KCNT1 mutations in seizure disorders: the phenotypic spectrum and functional effects.
Lim, CX, Ricos, MG, Dibbens, LM, Heron, SE
Journal of medical genetics. 2016;(4):217-25
Abstract
Mutations in the sodium-gated potassium channel subunit gene KCNT1 have recently emerged as a cause of several different epileptic disorders. This review describes the mutational and phenotypic spectrum associated with the gene and discusses the comorbidities found in patients, which include intellectual disability and psychiatric features. The gene may also be linked with cardiac disorders. KCNT1 missense mutations have been found in 39% of patients with the epileptic encephalopathy malignant migrating focal seizures of infancy (MMFSI), making it the most significant MMFSI disease-causing gene identified to date. Mutations in KCNT1 have also been described in eight unrelated cases of sporadic and familial autosomal-dominant nocturnal frontal lobe epilepsy (ADNFLE). These patients have a high frequency of associated intellectual disability and psychiatric features. Two mutations in KCNT1 have been associated with both ADNFLE and MMFSI, suggesting that the genotype-phenotype relationship for KCNT1 mutations is not straightforward. Mutations have also been described in several patients with infantile epileptic encephalopathies other than MMFSI. Notably, all mutations in KCNT1 described to date are missense mutations, and electrophysiological studies have shown that they result in increased potassium current. Together, these genetic and electrophysiological studies raise the possibility of delivering precision medicine by treating patients with KCNT1 mutations using drugs that alter the action of potassium channels to specifically target the biological effects of their disease-causing mutation. Such trials are now in progress. Better understanding of the mechanisms underlying KCNT1-related disease will produce further improvements in treatment of the associated severe seizure disorders.
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4.
KCTD7-related progressive myoclonus epilepsy.
Van Bogaert, P
Epileptic disorders : international epilepsy journal with videotape. 2016;(S2):115-119
Abstract
Progressive myoclonic epilepsy associated with KCTD7 mutations has been reported in 19 patients from 12 families. Patients show homozygous mutations in the coding regions of the KCTD7 gene. The disease starts in infancy. Patients typically show an initial severe epileptic disorder, with abundant epileptiform discharges on EEG and myoclonic seizures in the foreground, associated with cognitive regression and ataxia. Continuous multifocal myoclonus aggravated by action is observed in more than half of the cases. After a few years, the disease tends to stabilize and long survival can be expected. Some patients remain able to walk independently. The severity of the disease is variable from one patient to another, even within the same family. It is hypothesized that the epileptic disorder may influence the neurological regression observed in patients.
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5.
Genetic Control of Potassium Channels.
Amin, AS, Wilde, AA
Cardiac electrophysiology clinics. 2016;(2):285-306
Abstract
Approximately 80 genes in the human genome code for pore-forming subunits of potassium (K(+)) channels. Rare variants (mutations) in K(+) channel-encoding genes may cause heritable arrhythmia syndromes. Not all rare variants in K(+) channel-encoding genes are necessarily disease-causing mutations. Common variants in K(+) channel-encoding genes are increasingly recognized as modifiers of phenotype in heritable arrhythmia syndromes and in the general population. Although difficult, distinguishing pathogenic variants from benign variants is of utmost importance to avoid false designations of genetic variants as disease-causing mutations.
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6.
Clinical Features of Genetic Cardiac Diseases Related to Potassium Channelopathies.
Adler, A, Viskin, S
Cardiac electrophysiology clinics. 2016;(2):361-72
Abstract
Genetic cardiac diseases related to potassium channelopathies are a group of relatively rare syndromes that includes long QT syndrome, short QT syndrome, Brugada syndrome, and early repolarization syndrome. Patients with these syndromes share a propensity for the development of life-threatening ventricular arrhythmias in the absence of significant cardiac structural abnormalities. Familial atrial fibrillation has also been associated with potassium channel dysfunction but differs from the other syndromes by being a rare cause of a common condition. This article focuses on the clinical features, diagnosis, and management of these syndromes.
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7.
Ca(2+) and ion channels in hypoxia-mediated pulmonary hypertension.
Lai, N, Lu, W, Wang, J
International journal of clinical and experimental pathology. 2015;(2):1081-92
Abstract
Alveolar hypoxia, a consequence of many lung diseases, can have adverse effects on the pulmonary vasculature. The changes that occur in the pulmonary circulation with exposure to chronic hypoxia include reductions in the diameter of the pulmonary arteries due to structural remodeling of the vasculature. Although the structural and functional changes that occur in the development of pulmonary hypertension have been well investigated, less is known about the cellular and molecular mechanisms of this process. This review will discuss the role of several potassium and calcium channels in hypoxic pulmonary vasoconstriction, both in elevating calcium influx into pulmonary artery smooth muscle cells (PASMCs). In addition to other signal transduction pathways, Ca(2+) signaling in PASMCs plays an important role in the development and progression of pulmonary hypertension due to its central roles in vasoconstriction and vascular remodeling. This review will focus on the effect of chronic hypoxia on ion channels and the potential pathogenic role of Ca(2+) signaling and regulation in the progression of pulmonary hypertension.
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8.
Diversity of potassium channels in human umbilical artery smooth muscle cells: a review of their roles in human umbilical artery contraction.
Martín, P, Rebolledo, A, Palomo, AR, Moncada, M, Piccinini, L, Milesi, V
Reproductive sciences (Thousand Oaks, Calif.). 2014;(4):432-41
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Abstract
Through their control of cell membrane potential, potassium (K(+)) channels are among the best known regulators of vascular tone. This article discusses the expression and function of K(+) channels in human umbilical artery smooth muscle cells (HUASMCs). We review the bibliographic reports and also present single-channel data recorded in freshly isolated cells. Electrophysiological properties of big conductance, voltage- and Ca(2+)-sensitive K(+) channel and voltage-dependent K(+) channels are clearly established in this vessel, where they are involved in contractile state regulation. Their role in the maintenance of membrane potential is an important control mechanism in the determination of the vessel diameter. Additionally, small conductance Ca(2+)-sensitive K(+) channels, 2-pore domains K(+) channels and inward rectifier K(+) channels also appear to be present in HUASMCs, while intermediate conductance Ca(2+)-sensitive K(+) channels and ATP-sensitive K(+) channels could not be identified. In both cases, additional investigation is necessary to reach conclusive evidence of their expression and/or functional role in HUASMCs. Finally, we discuss the role of K(+) channels in pregnancy-related pathologies like gestational diabetes and preeclampsia.
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9.
Molecular biology of K+ transport across the plant cell membrane: what do we learn from comparison between plant species?
Véry, AA, Nieves-Cordones, M, Daly, M, Khan, I, Fizames, C, Sentenac, H
Journal of plant physiology. 2014;(9):748-69
Abstract
Cloning and characterizations of plant K(+) transport systems aside from Arabidopsis have been increasing over the past decade, favored by the availability of more and more plant genome sequences. Information now available enables the comparison of some of these systems between species. In this review, we focus on three families of plant K(+) transport systems that are active at the plasma membrane: the Shaker K(+) channel family, comprised of voltage-gated channels that dominate the plasma membrane conductance to K(+) in most environmental conditions, and two families of transporters, the HAK/KUP/KT K(+) transporter family, which includes some high-affinity transporters, and the HKT K(+) and/or Na(+) transporter family, in which K(+)-permeable members seem to be present in monocots only. The three families are briefly described, giving insights into the structure of their members and on functional properties and their roles in Arabidopsis or rice. The structure of the three families is then compared between plant species through phylogenic analyses. Within clusters of ortologues/paralogues, similarities and differences in terms of expression pattern, functional properties and, when known, regulatory interacting partners, are highlighted. The question of the physiological significance of highlighted differences is also addressed.
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10.
Cl- and K+ channels and their role in primary brain tumour biology.
Turner, KL, Sontheimer, H
Philosophical transactions of the Royal Society of London. Series B, Biological sciences. 2014;(1638):20130095
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Abstract
Profound cell volume changes occur in primary brain tumours as they proliferate, invade surrounding tissue or undergo apoptosis. These volume changes are regulated by the flux of Cl(-) and K(+) ions and concomitant movement of water across the membrane, making ion channels pivotal to tumour biology. We discuss which specific Cl(-) and K(+) channels are involved in defined aspects of glioma biology and how these channels are regulated. Cl(-) is accumulated to unusually high concentrations in gliomas by the activity of the NKCC1 transporter and serves as an osmolyte and energetic driving force for volume changes. Cell volume condensation is required as cells enter M phase of the cell cycle and this pre-mitotic condensation is caused by channel-mediated ion efflux. Similarly, Cl(-) and K(+) channels dynamically regulate volume in invading glioma cells allowing them to adjust to small extracellular brain spaces. Finally, cell condensation is a hallmark of apoptosis and requires the concerted activation of Cl(-) and Ca(2+)-activated K(+) channels. Given the frequency of mutation and high importance of ion channels in tumour biology, the opportunity exists to target them for treatment.