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1
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Transmembrane segment M2 of glycine receptor as a model system for the pore-forming structure of ion channels.

100%
Bednarczyk P., Szewczyk A., Dołowy K.
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2002
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vol. 49
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issue 4
869-875
EN
The glycine receptor belongs to the ligand-gated ion channel superfamily. It is a chloride conducting channel composed of four transmembrane domains. It was previously shown that the second transmembrane domain (M2) of the glycine receptor forms an ion conduction pathway throught lipid bilayers. The amino-acid sequence of the transmembrane segment M2 of the glycine receptor has a high homology to all receptors of the ligand-gated ion channel superfamily. In our report, we have used a synthetic M2 peptide. It was incorporated into a planar membrane of known lipid composition and currents induced by M2 were measured by the Black Lipid Membrane technique. When the planar lipid bilayer was composed of 75% phosphatidylethanolamine and 25% phosphatidylserine, the reversal potential measured in a 150/600 mM KCl (cis/trans) gradient was -19 mV suggesting that the examined pore was preferential to anions, PK/PCl = 0.25. In contrast, when 75% phosphatidylserine and 25% phosphatidylethanolamine was used, the reversal potential was +20 mV and the pore was preferential to cations, PK/PCl = 4.36. Single-channel currents were recorded with two predominant amplitudes corresponding to the main-conductance and sub-conductance states. Both conductance states (about 12 pS and 30 pS) were measured in a symmetric solution of 50 mM KCl. The observed single-channel properties suggest that the selectivity and conductance of the pore formed by the M2 peptide of the glycine receptor depend on the lipid composition of the planar bilayer.
2
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Molekularne metody stosowane w diagnostyce zespołu long-QT

75%
Moric-Janiszewska E., Głowacka M., Węglarz L.
Annales Academiae Medicae Silesiensis
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2012
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vol. 66
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issue 4
41-47
EN
LQTS (long QT syndrome) is a genetic disorder caused by the mutations of genes adversely aff ecting the ion channel function in the cellular membranes of cardiac myocytes. Prolonged repolarization detected on a ECG as a longer QT interval (> 450 ms) is responsible for syncope, cardiac arrest and sudden cardiac death (SCD), due to transient “torsade de pointes” (TdP) or ventricular fibrillation. Currently, 12 types of long-QT syndrome have been identifi ed, which are caused by 600 mutations of genes located on chromosomes: 3,4,6,7,11,17,21. Depending on the particular gene mutation in the LQT syndrome, subtypes from LQTS1 to LQTS12 were identifi ed. The knowledge of genetic disorders in diff erent types of LQTS has enabled the introduction of genotype-dependent therapy. Due to the frequent absence of clinical signs in 40% of mutant genes carriers, it is very important to develop fast and eff ective diagnostics. These patients do not always suit the clinical diagnostic criteria and therefore they should be diagnosed using molecular methods. In the present study we describe some molecular methods (SSCP, sequencing, quantitative PCR) most commonly used in genetic diagnostics of the long-QT syndrome.
PL
LQTS (long-QT syndrome) oznacza wrodzony zespół wydłużonego odcinka QT i jest chorobą kanałów jonowych uwarunkowaną genetycznie. U jej podstaw leżą mutacje genów kodujących białka i podjednostki kanałów jonowych błony podstawnej kardiomiocytów, istotne dla prawidłowego ich funkcjonowania. Jej głównymi cechami są: wydłużenie odstępu QT (> 450 ms) widoczne w obrazie EKG, pojawianie się omdleń, zatrzymania akcji serca oraz nagła śmierć sercowa SCD (sudden cardiac death), spowodowana występowaniem wielokształtnego częstoskurczu komorowego typu torsade de pointes (TdP) lub też migotaniem komór. Obecnie zidentyfi kowano 12 odmian zespołu long-QT, które spowodowane są aż 600 mutacjami genów zlokalizowanych w chromosomach: 3, 4, 6, 7, 11, 17, 21. Zależnie od mutacji konkretnego genu, w zespole LQT wyodrębniono podtypy od LQTS1 do LQTS12. Poznanie zaburzeń genetycznych w poszczególnych typach LQTS umożliwiło wprowadzenie terapii zależnej od genotypu. Ze względu na częste niewystępowanie objawów klinicznych aż u 40% nosicieli zmutowanych genów bardzo ważna jest szybka i skuteczna diagnostyka. U pacjentów takich nie zawsze sprawdzają się kliniczne kryteria diagnostyczne i dlatego należy ich diagnozować metodami molekularnymi. W przedstawionej pracy opisano niektóre (SSCP, sekwencjonowanie, ilościowy PCR) najczęściej stosowane, molekularne metody diagnostyki zespołu long-QT.
3
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Molecular dynamics simulations of potassium channels

75%
Domene C.
Open Chemistry
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2007
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vol. 5
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issue 3
635-671
EN
Despite the complexity of ion-channels, MD simulations based on realistic all-atom models have become a powerful technique for providing accurate descriptions of the structure and dynamics of these systems, complementing and reinforcing experimental work. Successful multidisciplinary collaborations, progress in the experimental determination of three-dimensional structures of membrane proteins together with new algorithms for molecular simulations and the increasing speed and availability of supercomputers, have made possible a considerable progress in this area of biophysics. This review aims at highlighting some of the work in the area of potassium channels and molecular dynamics simulations where numerous fundamental questions about the structure, function, folding and dynamics of these systems remain as yet unresolved challenges. [...]
4
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Mitochondrial potassium and chloride channels.

75%
Kicińska A., Dębska G., Kunz W., Szewczyk A.
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2000
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vol. 47
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issue 3
541-551
EN
Channels selective for potassium or chloride ions are present in inner mitochondrial membranes. They probably play an important role in mitochondrial events such as the formation of ΔpH and regulation of mitochondrial volume changes. Mitochondrial potassium and chloride channels could also be the targets for pharmacologically active compounds such as potassium channel openers and antidiabetic sulfonylureas. This review describes the properties, pharmacology, and current observations concerning the functional role of mitochondrial potassium and chloride channels.
5
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Intracellular potassium and chloride channels: An update.

75%
Dębska G., Kicińska A., Skalska J., Szewczyk A.
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2001
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vol. 48
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issue 1
137-144
EN
Channels selective for potassium or chloride ions are present in all intracellular membranes such as mitochondrial membranes, sarcoplasmic/endoplasmic reticulum, nuclear membrane and chromaffin granule membranes. They probably play an important role in events such as acidification of intracellular compartments and regulation of organelle volume. Additionally, intracellular ion channels are targets for pharmacologically active compounds, e.g. mitochondrial potassium channels interact with potassium channel openers such as diazoxide. This review describes current observations concerning the properties and functional roles of intracellular potassium and chloride channels.
6
Content available remote

Ion channels-related diseases.

75%
Dworakowska B., Dołowy K.
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2000
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vol. 47
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issue 3
685-703
EN
There are many diseases related to ion channels. Mutations in muscle voltage-gated sodium, potassium, calcium and chloride channels, and acetylcholine-gated channel may lead to such physiological disorders as hyper- and hypokalemic periodic paralysis, myotonias, long QT syndrome, Brugada syndrome, malignant hyperthermia and myasthenia. Neuronal disorders, e.g., epilepsy, episodic ataxia, familial hemiplegic migraine, Lambert-Eaton myasthenic syndrome, Alzheimer's disease, Parkinson's disease, schizophrenia, hyperekplexia may result from dysfunction of voltage-gated sodium, potassium and calcium channels, or acetylcholine- and glycine-gated channels. Some kidney disorders, e.g., Bartter's syndrome, policystic kidney disease and Dent's disease, secretion disorders, e.g., hyperinsulinemic hypoglycemia of infancy and cystic fibrosis, vision disorders, e.g., congenital stationary night blindness and total colour-blindness may also be linked to mutations in ion channels.
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