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Journal articles on the topic 'IK1'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Opdyke, C. A., and R. L. Calabrese. "Outward currents in heart motor neurons of the medicinal leech." Journal of Neurophysiology 74, no. 6 (1995): 2524–37. http://dx.doi.org/10.1152/jn.1995.74.6.2524.

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1. Outward currents were studied in isolation in heart motor neurons in the medicinal leech, using the single-electrode voltage-clamp technique. The currents were divided into four distinct types on the basis of their time and voltage characteristics and sensitivity to external Ca2+ concentration. 2. The four types were a fast transient current, IKA; a slow transient current. IK1; a noninactivating current, IK2, all measured in a bathing solution in which Co2+ was substituted for Ca2+; and a calcium-sensitive current. IK1Cal which was revealed in a bathing solution containing normal levels of

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2

Yagi, Tomohito, Shigeyoshi Hibi, Mami Takanashi, et al. "High frequency of Ikaros isoform 6 expression in acute myelomonocytic and monocytic leukemias: implications for up-regulation of the antiapoptotic protein Bcl-XL in leukemogenesis." Blood 99, no. 4 (2002): 1350–55. http://dx.doi.org/10.1182/blood.v99.4.1350.

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While studying Ikaros proteins in childhood acute myeloid leukemia (AML), Ikaros isoform 6 (Ik6) expression was detected in 7 of 10 cases of M4 and M5 leukemia, but in none of the remaining French-American-British subtypes (M2, 8 cases; M7, 6 cases). The spliced Ikaros isoforms 4 to 8 (Ik4-8) suppress the function of full-length Ik1 or Ik2 in a dominant-negative manner, owing to their reduced numbers of DNA binding sites. Thus, dominant-negative Ikaros isoforms may inhibit the normal transcriptional regulation of hematopoietic cell development. To clarify the function of Ik6 in developing bloo

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3

Vaidyanathan, Ravi, Yogananda S. Markandeya, Timothy J. Kamp, Jonathan C. Makielski, Craig T. January, and Lee L. Eckhardt. "IK1-enhanced human-induced pluripotent stem cell-derived cardiomyocytes: an improved cardiomyocyte model to investigate inherited arrhythmia syndromes." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 11 (2016): H1611—H1621. http://dx.doi.org/10.1152/ajpheart.00481.2015.

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Currently available induced pluripotent stem cell-derived cardiomyocytes (iPS-CMs) do not ideally model cellular mechanisms of human arrhythmic disease due to lack of a mature action potential (AP) phenotype. In this study, we create and characterize iPS-CMs with an electrically mature AP induced by potassium inward rectifier ( IK1) enhancement. The advantages of IK1-enhanced iPS-CMs include the absence of spontaneous beating, stable resting membrane potentials at approximately −80 mV and capability for electrical pacing. Compared with unenhanced, IK1-enhanced iPS-CMs calcium transient amplitu

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4

Thompson, Jill, and Ted Begenisich. "Membrane-delimited Inhibition of Maxi-K Channel Activity by the Intermediate Conductance Ca2+-activated K Channel." Journal of General Physiology 127, no. 2 (2006): 159–69. http://dx.doi.org/10.1085/jgp.200509457.

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The complexity of mammalian physiology requires a diverse array of ion channel proteins. This diversity extends even to a single family of channels. For example, the family of Ca2+-activated K channels contains three structural subfamilies characterized by small, intermediate, and large single channel conductances. Many cells and tissues, including neurons, vascular smooth muscle, endothelial cells, macrophages, and salivary glands express more than a single class of these channels, raising questions about their specific physiological roles. We demonstrate here a novel interaction between two

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5

Panama, Brian K., Meredith McLerie, and Anatoli N. Lopatin. "Heterogeneity of IK1 in the mouse heart." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 6 (2007): H3558—H3567. http://dx.doi.org/10.1152/ajpheart.00419.2007.

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Previous studies have shown that cardiac inward rectifier potassium current ( IK1) channels are heteromers of distinct Kir2 subunits and suggested that species- and tissue-dependent expression of these subunits may underlie variability of IK1. In this study, we investigated the contribution of the slowly activating Kir2.3 subunit and free intracellular polyamines (PAs) to variability of IK1 in the mouse heart. The kinetics of activation was measured in Kir2 concatemeric tetramers with known subunit stoichiometry. Inclusion of only one Kir2.3 subunit to a Kir2.1 channel led to an approximate th

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6

Wahler, G. M. "Developmental increases in the inwardly rectifying potassium current of rat ventricular myocytes." American Journal of Physiology-Cell Physiology 262, no. 5 (1992): C1266—C1272. http://dx.doi.org/10.1152/ajpcell.1992.262.5.c1266.

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The neonatal rat ventricular action potential has a shape similar to that of most adult mammals. However, shortly after birth, the action potential shortens to a spike-like configuration. The contribution of changes in repolarizing currents to the shortening is unclear. Thus the inwardly rectifying potassium current (IK1) was measured in heart cells from rats of varying ages using patch-clamp techniques. In freshly isolated cells, whole cell IK1 currents increased greatly between ages 3 and 9-13 days and remained constant thereafter. In culture, IK1 disappeared preferentially in older cells, o

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7

Romanenko, Victor G., Kurt S. Roser, James E. Melvin, and Ted Begenisich. "The role of cell cholesterol and the cytoskeleton in the interaction between IK1 and maxi-K channels." American Journal of Physiology-Cell Physiology 296, no. 4 (2009): C878—C888. http://dx.doi.org/10.1152/ajpcell.00438.2008.

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Recently, we demonstrated a novel interaction between large-conductance (maxi-K or KCa1.1) and intermediate-conductance (IK1 or KCa3.1) Ca2+-activated K channels: activation of IK1 channels causes the inhibition of maxi-K activity (Thompson J and Begenisich T. J Gen Physiol 127: 159–169, 2006). Here we show that the interaction between these two channels can be regulated by the membrane cholesterol level in parotid acinar cells. Depletion of cholesterol using methyl-β-cyclodextrin weakened, while cholesterol enrichment increased, the ability of IK1 activation to inhibit maxi-K channels. Choles

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8

Masuda, H., and N. Sperelakis. "Inwardly rectifying potassium current in rat fetal and neonatal ventricular cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (1993): H1107—H1111. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1107.

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Whole cell and single-channel inwardly rectifying potassium currents (IK1) of freshly isolated single fetal (12 and 18 days) and neonatal (1, 5, and 10 days) rat ventricular myocytes were recorded using patch-clamp techniques. Whole cell IK1 was elicited by hyperpolarizing test pulses from a holding potential of -40 mV. IK1 densities increased markedly during heart development between fetal day 12 and until neonatal day 5; there was no further increase on neonatal day 10. Cell-attached patch recordings of single IK1 channels were employed with 150 mM K+ both in the pipette and bath solutions.

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9

Cheng, Lu-Feng, Fuzhen Wang, and Anatoli N. Lopatin. "Metabolic stress in isolated mouse ventricular myocytes leads to remodeling of t tubules." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (2011): H1984—H1995. http://dx.doi.org/10.1152/ajpheart.00304.2011.

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Cardiac ventricular myocytes possess an extensive t-tubular system that facilitates the propagation of membrane potential across the cell body. It is well established that ionic currents at the restricted t-tubular space may lead to significant changes in ion concentrations, which, in turn, may affect t-tubular membrane potential. In this study, we used the whole cell patch-clamp technique to study accumulation and depletion of t-tubular potassium by measuring inward rectifier potassium tail currents ( IK1,tail), and inward rectifier potassium current ( IK1) “inactivation”. At room temperature

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10

Poelzing, Steven, and Rengasayee Veeraraghavan. "Heterogeneous ventricular chamber response to hypokalemia and inward rectifier potassium channel blockade underlies bifurcated T wave in guinea pig." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (2007): H3043—H3051. http://dx.doi.org/10.1152/ajpheart.01312.2006.

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It was previously demonstrated that transmural electrophysiological heterogeneities can inscribe the ECG T wave. However, the bifurcated T wave caused by loss of inward rectifier potassium current ( IK1) function is not fully explained by transmural heterogeneities. Since right ventricular (RV) guinea pig myocytes have significantly lower IK1 than left ventricular (LV) myocytes, we hypothesized that the complex ECG can be inscribed by heterogeneous chamber-specific responses to hypokalemia and partial IK1 blockade. Ratiometric optical action potentials were recorded from the epicardial surface

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Costa, Ana Da Silva, Peter Mortensen, Maria P. Hortigon-Vinagre, et al. "Electrophysiology of hiPSC-Cardiomyocytes Co-Cultured with HEK Cells Expressing the Inward Rectifier Channel." International Journal of Molecular Sciences 22, no. 12 (2021): 6621. http://dx.doi.org/10.3390/ijms22126621.

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The immature electrophysiology of human-induced pluripotent stem cell-derived cardiomyocytes (hiCMs) complicates their use for therapeutic and pharmacological purposes. An insufficient inward rectifying current (IK1) and the presence of a funny current (if) cause spontaneous electrical activity. This study tests the hypothesis that the co-culturing of hiCMs with a human embryonic kidney (HEK) cell-line expressing the Kir2.1 channel (HEK-IK1) can generate an electrical syncytium with an adult-like cardiac electrophysiology. The mechanical activity of co-cultures using different HEK-IK1:hiCM rat

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12

Li, Yacong, Kuanquan Wang, Qince Li, Jules C. Hancox, and Henggui Zhang. "Reciprocal interaction between IK1 and If in biological pacemakers: A simulation study." PLOS Computational Biology 17, no. 3 (2021): e1008177. http://dx.doi.org/10.1371/journal.pcbi.1008177.

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Pacemaking dysfunction (PD) may result in heart rhythm disorders, syncope or even death. Current treatment of PD using implanted electronic pacemakers has some limitations, such as finite battery life and the risk of repeated surgery. As such, the biological pacemaker has been proposed as a potential alternative to the electronic pacemaker for PD treatment. Experimentally and computationally, it has been shown that bio-engineered pacemaker cells can be generated from non-rhythmic ventricular myocytes (VMs) by knocking out genes related to the inward rectifier potassium channel current (IK1) or

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13

Volejnikova, Jana, Ester Mejstrikova, Karel Svojgr, Jan Stary, Jan Trka, and Eva Fronkova. "Prognostic Impact of Ikaros (IKZF1) Gene Alterations In Childhood ALL Treated with ALL IC-BFM 2002 Protocol: A Comparison of Gene Expression and Genomic-Based Methods." Blood 116, no. 21 (2010): 1656. http://dx.doi.org/10.1182/blood.v116.21.1656.1656.

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Abstract Abstract 1656 Introduction: Recently, Ikaros (IKZF1) gene alterations were found to predict poor prognosis in childhood acute lymphoblastic leukemia (ALL). Thus, the implementation of IKZF1 status into the risk group stratification is discussed. So far, limited data are available concerning both IKZF1 importance in different treatment protocols for Ph-negative ALL and the choice of the best diagnostic method. In this study, we compared two methods based on either genomic DNA examination or gene expression analysis, and their prognostic impact within a treatment protocol for childhood

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14

Husti, Zoltán, Katalin Tábori, Viktor Juhász, Tibor Hornyik, András Varró, and István Baczkó. "Combined inhibition of key potassium currents has different effects on cardiac repolarization reserve and arrhythmia susceptibility in dogs and rabbits." Canadian Journal of Physiology and Pharmacology 93, no. 7 (2015): 535–44. http://dx.doi.org/10.1139/cjpp-2014-0514.

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A reliable assessment of the pro-arrhythmic potential for drugs in the development phase remains elusive. Rabbits and dogs are commonly used to create models of pro-arrhythmia, but the differences between them with respect to repolarizing potassium currents are poorly understood. We investigated the incidence of drug-induced torsades de pointes (TdP) and measured conventional ECG parameters and the short-term variability of the QT interval (STVQT) following combined pharmacological inhibition of IK1+IKs and IK1+IKr in conscious dogs and anesthetized rabbits. A high incidence of TdP was observe

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15

Curtis, Michael J. "Activation of IK1 by Zacopride." Journal of Cardiovascular Pharmacology 64, no. 4 (2014): 343–44. http://dx.doi.org/10.1097/fjc.0000000000000140.

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16

SAKAGUCHI, Y. "Aprindine block on IK1 channel." Journal of Molecular and Cellular Cardiology 23 (March 1991): 25. http://dx.doi.org/10.1016/0022-2828(91)90449-v.

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17

Lin, Yuanyuan, Junhu Li, Baozhong Zhu, et al. "Zacopride Exerts an Antiarrhythmic Effect by Specifically Stimulating the Cardiac Inward Rectifier Potassium Current in Rabbits: Exploration of a New Antiarrhythmic Strategy." Current Pharmaceutical Design 26, no. 44 (2020): 5746–54. http://dx.doi.org/10.2174/1381612826666200701135508.

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Background: Zacopride, a potent antagonist of 5-HT3 receptors and an agonist of 5-HT4 receptors, is a gastrointestinal prokinetic agent. In a previous study, we discovered that zacopride selectively stimulated the inward rectifier potassium current (IK1) in the rat and that agonizing IK1 prevented or eliminated aconitine-induced arrhythmias in rats. Objective: Our aims were to confirm that the antiarrhythmic effects of zacopride are mediated by selectively enhancing IK1 in rabbits. Methods: The effects of zacopride on the function of the main ion channels were investigated using a whole-cell p

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Lin, Mike T., John P. Adelman, and James Maylie. "Modulation of endothelial SK3 channel activity by Ca2+-dependent caveolar trafficking." American Journal of Physiology-Cell Physiology 303, no. 3 (2012): C318—C327. http://dx.doi.org/10.1152/ajpcell.00058.2012.

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Small- and intermediate-conductance Ca2+-activated K+ channels (SK3/Kcnn3 and IK1/Kcnn4) are expressed in vascular endothelium. Their activities play important roles in regulating vascular tone through their modulation of intracellular concentration ([Ca2+]i) required for the production of endothelium-derived vasoactive agents. Activation of endothelial IK1 or SK3 channels hyperpolarizes endothelial cell membrane potential, increases Ca2+ influx, and leads to the release of vasoactive factors, thereby impacting blood pressure. To examine the distinct roles of IK1 and SK3 channels, we used elec

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19

Oliva, C., I. S. Cohen, and P. Pennefather. "The mechanism of rectification of iK1 in canine Purkinje myocytes." Journal of General Physiology 96, no. 2 (1990): 299–318. http://dx.doi.org/10.1085/jgp.96.2.299.

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We have characterized the inward rectifying background potassium current, iK1, of canine cardiac Purkinje myocytes in terms of its reversal potential, voltage activation curve, and "steady-state" current-voltage relation. The latter parameter was defined from the difference current between holding currents in the presence and absence of 20 mM cesium. Our data suggest that iK1 rectification does not arise exclusively from voltage-dependent gating or exclusively from voltage-dependent blockade by internal magnesium ions. The voltage activation curve constructed from tail currents fit to a Boltzm

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20

Huguenard, J. R., and D. A. Prince. "Slow inactivation of a TEA-sensitive K current in acutely isolated rat thalamic relay neurons." Journal of Neurophysiology 66, no. 4 (1991): 1316–28. http://dx.doi.org/10.1152/jn.1991.66.4.1316.

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1. Voltage-gated K currents were studied in relay neurons (RNs) acutely isolated from somatosensory (VB) thalamus of 7- to 14-day-old rats. In addition to a rapidly activated, transient outward current, IA, depolarizations activated slower K+ currents, which were isolated through the use of appropriate ionic and pharmacological conditions and measured via whole-cell voltage-clamp. 2. At least two slow components of outward current were observed, both of which were sensitive to changes in [K+]o, as expected for K conductances. The first, IK1, had an amplitude that was insensitive to holding pot

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Kleiman, R. B., and S. R. Houser. "Outward currents in normal and hypertrophied feline ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 5 (1989): H1450—H1461. http://dx.doi.org/10.1152/ajpheart.1989.256.5.h1450.

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The properties of the inward rectifier K current (IK1) and the delayed rectifier K current (IK) were studied in single feline myocytes isolated from the right ventricle of normal cats and cats with experimentally induced right ventricular hypertrophy (RVH). IK1 demonstrated time-dependent decay during hyperpolarizations and showed inward rectification with a prominent negative-slope region between -30 and -10 mV. Both IK1 and IK was carried primarily by K ions. The activation of IK during depolarizations followed a monoexponential time course, whereas the deactivation of IK tail currents was e

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22

Hayashi, M., C. Kunii, T. Takahata, and T. Ishikawa. "ATP-dependent regulation of SK4/IK1-like currents in rat submandibular acinar cells: possible role of cAMP-dependent protein kinase." American Journal of Physiology-Cell Physiology 286, no. 3 (2004): C635—C646. http://dx.doi.org/10.1152/ajpcell.00283.2003.

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SK4/IK1 encodes an intermediate conductance, Ca2+-activated K+ channel and fulfills a variety of physiological functions in excitable and nonexcitable cells. Although recent studies have provided evidence for the presence of SK4/IK1 channels in salivary acinar cells, the regulatory mechanisms and the physiological function of the channel remain unknown in these cells. Using molecular and electrophysiological techniques, we examined whether cytosolic ATP-dependent regulation of native SK4/IK1-like channel activity would involve endogenous cAMP-dependent protein kinase (PKA) in rat submandibular

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23

Holt, J. R., and R. A. Eatock. "Inwardly rectifying currents of saccular hair cells from the leopard frog." Journal of Neurophysiology 73, no. 4 (1995): 1484–502. http://dx.doi.org/10.1152/jn.1995.73.4.1484.

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1. Inwardly rectifying currents were characterized in sensory hair cells isolated from the saccules of leopard frogs, using the whole cell configuration of the patch-clamp technique in voltage-clamp mode. 2. Two types of inwardly rectifying currents were distinguishable based on their ionic selectivity, activation and deactivation kinetics, voltage dependence, dependence on external K+ and sensitivity to divalent cations. 3. One inwardly rectifying current displayed K+ selectivity, rapid monoexponential activation (tau approximately 1 ms at -120 mV), steep voltage dependence, dependence of the

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Teos, Leyla Y., Aiqiu Zhao, Zikiar Alvin, Graham G. Laurence, Chuanfu Li, and Georges E. Haddad. "Basal and IGF-I-dependent regulation of potassium channels by MAP kinases and PI3-kinase during eccentric cardiac hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 5 (2008): H1834—H1845. http://dx.doi.org/10.1152/ajpheart.321.2008.

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The potassium channels IK and IK1, responsible for the action potential repolarization and resting potential respectively, are altered during cardiac hypertrophy. The activation of insulin-like growth factor-I (IGF-I) during hypertrophy may affect channel activity. The aim was to examine the modulatory effects of IGF-I on IK and IK1 through mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways during hypertrophy. With the use of specific inhibitors for ERK1/2 (PD98059), p38 MAPK (SB203580) and PI3K/Akt (LY294002), Western blot and whole cell patch-clamp were

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van der Schoor, Laura, Emma J. van Hattum, Sophie M. de Wilde, et al. "Towards the Development of AgoKirs: New Pharmacological Activators to Study Kir2.x Channel and Target Cardiac Disease." International Journal of Molecular Sciences 21, no. 16 (2020): 5746. http://dx.doi.org/10.3390/ijms21165746.

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Inward rectifier potassium ion channels (IK1-channels) of the Kir2.x family are responsible for maintaining a stable negative resting membrane potential in excitable cells, but also play a role in processes of non-excitable tissues, such as bone development. IK1-channel loss-of-function, either congenital or acquired, has been associated with cardiac disease. Currently, basic research and specific treatment are hindered by the absence of specific and efficient Kir2.x channel activators. However, twelve different compounds, including approved drugs, show off-target IK1 activation. Therefore, th

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26

Kleber, A. G. "Commentary on the IK1 blockade controversy." Cardiovascular Research 28, no. 5 (1994): 720. http://dx.doi.org/10.1093/cvr/28.5.720.

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Ichikawa, H. "Is IK1 blockade proarrhgthmic or antiarrhythmic?" Cardiovascular Research 28, no. 7 (1994): 1120–21. http://dx.doi.org/10.1093/cvr/28.7.1120.

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Beaumont, J., D. C. Michaels, M. Delmar, J. Davidenko, and J. Jalife. "A model study of changes in excitability of ventricular muscle cells: inhibition, facilitation, and hysteresis." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 3 (1995): H1181—H1194. http://dx.doi.org/10.1152/ajpheart.1995.268.3.h1181.

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A model study was carried out to investigate the mechanism of changes in excitability at long cycle lengths (i.e., > 1,000 ms), which are responsible for various phenomena, including electrotonic inhibition, active facilitation, and hysteresis of excitability in ventricular muscle at slow frequencies of stimulation. Experimental studies suggested that with repetitive activity the inward rectifier potassium current (IK1) is not a passive component of membrane response and that the dynamics of IK1 are responsible for the changes in excitability at long cycle lengths. In the present study, we

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Hassinen, Minna, Vesa Paajanen, Jaakko Haverinen, Heli Eronen, and Matti Vornanen. "Cloning and expression of cardiac Kir2.1 and Kir2.2 channels in thermally acclimated rainbow trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 6 (2007): R2328—R2339. http://dx.doi.org/10.1152/ajpregu.00354.2006.

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Potassium currents are plastic entities that modify electrical activity of the heart in various physiological conditions including chronic thermal stress. We examined the molecular basis of the inward rectifier K+ current ( IK1) in rainbow trout acclimated to cold (4°C, CA) and warm (18°C, WA) temperature. Inward rectifier K+ channel (Kir)2.1 and Kir2.2 transcripts were expressed in atrium and ventricle of the trout heart, Kir2.1 being the major component in both cardiac chambers. The relative expression of Kir2.2 was, however, higher ( P < 0.05) in atrium than ventricle. The density of ven

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Iacobucci, Ilaria, Annalisa Lonetti, Francesca Messa, et al. "Expression of spliced oncogenic Ikaros isoforms in Philadelphia-positive acute lymphoblastic leukemia patients treated with tyrosine kinase inhibitors: implications for a new mechanism of resistance." Blood 112, no. 9 (2008): 3847–55. http://dx.doi.org/10.1182/blood-2007-09-112631.

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Ikaros plays an important role in the control of differentiation and proliferation of all lymphoid lineages. The expression of short isoforms lacking DNA-binding motifs alters the differentiation capacities of hematopoietic progenitors, arresting lineage commitment. We sought to determine whether molecular abnormalities involving the IKZF1 gene were associated with resistance to tyrosine kinase inhibitors (TKIs) in Ph+ acute lymphoblastic leukemia (ALL) patients. Using reverse-transcribed polymerase chain reaction, cloning, and nucleotide sequencing, only the non–DNA-binding Ik6 isoform was de

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Kurata, Yasutaka, Hiroyuki Matsuda, Ichiro Hisatome, and Toshishige Shibamoto. "Effects of pacemaker currents on creation and modulation of human ventricular pacemaker: theoretical study with application to biological pacemaker engineering." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (2007): H701—H718. http://dx.doi.org/10.1152/ajpheart.00426.2006.

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A cardiac biological pacemaker (BP) has been created by suppression of the inward rectifier K+ current ( IK1) or overexpression of the hyperpolarization-activated current ( Ih). We theoretically investigated the effects of incorporating Ih, T-type Ca2+ current ( ICa,T), sustained inward current ( Ist), and/or low-voltage-activated L-type Ca2+ channel current ( ICa,LD) on 1) creation of BP cells, 2) robustness of BP activity to electrotonic loads of nonpacemaking (NP) cells, and 3) BP cell ability to drive NP cells. We used a single-cell model for human ventricular myocytes (HVMs) and also coup

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Hegyi, Bence, Ye Chen-Izu, Leighton T. Izu та Tamás Bányász. "Altered K+ current profiles underlie cardiac action potential shortening in hyperkalemia and β-adrenergic stimulation". Canadian Journal of Physiology and Pharmacology 97, № 8 (2019): 773–80. http://dx.doi.org/10.1139/cjpp-2019-0056.

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Hyperkalemia is known to develop in various conditions including vigorous physical exercise. In the heart, hyperkalemia is associated with action potential (AP) shortening that was attributed to altered gating of K+ channels. However, it remains unknown how hyperkalemia changes the profiles of each K+ current under a cardiac AP. Therefore, we recorded the major K+ currents (inward rectifier K+ current, IK1; rapid and slow delayed rectifier K+ currents, IKr and IKs, respectively) using AP-clamp in rabbit ventricular myocytes. As K+ may accumulate at rapid heart rates during sympathetic stimulat

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Sridhar, Arun, Spencer J. Dech, Veronique A. Lacombe, et al. "Abnormal diastolic currents in ventricular myocytes from spontaneous hypertensive heart failure rats." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 5 (2006): H2192—H2198. http://dx.doi.org/10.1152/ajpheart.01146.2005.

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Hypertension is a common cause of heart failure, and ventricular arrhythmias are a major cause of death in heart failure. The spontaneous hypertension heart failure (SHHF) rat model was used to study altered ventricular electrophysiology in hypertension and heart failure. We hypothesized that a reduction in the inward rectifier K+ current ( IK1) and expression of pacemaker current ( If) would favor abnormal automaticity in the SHHF ventricle. SHHF ventricular myocytes were isolated at 2 and 8 mo of age and during end-stage heart failure (≥17 mo); myocytes from age-matched rats served as contro

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Li, Yue, Hongxiang Hu, Jin-Bin Tian, Michael X. Zhu, and Roger G. O’Neil. "Dynamic coupling between TRPV4 and Ca2+-activated SK1/3 and IK1 K+ channels plays a critical role in regulating the K+-secretory BK channel in kidney collecting duct cells." American Journal of Physiology-Renal Physiology 312, no. 6 (2017): F1081—F1089. http://dx.doi.org/10.1152/ajprenal.00037.2017.

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The large-conductance Ca2+-activated K+ channel, BK (KCNMA1), is expressed along the connecting tubule (CNT) and cortical collecting duct (CCD) where it underlies flow- and Ca2+-dependent K+ secretion. Its activity is partially under the control of the mechanosensitive transient receptor potential vanilloid type 4 (TRPV4) Ca2+-permeable channel. Recently, we identified three small-/intermediate-conductance Ca2+-activated K+ channels, SK1 (KCNN1), SK3 (KCNN3), and IK1 (KCNN4), with notably high Ca2+-binding affinities, that are expressed in CNT/CCD and may be regulated by TRPV4-mediated Ca2+ in

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Li, Yue, Hongxiang Hu, and Roger G. O’Neil. "Caveolae facilitate TRPV4-mediated Ca2+ signaling and the hierarchical activation of Ca2+-activated K+ channels in K+-secreting renal collecting duct cells." American Journal of Physiology-Renal Physiology 315, no. 6 (2018): F1626—F1636. http://dx.doi.org/10.1152/ajprenal.00076.2018.

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Transient receptor potential cation channel subfamily V member 4 (TRPV4)-mediated Ca2+ signaling induces early activation of small/intermediate Ca2+-activated K+ channels, SK3 (KCNN3) and IK1 (KCNN4), which leads to membrane hyperpolarization and enhanced Ca2+ influx, which is critical for subsequent activation of the large conductance Ca2+-activated K+ channel BK (KCNMA1) and K+ secretion in kidney cortical collecting duct (CCD) cells. The focus of the present study was to determine if such coordinated hierarchical/sequential activation of these channels in CCD was orchestrated within caveola

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36

Collins-Underwood, J. Racquel, Nidal Boulos, Debbie Payne-Turner, Shann-Ching Chen, Richard Williams, and Charles Mullighan. "The Role of Dominant-Negative IKAROS Mutations In the Pathogenesis and Treatment Responsiveness of BCR-ABL1 positive Acute Lymphoblastic Leukemia." Blood 116, no. 21 (2010): 540. http://dx.doi.org/10.1182/blood.v116.21.540.540.

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Abstract Abstract 540 Expression of the constitutively active tyrosine kinase BCR-ABL1 is the hallmark of two diseases with distinct pathologic and clinical features: chronic myeloid leukemia (CML), an expansion of relatively mature granulocytes that typically responds well to kinase inhibition, and pre-B cell acute lymphoblastic leukemia (ALL), an aggressive malignancy of lymphoid progenitors that has a dismal prognosis. The basis for this dichotomy has been poorly understood. Recent studies profiling genome-wide DNA copy number alterations in CML and ALL have identified common deletions of I

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Liu, Qing-Hua, Xiao-Li Li, Yan-Wu Xu, Yuan-Yuan Lin, Ji-Min Cao, and Bo-Wei Wu. "A Novel Discovery of IK1 Channel Agonist." Journal of Cardiovascular Pharmacology 59, no. 1 (2012): 37–48. http://dx.doi.org/10.1097/fjc.0b013e3182350bcc.

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Harvey, R. D., and R. E. Ten Eick. "Voltage-dependent block of cardiac inward-rectifying potassium current by monovalent cations." Journal of General Physiology 94, no. 2 (1989): 349–61. http://dx.doi.org/10.1085/jgp.94.2.349.

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The inward-rectifying K+ current (IK1) in cat ventricular myocytes, like inward-rectifying K+ currents in many other preparations, exhibited a negative slope conductance region at hyperpolarized membrane potentials that was time-dependent. This was evident as an inactivation of inward current elicited by hyperpolarizing voltage-clamp pulses resulting in a negative slope region of the steady-state current-voltage relationship at potentials negative to -140 mV. Removing extracellular Na+ prevented the development of the negative slope in this voltage region, suggesting that Na+ can block IK1 cha

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Li, Xiantao, Alexei Surguchev, Shumin Bian, Dhasakumar Navaratnam, and Joseph Santos-Sacchi. "Extracellular chloride regulation of Kv2.1, contributor to the major outward Kv current in mammalian outer hair cells." American Journal of Physiology-Cell Physiology 302, no. 1 (2012): C296—C306. http://dx.doi.org/10.1152/ajpcell.00177.2011.

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Outer hair cells (OHC) function as both receptors and effectors in providing a boost to auditory reception. Amplification is driven by the motor protein prestin, which is under anionic control. Interestingly, we now find that the major, 4-AP-sensitive, outward K+ current of the OHC ( IK) is also sensitive to Cl−, although, in contrast to prestin, extracellularly. IK is inhibited by reducing extracellular Cl− levels, with a linear dependence of 0.4%/mM. Other voltage-dependent K+ (Kv) channel conductances in supporting cells, such as Hensen and Deiters' cells, are not affected by reduced extrac

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Volejnikova, Jana, Ester Mejstrikova, Jan Stary, Jan Trka, and Eva Fronkova. "Relative Expression of Ikaros Isoforms Has a Prognostic Impact in Phildelphia-Negative Childhood Acute Lymphoblastic Leukemia." Blood 114, no. 22 (2009): 1282. http://dx.doi.org/10.1182/blood.v114.22.1282.1282.

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Abstract Abstract 1282 Poster Board I-304 Ikaros, encoded by the IKZF1 gene, is a zinc-finger transcription factor crucial for normal differentiation of the lymphoid lineage. Multiple isoforms of Ikaros are generated by alternative splicing in lymphoid progenitors. Recent studies based primarily on high-risk (HR) patients with ALL, including Philadelphia-positive cases, have shown an inferior prognosis of patients with Ikaros alterations, leading in most cases to the expression of short, non-DNA binding isoforms of IKZF1. There is only a limited information about the overall frequency and prog

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Xiao, Guo-Sheng, Jing-Jun Zhou, Guan-Ying Wang, Chun-Mei Cao, Gui-Rong Li, and Tak-Ming Wong. "In Vitro Electrophysiologic Effects of Morphine in Rabbit Ventricular Myocytes." Anesthesiology 103, no. 2 (2005): 280–86. http://dx.doi.org/10.1097/00000542-200508000-00011.

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Background Morphine is widely used in patients undergoing surgical operations and is also reported to mediate cardioprotection of preconditioning. The current study determined effects of morphine at therapeutic to pharmacologic concentrations on cardiac action potential, L-type Ca2+ current (ICa.L), delayed rectifier K+ current (IK), and inward rectifier K+ current (IK1) in isolated rabbit ventricular myocytes. Methods Ventricular myocytes were enzymatically isolated from rabbit hearts. Action potential and membrane currents were recorded in current and voltage clamp modes. Results Morphine at

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Stecyk, Jonathan A. W., Christine S. Couturier, Denis V. Abramochkin, et al. "Cardiophysiological responses of the air-breathing Alaska blackfish to cold acclimation and chronic hypoxic submergence at 5°C." Journal of Experimental Biology 223, no. 22 (2020): jeb225730. http://dx.doi.org/10.1242/jeb.225730.

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ABSTRACTThe Alaska blackfish (Dallia pectoralis) remains active at cold temperatures when experiencing aquatic hypoxia without air access. To discern the cardiophysiological adjustments that permit this behaviour, we quantified the effect of acclimation from 15°C to 5°C in normoxia (15N and 5N fish), as well as chronic hypoxic submergence (6–8 weeks; ∼6.3–8.4 kPa; no air access) at 5°C (5H fish), on in vivo and spontaneous heart rate (fH), electrocardiogram, ventricular action potential (AP) shape and duration (APD), the background inward rectifier (IK1) and rapid delayed rectifier (IKr) K+ cu

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Rees, S. A., and M. J. Curtis. "IK1 blockade is a potentially useful antiarrhythmic mechanism." Cardiovascular Research 28, no. 3 (1994): 421. http://dx.doi.org/10.1093/cvr/28.3.421.

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Zhang, Guangsi, Cao Panxiang, Fang Wang, et al. "Classification and Quantification of Oncogenic Ikaros Isoforms in B Cell Precursor Acute Lymphoblastic Leukemia By RNA-Seq." Blood 136, Supplement 1 (2020): 2–3. http://dx.doi.org/10.1182/blood-2020-140285.

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Background Ikaros, encoded by IKZF1, is a critical transcriptional factor in the B cell development, and the oncogenic isoforms could contribute to leukemia transformation and poor outcome in B cell precursor acute lymphoblastic leukemia (BCP-ALL). Truncated oncogenic isoforms lacking DNA binding domains could be originated from intragenic deletion and alternative splicing, and act as dominant-negative manner. Because of the variable transcripts and sequence homology of IKZF1, there are still challenges to identify the ikaros isoforms by traditional PCR. Methods Here, we developed an integrate

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Lee, Elbert L., Yuichi Hasegawa, Takahiro Shimizu, and Yasunobu Okada. "IK1 channel activity contributes to cisplatin sensitivity of human epidermoid cancer cells." American Journal of Physiology-Cell Physiology 294, no. 6 (2008): C1398—C1406. http://dx.doi.org/10.1152/ajpcell.00428.2007.

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Cisplatin, a platinum-based drug, is an important weapon against many types of cancer. It induces apoptosis by forming adducts with DNA, although many aspects of its mechanism of action remain to be clarified. Previously, we found a role for the volume-sensitive, outwardly rectifying Cl− channel in cisplatin-induced apoptosis. To investigate the possibility that cation channels also have a role in the cellular response to cisplatin, we examined the activity of cation channels in cisplatin-sensitive KB-3-1 (KB) epidermoid cancer cells by the whole cell patch-clamp method. A cation channel in KB

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Takahata, T., M. Hayashi, and T. Ishikawa. "SK4/IK1-like channels mediate TEA-insensitive, Ca2+-activated K+ currents in bovine parotid acinar cells." American Journal of Physiology-Cell Physiology 284, no. 1 (2003): C127—C144. http://dx.doi.org/10.1152/ajpcell.00250.2002.

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Although Ca2+-activated K+ (KCa) channels distinct from maxi-K+ channels have been suggested to contribute to muscarinically stimulated K+ currents in salivary acinar cells, the molecular nature of the channels is unclear. Using electrophysiological and RT-PCR techniques, we have now investigated the involvement of SK4/IK1-like channels in native KCacurrents in bovine parotid acinar (BPA) cells. Ca2+-dependent K+ efflux from perfused bovine parotid tissues was not inhibited by a maxi-K+ channel blocker, tetraethylammonium (TEA). Whole cell recordings from BPA cells showed a TEA-insensitive KCa

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He, Jianying, Margaret E. Kargacin, Gary J. Kargacin, and Christopher A. Ward. "Tamoxifen inhibits Na+ and K+ currents in rat ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 2 (2003): H661—H668. http://dx.doi.org/10.1152/ajpheart.00686.2002.

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Tamoxifen is an estrogen receptor antagonist used in the treatment of breast cancer. However, tamoxifen has been shown to induce QT prolongation of the electrocardiogram, thereby potentially causing life-threatening polymorphic ventricular arrhythmias. The purpose of the present study was to elucidate the electrophysiological mechanism(s) that underlie the arrhythmogenic effects of tamoxifen. We used standard ruptured whole cell and perforated patch-clamping techniques on rat ventricular myocytes to investigate the effects of tamoxifen on cardiac action potential (AP) waveforms and the underly

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Imoto, Y., T. Ehara, and H. Matsuura. "Voltage- and time-dependent block of iK1 underlying Ba2+-induced ventricular automaticity." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 2 (1987): H325—H333. http://dx.doi.org/10.1152/ajpheart.1987.252.2.h325.

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The mechanism underlying the Ba2+-induced automaticity was studied in isolated guinea pig ventricular myocytes using the whole-cell clamp method and a patch electrode. In the presence of 0.1–0.3 mM Ba2+, application of a weak depolarizing current induced repetitive firing of spontaneous action potentials. Application of tetrodotoxin or Ca2+ channel blockers and removal of external Na+ and Ca2+ did not abolish the rhythmic activity, thereby suggesting that activation of inward currents played no crucial role in the generation of this rhythmicity. Voltage-clamp studies revealed that Ba2+ blocked

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Suhartanto, Ari, Ismail Abdurrozzaq Zulkarnain, and Yoga Prisma Yuda. "Simple Additive Weighting Method for The Assessment of Sharia Banking Performance." INTENSIF: Jurnal Ilmiah Penelitian dan Penerapan Teknologi Sistem Informasi 4, no. 1 (2020): 108–22. http://dx.doi.org/10.29407/intensif.v4i1.13799.

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The interest in Sharia-based financial industry products has increased rapidly, as evidenced by a large number of conventional Bank customers migrating to Islamic Commercial Banks (BUS). With this phenomenon, it is necessary to measure BUS financial performance in Indonesia by using the analysis of the Shariah Maqashid Index (SMI) concept as control and reference for the public to choose and utilize Islamic financial products in Indonesia with an empirical study approach. The object of this study is Islamic banks in Indonesia using purposive sampling techniques with the condition that only the

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Xu, Z., K. P. Patel, and G. J. Rozanski. "Intracellular protons inhibit transient outward K+ current in ventricular myocytes from diabetic rats." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 5 (1996): H2154—H2161. http://dx.doi.org/10.1152/ajpheart.1996.271.5.h2154.

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This study examined the effects of protons on cardiac ion channel function in early stages of diabetes mellitus. Transient outward (I(to)) and inward rectifier K+ (IK1) currents were recorded by the whole cell, voltage-clamp technique in ventricular myocytes isolated from hearts of streptozotocin-induced diabetic and control rats. Proton concentration was controlled by independently varying the pH of buffered external or pipette (pHp) solutions. External acidification did not alter I(to) in diabetic rat myocytes when initiated after intracellular dialysis with standard pHp 7.2, but when these

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