TY - JOUR. T1 - Functional blockade of the voltage-gated potassium channel Kv1.3 mediates reversion of T effector to central memory lymphocytes through SMAD3/p21 cip1 signaling. AU - Hu, Lina. AU - Gocke, Anne R.. AU - Knapp, Edward. AU - Rosenzweig, Jason M.. AU - Grishkan, Inna V.. AU - Baxi, Emily Grace. AU - Zhang, Hao. AU - Margolick, Joseph Bernard. AU - Whartenby, Katharine. AU - Calabresi, Peter. PY - 2012/1/6. Y1 - 2012/1/6. N2 - The maintenance of T cell memory is critical for the development of rapid recall responses to pathogens, but may also have the undesired side effect of clonal expansion of T effector memory (T EM) cells in chronic autoimmune diseases. The mechanisms by which lineage differentiation of T cells is controlled have been investigated, but are not completely understood. Our previous work demonstrated a role of the voltage-gated potassium channel Kv1.3 in effector T cell function in autoimmune disease. In the present study, we have identified a mechanism by which ...
Looking for online definition of Tandem pore domain potassium channel in the Medical Dictionary? Tandem pore domain potassium channel explanation free. What is Tandem pore domain potassium channel? Meaning of Tandem pore domain potassium channel medical term. What does Tandem pore domain potassium channel mean?
TY - JOUR. T1 - Short-term effects of glipizide (an adenosine triphosphate-sensitive potassium channel inhibitor) on cardiopulmonary hemodynamics and global oxygen transport in healthy and endotoxemic sheep. AU - Lange, Matthias. AU - Szabo, Csaba. AU - Van Aken, Hugo. AU - Williams, William. AU - Traber, Daniel L.. AU - Daudel, Fritz. AU - Bröking, Katrin. AU - Salzman, Andrew L.. AU - Bone, Hans Georg. AU - Westphal, Martin. PY - 2006/11. Y1 - 2006/11. N2 - In severe sepsis and septic shock, hemodynamic support is often complicated by a tachyphylaxis against exogenous catecholamines. Because activation of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels plays a pivotal role in the pathogenesis of hyperdynamic vasodilatory shock, we hypothesized that it may be beneficial to administer a specific KATP channel inhibitor to prevent, or at least attenuate, hemodynamic dysfunction in sepsis. The present study was designed as a prospective and controlled laboratory experiment to ...
Inward-rectifier potassium channels (Kir, IRK) are a specific subset of potassium channels. To date, seven subfamilies have been identified in various mammalian cell types, plants, and bacteria. They are the targets of multiple toxins, and malfunction of the channels has been implicated in several diseases. IRK channels possess a pore domain, homologous to that of voltage-gated ion channels, and flanking transmembrane segments (TMSs). They may exist in the membrane as homo- or heterooligomers and each monomer possesses between 2 and 4 TMSs. In terms of function, these proteins transport potassium (K+), with a greater tendency for K+ uptake than K+ export. A channel that is "inwardly-rectifying" is one that passes current (positive charge) more easily in the inward direction (into the cell) than in the outward direction (out of the cell). It is thought that this current may play an important role in regulating neuronal activity, by helping to stabilize the resting membrane potential of the cell. ...
Andersen-Tawil Syndrome is a genetic condition that causes periods of muscle weakness (periodic paralysis), changes in heart rhythm (arrhythmia), and intellectual and developmental abnormalities. Other features can include low-set ears, widely spaced eyes, small mandible, fifth-digit clinodactyly, syndactyly, short stature, and scoliosis. Speak to a genetic counselor or a medical geneticist if you have questions about Andersen-Tawil syndrome. ...
BioAssay record AID 623912 submitted by Johns Hopkins Ion Channel Center: SAR Analysis for the identification of inhibitors of the two-pore domain potassium channel KCNK9 - Selectivity assay against KCNK3: FluxOR Assay CRC 2.
Definition of potassium-sensitive periodic paralysis in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is potassium-sensitive periodic paralysis? Meaning of potassium-sensitive periodic paralysis as a legal term. What does potassium-sensitive periodic paralysis mean in law?
Action potentials in vertebrate neurons are followed by an afterhyperpolarization (AHP) that may persist for several seconds and may have profound consequences for the firing pattern of the neuron. Each component of the AHP is kinetically distinct and is mediated by different calcium-activated potassium channels. The protein encoded by this gene is activated before membrane hyperpolarization and is thought to regulate neuronal excitability by contributing to the slow component of synaptic AHP. This gene is a member of the KCNN family of potassium channel genes. The encoded protein is an integral membrane protein that forms a voltage-independent calcium-activated channel with three other calmodulin-binding subunits. Alternate splicing of this gene results in multiple transcript variants. [provided by RefSeq, May 2013 ...
To more clearly define the role of the transepithelial electrical potential difference (V m→s), potassium permeability, and sodium-potassium pump rate in transcellular potassium transport by isolated turtle colon, we measured transmural potassium fluxes under open-circuit conditions in the presence and absence of putative blockers of potassium transport: amiloride and barium. The results were consistent with the notion that V m→s is a major determinant of cellular potassium secretion, whereas active potassium absorption is insensitive to changes in V m→s. These observations suggest that coupling between colonic sodium absorption and potassium secretion in vivo could be due primarily to the effect of the lumen negative V m→s on transcellular secretory potassium flow. Amiloride-induced inhibition of potassium secretion appeared to be due to the reductions in V m→s and sodium-potassium pump rate that accompanied the inhibition of active sodium absorption.
Hyperpolarization-activated cyclic nucleotide-gated channels (HCN) are responsible for the functional hyperpolarization-activated current (I(h)) in dorsal root ganglion (DRG) neurons. We studied HCN1-4 channel mRNA and protein expression and correlated these findings with I(h) functional properties in rat DRG neurons of different size. Quantitative RT-PCR (TaqMan) analysis demonstrated that HCN2 and HCN1 mRNAs were more abundantly expressed in large diameter (55-80 microm) neurons, while HCN3 mRNA was preferentially expressed in small diameter (20-30 microm) neurons. HCN4 mRNA expression was very low in neurons of all sizes. At the protein level, subunit-selective polyclonal antibodies and immunofluorescence indicated that HCN1 and HCN3 are present in large diameter neurons and small diameter neurons. Staining in small diameter neurons was in IB4-positive (non-peptidergic) and IB4-negative (peptidergic) cells. HCN2 immunofluorescent staining was heterogeneous and predominantly in large diameter ...
Potassium Channels Inhibitors on signaling pathway are available at Adooq Bioscience. Check Potassium Channels pathway , inhibitors reviews and assay information.
TY - JOUR. T1 - ATP sensitive potassium channel openers. T2 - A new class of ocular hypotensive agents. AU - Roy Chowdhury, Uttio. AU - Dosa, Peter I.. AU - Fautsch, Michael P. PY - 2016/3/2. Y1 - 2016/3/2. N2 - ATP sensitive potassium (KATP) channels connect the metabolic and energetic state of cells due to their sensitivity to ATP and ADP concentrations. KATP channels have been identified in multiple tissues and organs of the body including heart, pancreas, vascular smooth muscles and skeletal muscles. These channels are obligatory hetero-octamers and contain four sulfonylurea (SUR) and four potassium inward rectifier (Kir) subunits. Based on the particular type of SUR and Kir present, there are several tissue specific subtypes of KATP channels, each with their own unique set of functions. Recently, KATP channels have been reported in human and mouse ocular tissues. In ex vivo and in vivo model systems, KATP channel openers showed significant ocular hypotensive properties with no appearance of ...
Martial arts expert, Mitch Gooch, teaches people how to do Kung Fu and martial arts all from his wheelchair. The 36-year-old British man suffers from a rare illness that causes his whole body to feel like "blocks of ice" and has left him disabled.. "I can only describe it as being frozen. You know you can move but you are just unable to. It literally feels like parts of your body are blocks of ice," Gooch told the Daily Mail.. When Gooch was 24, he woke up one morning fully paralyzed and could not move for a week. The hospital staff previously diagnosed his condition as growing pains before it was revealed he suffered from a rare hereditary illness- Andersen-Tawil syndrome- a type of long QT syndrome.. Andersen-Tawil syndrome is a rare condition and a rare form of periodic paralysis that affects approximately 100 people worldwide. According to the Mayo Clinic, this syndrome can cause episodes of muscle weakness, changes in heart rhythm, and developmental abnormalities. Patients commonly develop ...
We describe a patient presenting with a combination of muscle fasciculations, paresthesias, hyperhidrosis, as well as insomnia, agitation and confusion. He went on to develop psychosis and respiratory failure requiring intensive care. Electromyography confirmed the presence of neuromyotonia and CSF showed mild pleocytosis. Routine testing for voltage-gated potassium channel complex (VGKC-complex) antibodies was highly positive, confirming the clinical diagnosis of Morvans syndrome. The patient improved after treatment with intravenous immunoglobulin and methylprednisolone. Further investigation of the antigenic targets using immunohistochemistry and cell-based assays revealed that he had autoantibodies targeting Lgi1, Caspr2 and Contactin-2/Tag-1, all proteins known to be complexed with VGKC in peripheral nerves and CNS. This is the first case of Morvans syndrome from Cyprus and illustrates the clinical features as well as the emerging complexity of antigenic targets involved in the pathogenesis.
The passive K influx in low K(LK) red blood cells of sheep saturates with increasing external K concentration, indicating that this mode of transport is mediated by membrane-associated sites. The passive K influx, iMLK, is inhibited by external Na. Isoimmune anti-L serum, known to stimulate active K transport in LK sheep red cells, inhibits iMLK about twofold. iMLK is affected by changes in intracellular K concentration, [K]i, in a complex fashion: increasing [K]i from near zero stimulates iMLK, while further increases in [K]i, above 3 mmol/liter cells, inhibit iMLK. The passive K influx is not mediated by K-K exchange diffusion. The effects of anti-L antibody and [K]i on passive cation transport are specific for K: neither factor affects passive Na transport. The common characteristics of passive and active K influx suggest that iMLK is mediated by inactive Na-K pump sites, and that the inability to translocate Na characterizes the inactive pumps. Anti-L antibody stimulates the K pump in ...
Potassium deficiency symptoms appear as interveinal chlorosis on older leaves, that eventually progress to a red and/or gold coloration of the leaves. In cotton prior to bloom these symptoms will be visible on the lower leaves first because the plant is able to translocate Potassium from the older leaves to the newer leaves of the plant. After peak bloom similar deficiency symptoms can appear as well but will appear on the upper third of the plant.. In addition to the traditional leaf discolorations caused by Potassium deficiency, after peak bloom leaves may also begin to curl downward and the leaves to become thicker. If the Potassium deficiency is severe enough the plants may start to defoliate early, which can cause the deficiency to be confused with the vascular wilt disease called Verticillium wilt.. To distinguish between Potassium deficiency and Verticillium wilt, slice the stem and look for vascular discoloration. If the vascular tissue is bright white with no discoloration, then it is ...
BACKGROUND: GQ1b antibody (GQ1b-Ab) is detected in approximately two-thirds of sera of patients with Bickerstaffs encephalitis (BE). Whilst some of the remaining patients have antibodies to other gangliosides, many patients with BE are reported to be seronegative. METHODS AND RESULTS: Voltage-gated potassium channel antibody (VGKC-Ab) at high titer was detected during the diagnostic work-up of one patient with BE. Sera of an additional patient with BE and nine patients with Miller Fisher syndrome (MF) (all GQ1b-Ab positive) were investigated for VGKC-Ab and other anti-neuronal antibodies by radioimmunoprecipitation using 125I-dendrotoxin-VGKC and immunohistochemistry, respectively. Two patients with MF exhibited moderate titer VGKC-Abs. Regardless of positivity for VGKC or GQ1b antibodies, serum IgG of all patients with BE and MF reacted with the molecular layer and Purkinje cells of the cerebellum in a distinctive pattern. CONCLUSION: Voltage-gated potassium channel antibodies might be involved in some
Potassium channels, found throughout the animal and plant kingdoms, play important roles in maintaining membrane potentials and regulating action potential firing, shape, and duration, among other functions. Using the Xenopus laevis (frog) oocyte as model system, we induced high expression of sodium and potassium voltage-gated channels and recorded action potentials by a modification of the two-electrode voltage-clamp recording technique. The voltage-dependent sodium conductance was due to expression of the skeletal muscle NaV channel (NaV1.4) and the delayed rectifier voltage-dependent potassium conductance was due to expression of a Shaker (Kv1) potassium channel. Upon this background, we mixed different potassium-selective ion channels, such as inwardly rectifying potassium (KIR) channels, tandem pore domain (K2P) potassium channels and voltage-gated (KV) channels. We analyzed how these potassium channels affected firing thresholds, reliability of action potential generation, action potential
Forms a voltage-independent potassium channel activated by intracellular calcium. Activation is followed by membrane hyperpolarization. Thought to regulate neuronal excitability by contributing to the slow component of synaptic afterhyperpolarization. The channel is blocked by apamin (By similarity).
An alkaline hydrolysate of Bacillus thuringiensis var kurstaki HD1 (Btk) parasporal crystals was administered at 25 micrograms ml-1 (f.c.) to isolated, short-circuited, midguts of tobacco hornworm (Manduca sexta) larvae. The short-circuit current (s.c.c.), a precise measure of K+ active transport, was inhibited by 78% in 10 min in Btk-treated midguts as compared to controls. The elemental concentrations of K, together with Na, Mg, P, S, Cl and Ca, as well as the water content, were determined by electron probe X-ray microanalysis (EPXMA) in the muscle cells, columnar cells and goblet cells, as well as in the extracellular goblet cavity and the bathing media. The average K concentration in the goblet cell cavity was 129 mmol/kg wet wt in control midguts but only 37 mmol/kg wet wt in Btk-treated midguts. The elemental concentrations, including that of K, in other cell compartments were much less affected by Btk, but a rise in total cell calcium is suggested. It has been previously suggested that ...
The inhibition of voltage-gated potassium channels (Kv) plays a significant role in the cerebral hypoxia-induced cell death. of cerebral hypoxia. In conclusion AA/15-LOX/15-HETE induces vasoconstriction by down-regulating Kv channels and Kv2.1/1.5 channels are the targets. Our study also suggests a therapeutic strategy to improve ischemic vascular occlusion by lowering 15-HETE level and preventing Kv channel down-regulation which makes 15-LOX as a new target for the treatment of cerebral hypoxia. Keywords: 15-lipoxygenase (15-LOX) 15 acid (15-HETE) hypoxia Kv1.5 Kv2.1 Introduction Cerebral vascular disease is MP470 one of diseases with high morbidity and mortality 75 of which is caused by ischemic cerebrovascular. Hypoxia-induced vascular constriction was an important pathogenesis which could lead to cell death in cerebral ischemia [1 2 However the underlying mechanism is still unknown and the treatment could not accomplish the desired effect. In recent years hypoxia inhibits voltage-gated ...
OBJECTIVE: To assess the influence of blocking smooth muscle large conductance Ca(2+) -activated K+ channels and voltage-gated K+ channels on the conducted dilation to ACh and isoproterenol. MATERIALS AND METHODS: Rat mesenteric arteries were isolated with a bifurcation, triple-cannulated, pressurized and imaged using confocal microscopy. Phenylephrine was added to the superfusate to generate tone, and agonists perfused into a sidebranch to evoke local dilation and subsequent conducted dilation into the feed artery. RESULTS: Both ACh- and isoproterenol-stimulated local and conducted dilation with similar magnitudes of decay with distance along the feed artery (2000μm: ∼15% maximum dilation). The gap junction uncoupler carbenoxolone prevented both conducted dilation and intercellular spread of dye through gap junctions. IbTx, TEA or 4-AP, blockers of large conductance Ca(2+) -activated K+ channels and voltage-gated K+ channels, did not affect conducted dilation to either agonist. A combination
Hyperinsulinism can occur throughout childhood but is most common in infancy. Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) is the most important cause of hypoglycemia in early infancy. The excessive secretion of insulin is responsible for profound hypoglycemia and requires aggressive treatment to prevent severe and irreversible brain damage. Onset can be in the neonatal period or later, with the severity of hypoglycemia decreasing with age. PHHI is a heterogeneous disorder with two histopathological lesions, diffuse (DiPHHI) and focal (FoPHHI), which are clinically indistinguishable. FoPHHI is sporadic and characterized by somatic islet-cell hyperplasia. DiPHHI corresponds to a functional abnormality of insulin secretion in the whole pancreas and is most often recessive although rare dominant forms can occur, usually outside the newborn period. Differentiation between focal and diffuse lesions is important because the therapeutic approach and genetic counselling differ radically. ...
R Lim, MJ Walshaw, S Saltissi, CRK Hind; Serum Potassium Concentrations during Acute Exacerbations of Chronic Airflow Limitation and following Recovery: Effect of Beta Agonists Delivered by Home Nebulisers. Clin Sci (Lond) 1 January 1988; 75 (s19): 24P. doi: https://doi.org/10.1042/cs075024Pa. Download citation file:. ...
Multiwalled carbon nanotube (MWNT)/BaTiO3 functional nanocomposites were fabricated via the spark plasma sintering technique. The resistivity of MWNT/BaTiO3 nanocomposites was found higher than that of MWNT-free BaTiO3 ceramics. In addition, the temperature dependence of resistivity showed abnormal metallic conductance behavior in the 1 wt. % MWNT/BaTiO3 nanocomposite. It was proposed to be due to the additional subgrain boundary between MWNT and BaTiO3 matrix, which led to transformation from an impurity-scattering mechanism to a dominant lattice-scattering mechanism in the MWNT/BaTiO3 nanocomposites as the content of carbon nanotubes increased. Based on observed unique electrical properties, bilayer ceramics stacked by one layer of MWNT-free BaTiO3 and another layer of MWNT/BaTiO3 nanocomposite were fabricated and showed excellent rectification property ...
Congenital Hyperinsulinism International (CHI) held the Fifth Congenital Hyperinsulinism Family Conference at the NH Milano 2 Hotel in Segrate, Italy just outside of Milan on September 17 and 18, 2013. It was an intensive two days of presentations on many aspects of congenital hyperinsulinism, from the experience of living with the condition, to the latest research on potential new treatment options. The meeting was remarkable for showcasing a good number of new research projects, treatment options being pursued, and patient advocates working to support congenital hyperinsulinism families. The take away from this meeting is that so much is happening worldwide to improve the lives of children born with the condition. You can read a full summary of the meeting in English here or in French here.. Click here to access PDFs from the 22 presentations that were made at this conference.. ...
Data Synthesis:. The congenital long QT syndrome is characterized by abnormally prolonged ventricular repolarization, which predisposes patients to syncope, ventricular arrhythmias, and sudden cardiac death. The recent discovery of mutations in genes encoding ion channels has improved our understanding of the cellular origin of this condition. The congenital long QT syndrome may result from inherited defects in cardiac K+ and Na+ channels, which both result in prolongation of the ventricular action potential. The diagnosis is based on electrocardiographic and clinical criteria. Genetic screening of symptomatic patients or asymptomatic family members may identify patients at risk for life-threatening ventricular arrhythmias. β-Blocking agents are the mainstay of treatment. Certain patients may also benefit from a pacemaker or implantable cardioverter defibrillator. Recent studies suggest that genotype-specific treatment of the congenital long QT syndrome will be feasible in the near future. ...
No. Although having low levels of blood potassium during attacks is typical of hypokalemic periodic paralysis, between attacks, people with hypokalemic periodic paralysis can have a normal blood potassium level (frequently in the low normal range). Attacks of paralysis are typically triggered by the level of potassium dropping in the blood. Such potassium fluctuations occur in everyone, but in people with familial hypokalemic periodic paralysis, these drops in potassium can produce episodes of paralysis. For example, a large carbohydrate meal results in secretion of insulin into the blood, which results in a drop of the blood potassium level as potassium and glucose enter cells. In normal people, such a drop in blood potassium produces no symptoms. In people with familial hypokalemic periodic paralysis, however, the drop in blood potassium often triggers an episode of paralysis. Potassium levels in the blood can remain low as muscle is recovering from a recent attack. During an attack, muscles ...
Localization of voltage-gated potassium channels to specific subcellular compartments in neurons allows them to perform specific functions that modulate the overall electrophysiological properties of neurons. For instance, members of the Shaker family are localized to the axon of cortical pyramidal neurons where they contribute to the propagation of action potentials. Conversely, members of the Shal family of K+ channels are localized to the somatodendritic compartment of cortical pyramidal neurons where they inhibit initiation and propagation of action potentials. My research focuses on molecular mechanisms involved in targeting of these specific voltage-gated potassium channels to different subcellular compartments in neurons. By expressing chimeras between Kv1.4 and Kv4.2, two channels that are targeted to different neuronal compartments, the axon and the dendrites, respectively, as well as deletion mutants of Kv4.2 in cultured slices of rat cortical tissue we were able to identify a sixteen ...
Hypokalemic Periodic Paralysis. by: Joe Hing Kwok Chu. Other names: familial periodic paralysis, periodic paralysis. @. Hypokalemic periodic paralysis is a congenital disorder that occurs within certain families and causes intermittent episodes of muscle weakness or paralysis. The attacks can occur from daily to yearly and may last for a few hours or for several days. There is a low level of potassium in the bloodstream (hypokalemia) during the attack. But the serum potassium levels are normal between attacks.. There is no potassium deficiency in the whole body. Hypokalemia is low blood levels of potassium (low serum potassium). The following can cause hypokalemia. Alcoholism. Hypokalemic attack may be precipitated by the administration of oral glucose, 1.5g/kg body weight (up to 100 g). Intravenous administration of insulin, maximum 0.1 U/kg body weight at 30 and 60 minutes, during the infusion may aid in precipitating attacks. Diet high in sugar (carbohydrates). Diuretic therapy without ...
TY - JOUR. T1 - Destabilization of ATP-sensitive potassium channel activity by novel KCNJ11 mutations identified in congenital hyperinsulinism. AU - Lin, Yu Wen. AU - Bushman, Jeremy D.. AU - Yan, Fei Fei. AU - Haidar, Sara. AU - MacMullen, Courtney. AU - Ganguly, Arupa. AU - Stanley, Charles A.. AU - Shyng, Show-Ling. PY - 2008/4/4. Y1 - 2008/4/4. N2 - The inwardly rectifying potassium channel Kir6.2 is the pore-forming subunit of the ATP-sensitive potassium (KATP) channel, which controls insulin secretion by coupling glucose metabolism to membrane potential in β-cells. Loss of channel function because of mutations in Kir6.2 or its associated regulatory subunit, sulfonylurea receptor 1, causes congenital hyperinsulinism (CHI), a neonatal disease characterized by persistent insulin secretion despite severe hypoglycemia. Here, we report a novel KATP channel gating defect caused by CHI-associated Kir6.2 mutations at arginine 301 (to cysteine, glycine, histidine, or proline). These mutations in ...
The human ether-à-go-go channel (hEag1 or KV10.1) is a cancer-relevant voltage-gated potassium channel that is overexpressed in a majority of human tumors. Peptides that are able to selectively inhibit this channel can be lead compounds in the search for new anticancer drugs. Here, we report the activity-guided purification and electrophysiological characterization of a novel KV10.1 inhibitor from the sea anemone Anthopleura elegantissima. Purified sea anemone fractions were screened for inhibitory activity on KV10.1 by measuring whole-cell currents as expressed in Xenopus laevis oocytes using the two-microelectrode voltage clamp technique. Fractions that showed activity on Kv10.1 were further purified by RP-HPLC. The amino acid sequence of the peptide was determined by a combination of MALDI- LIFT-TOF/TOF MS/MS and CID-ESI-FT-ICR MS/MS and showed a high similarity with APETx1 and APETx3 and was therefore named APETx4. Subsequently, the peptide was electrophysiologically characterized on KV10.1. The
TY - JOUR. T1 - Episodic ataxia results from voltage-dependent potassium channels with altered functions. AU - Adelman, John P.. AU - Bond, Chris T.. AU - Pessia, Mauro. AU - Mayliet, James. PY - 1995/12. Y1 - 1995/12. N2 - Episodic ataxia (EA) is an autosomal dominant human disorder that produces persistent myokymia and attacks of generalized ataxia. Recently, familial EA has been linked to the voltage-dependent delayed rectifier, Kv1.1, on chromosome 12. Six EA families have been identified that carry distinct Kv1.1 missense mutations; all individuals are heterozygous. Expression in Xenopus oocytes demonstrates that two of the EA subunits form homomeric channels with altered gating properties. V408A channels have voltage dependence similar to that of wild-type channels, but with faster kinetics and increased C-type inactivation, while the voltage dependence of F1 84C channels is shifted 20 mV positive. The other four EA subunits do not produce functional homomeric channels but reduce the ...
This potassium channel is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by external barium (By similarity).
This potassium channel is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by external barium.
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The human ether-á-go-go (eag)-related gene (hERG) voltage-gated potassium channel is the primary pore-forming subunit of the rapidly activating delayed-rectifier potassium current (IKr) in the heart (Warmke and Ganetzky, 1994; Sanguinetti et al., 1995; Trudeau et al., 1995). The physiological role of cardiac IKr is to repolarize myocytes during the terminal phase of cardiac action potentials (Sanguinetti and Jurkiewicz, 1990, 1991). Loss of function in hERG, either caused by inheritable mutations or pharmacological block, causes long QT syndrome, which can develop into ventricular arrhythmias and sudden cardiac death (Curran et al., 1995; Sanguinetti et al., 1995).. hERG is a member of the KCNH family of voltage-activated potassium (K+) channels, which are closely related to CNG and hyperpolarization-activated, cyclic nucleotide-modulated (HCN) channels (Guy et al., 1991; Warmke and Ganetzky, 1994). Like other voltage-gated potassium channels, KCNH channels are tetrameric, and each subunit has ...
The properties of single Ca2+-activated K+ (BK) channels in neonatal rat intracardiac neurons were investigated using the patch-clamp recording technique. In symmetrical 140 mM K+. the single-channel slope conductance was linear in the voltage range -60/+60 mV, and was 207±19 pS. Na+ ions were not measurably permeant through the open channel. Channel activity increased with the cytoplasmic free Ca2+ concentration ([Ca2+]i) with a Hill plot giving a half-saturating [Ca2+] (K0.5) of 1.35 μM and slope of ≅3. The BK channel was inhibited reversibly by external tetraethylammonium (TEA) ions, charybdotoxin, and quinine and was resistant to block by 4-aminopyridine and apamin. Ionomycin (1-10 μM) increased BK channel activity in the cell-attached recording configuration. The resting activity was consistent with a [Ca2+]i |100 nM and the increased channel activity evoked by ionomycin was consistent with a rise in|[Ca2+]i to ≥ 0.3 μM. TEA (0.2-1 mM) increased the action potential duration 1.5-fold and
TY - JOUR. T1 - Up-regulation of A-type potassium currents protects neurons against cerebral ischemia. AU - Deng, Ping. AU - Pang, Zhi Ping. AU - Lei, Zhigang. AU - Shikano, Sojin. AU - Xiong, Qiaojie. AU - Harvey, Brandon K.. AU - London, Barry. AU - Wang, Yun. AU - Li, Min. AU - Xu, Zao C.. PY - 2011/9/1. Y1 - 2011/9/1. N2 - Excitotoxicity is the major cause of many neurologic disorders including stroke. Potassium currents modulate neuronal excitability and therefore influence the pathological process. A-type potassium current (IA) is one of the major voltage-dependent potassium currents, yet its roles in excitotoxic cell death are not well understood. We report that, following ischemic insults, the IA increases significantly in large aspiny (LA) neurons but not medium spiny (MS) neurons in the striatum, which correlates with the higher resistance of LA neurons to ischemia. Activation of protein kinase Cα increases IA in LA neurons after ischemia. Cultured neurons from transgenic mice lacking ...
Hyperkalemic periodic paralysis (HyperKPP) produces myotonia and attacks of muscle weakness triggered by rest after exercise or by K+ ingestion. We introduced a missense substitution corresponding to a human familial HyperKPP mutation (Met1592Val) into the mouse gene encoding the skeletal muscle voltage-gated Na+ channel NaV1.4. Mice heterozygous for this mutation exhibited prominent myotonia at rest and muscle fiber-type switching to a more oxidative phenotype compared with controls. Isolated mutant extensor digitorum longus muscles were abnormally sensitive to the Na+/K+ pump inhibitor ouabain and exhibited age-dependent changes, including delayed relaxation and altered generation of tetanic force. Moreover, rapid and sustained weakness of isolated mutant muscles was induced when the extracellular K+ concentration was increased from 4 mM to 10 mM, a level observed in the muscle interstitium of humans during exercise. Mutant muscle recovered from stimulation-induced fatigue more slowly than did ...
The present invention describes novel nitrosated and/or nitrosylated potassium channel activators, and novel compositions comprising at least one nitrosated and/or nitrosylated potassium channel activator, and, optionally, at least one compound that donates, transfers or releases nitric oxide, elevates endogenous levels of endothelium-derived relaxing factor, stimulates endogenous synthesis of nitric oxide or is a substrate for nitric oxide synthase and/or at least one vasoactive agent. The present invention also provides novel compositions comprising at least one potassium channel activator, and at least one compound that donates, transfers or releases nitric oxide, elevates endogenous levels of endothelium-derived relaxing factor, stimulates endogenous synthesis of nitric oxide or is a substrate for nitric oxide synthase and/or at least one vasoactive agent. The present invention also provides methods for treating or preventing sexual dysfunctions in males and females, for enhancing sexual responses
Looking for online definition of potassium voltage-gated channel subfamily H member 5 in the Medical Dictionary? potassium voltage-gated channel subfamily H member 5 explanation free. What is potassium voltage-gated channel subfamily H member 5? Meaning of potassium voltage-gated channel subfamily H member 5 medical term. What does potassium voltage-gated channel subfamily H member 5 mean?
In response to intracellular energy supply, ATP-sensitive potassium (KATP) channels alter membrane potential and mediate cell stress response. The Abcc9 gene encodes the major regulatory subunit in the heart, sulfonylurea receptor 2 (SUR2), as well as smaller mitochondria-enriched proteins that contribute to sulfonylurea-insensitive KATP channels. Pharmacological studies suggest mitochondrial KATP channels are critical regulators of cell stress, however the molecular composition of this channel has been unclear. We now studied the role of KATP channels by deleting exon 5 of Abcc9. This strategy ablated expression of both full length SUR2 protein as well as the smaller mitochondrial 55 KDa protein. Homozygous exon 5 (Ex5) mice died within 14 days of birth with progressive cardiac contractile dysfunction. Diazoxide was found to depolarize mitochondria from wildtype cardiomyocytes but not Ex5 mitochondria, consistent with disrupted mitochondrial KATP channels. Ex5 mitochondria had a reduced cross ...
Antibodies for proteins involved in positive regulation of voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization pathways, according to their Panther/Gene Ontology Classification
3 Studies found for: long QT syndrome OR Jervell and Lange-Nielsen syndrome OR Romano-Ward syndrome OR Andersen-Tawil , Recruiting, Not yet recruiting, Available Studies , NIH, U.S. Fed ...
Long QT syndrome (LQTS) is an inherited cardiac arrhythmia characterized by a prolonged heart rate-corrected QT (QTc) interval, which is associated with syncope and sudden death caused by torsades de pointes or polymorphic ventricular tachycardia. LQTS can be an autosomal recessive disorder (1), but the most common form is an autosomal dominant disorder called Romano-Ward syndrome (2,3). LQTS affects between 1 in 5,000 and 1 in 2,000 individuals (4,5). Molecular diagnosis is an important tool to guide diagnosis, treatment, and prevention strategies in LQTS patients. To date, more than 600 mutations (6) have been identified among 12 different genes: 5 genes encoding ion channel alpha subunits (KCNQ1 [7], KCNH2 [8], SCN5A [9], KCNJ2 [10], and CACNA1C [11]) and 7 genes encoding ion channel regulatory proteins (ANKB [12], KCNE1 [13], KCNE2 [14], CAV3 [15], SCN4B [16], AKAP9 [17], and SNTA1 [18]). In total, molecular diagnosis can resolve up to 70% of cases. More than 90% of those cases are due to ...
Elezgarai I, Diez J, Puente N, Azkue JJ, Benitez R, Bilbao A, Knopfel T, Donate-Oliver F & Grandes P (2003). Subcellular localization of the voltage-dependent potassium channel Kv3. 1b in postnatal and adult rat medial nucleus of the trapezoid body. Neuroscience 118, 889-898 ...
A surprising result of these studies is the augmentation of IL-4 production by Kv channel blockers in anergized CD4+ lymphocytes. This finding suggests that a more complex repertoire of functions may exist for Kv channels during other immunological responses of T cells. In anergized cells, IL-4 augmentation by Kv channel inhibitors may reflect the fact that low amplitude calcium signals bias the cytokine profile toward the transcription/production of IL-4 (and not IL-2) via the differential activation of NFATc and NFATp (44). Thus, diminished calcium signaling in partially primed (anergic) T cells may be analogous to diminished (APL-like) calcium signaling, which has been shown to induce IL-4 production upon restimulation of incompletely primed cells.. Another unexpected finding was that Kv channels do not regulate secondary physiological and immunological responses of effector cells. Thus, although Kv1.3 expression is increased, Kv channels neither contribute significantly to the membrane ...
by Barbara Stranger, Hu X, Kim H, Raj T, Brennan PJ, Trynka G, Teslovich N, Slowikowski K, Chen WM, Onengut S, Baecher-Allan C, De Jager PL, Rich SS, Stranger BE, Brenner MB, Raychaudhuri S. Genome-wide association studies (GWAS) and subsequent dense-genotyping of associated loci identified over a hundred single-nucleotide polymorphism (SNP) variants associated with the risk of rheumatoid arthritis (RA), type 1 diabetes (T1D), and celiac disease (CeD). Immunological and genetic studies suggest a role for CD4-positive effector memory T (CD+ TEM) cells in the pathogenesis of these diseases. To elucidate mechanisms of autoimmune disease alleles, we investigated molecular phenotypes in CD4+ effector memory T cells potentially affected by these variants. In a cohort of genotyped healthy individuals, we isolated high purity CD4+ TEM cells from peripheral blood, then assayed relative abundance, proliferation upon T cell receptor (TCR) stimulation, and the transcription of 215 genes within disease loci ...
integral component of plasma membrane, potassium ion leak channel activity, voltage-gated potassium channel activity, cellular potassium ion transport, stabilization of membrane potential