Bibliografías temáticas / L-typa calcium channels

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Literatura académica sobre el tema "L-typa calcium channels"

Autor: Grafiati
Publicado: 11 de marzo de 2023

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Artículos de revistas sobre el tema "L-typa calcium channels"

1

Collier, M. L., G. Ji, Y. X. Wang y M. I. Kotlikoff. "Calcium-Induced Calcium Release in Smooth Muscle". Journal of General Physiology 115, n.º 5 (1 de mayo de 2000): 653–62. http://dx.doi.org/10.1085/jgp.115.5.653.

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Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca2+ channels. In heart cells, a tight coupling between the gating of single L-type Ca2+ channels and ryanodine receptors (RYRs) underlies calcium release. Here we demonstrate that L-type Ca2+ channels activate RYRs to produce CICR in smooth muscle cells in the form of Ca2+ sparks and propagated Ca2+ waves. However, unlike CICR in cardiac muscle, RYR channel opening is not tightly linked to the gating of L-type Ca2+ channels. L-type Ca2+ channels can open without triggering Ca2+ sparks and triggered Ca2+ sparks are often observed after channel closure. CICR is a function of the net flux of Ca2+ ions into the cytosol, rather than the single channel amplitude of L-type Ca2+ channels. Moreover, unlike CICR in striated muscle, calcium release is completely eliminated by cytosolic calcium buffering. Thus, L-type Ca2+ channels are loosely coupled to RYR through an increase in global [Ca2+] due to an increase in the effective distance between L-type Ca2+ channels and RYR, resulting in an uncoupling of the obligate relationship that exists in striated muscle between the action potential and calcium release.
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2

BIEDA, MARK C. y DAVID R. COPENHAGEN. "N-type and L-type calcium channels mediate glycinergic synaptic inputs to retinal ganglion cells of tiger salamanders". Visual Neuroscience 21, n.º 4 (julio de 2004): 545–50. http://dx.doi.org/10.1017/s0952523804214055.

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Synaptically localized calcium channels shape the timecourse of synaptic release, are a prominent site for neuromodulation, and have been implicated in genetic disease. In retina, it is well established that L-type calcium channels play a major role in mediating release of glutamate from the photoreceptors and bipolar cells. However, little is known about which calcium channels are coupled to synaptic exocytosis of glycine, which is primarily released by amacrine cells. A recent report indicates that glycine release from spiking AII amacrine cells relies exclusively upon L-type calcium channels. To identify calcium channel types controlling neurotransmitter release from the population of glycinergic neurons that drive retinal ganglion cells, we recorded electrical and potassium evoked inhibitory synaptic currents (IPSCs) from these postsynaptic neurons in retinal slices from tiger salamanders. The L-channel antagonist nifedipine strongly inhibited release and FPL64176, an L-channel agonist, greatly enhanced it, indicating a significant role for L-channels. ω-Conotoxin MVIIC, an N/P/Q-channel antagonist, strongly inhibited release, indicating an important role for non-L channels. While the P/Q-channel blocker ω-Aga IVA produced only small effects, the N-channel blocker ω-conotoxin GVIA strongly inhibited release. Hence, N-type and L-type calcium channels appear to play major roles, overall, in mediating synaptic release of glycine onto retinal ganglion cells.
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3

Mangel, A. W., L. Scott y R. A. Liddle. "Depolarization-stimulated cholecystokinin secretion is mediated by L-type calcium channels in STC-1 cells". American Journal of Physiology-Gastrointestinal and Liver Physiology 270, n.º 2 (1 de febrero de 1996): G287—G290. http://dx.doi.org/10.1152/ajpgi.1996.270.2.g287.

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To examine the role of calcium channels in depolarization-activated cholecystokinin (CCK) release, studies were performed in an intestinal CCK-secreting cell line, STC-1. Blockade of potassium channels with barium chloride (5 mM) increased the release of CCK by 374.6 +/- 46.6% of control levels. Barium-induced secretion was inhibited by the L-type calcium-channel blocker, nicardipine. Nicardipine (10(-9)-10(-5) M) produced a dose-dependent inhibition in barium-stimulated secretion with a half-maximal inhibition (IC50) value of 0.1 microM. A second L-type calcium-channel blocker, diltiazem (10(-9)-10(-4) M), also inhibited barium-induced CCK secretion with an IC50 value of 5.1 microM. By contrast, the T-type calcium-channel blocker, nickel chloride (10(-7)-10(-8) M), failed to significantly inhibit barium-induced CCK secretion. To further evaluate a role for L-type calcium channels in the secretion of CCK, the effects of the L-type calcium channel opener, BAY K 8644, were examined. BAY K 8644 (10(-8)-10(-4) M) produced a dose-dependent stimulation in CCK release with a mean effective concentration value of 0.2 microM. Recordings of single-channel currents from inside-out membrane patches showed activation of calcium channels by BAY K 8644 (1 microM), with a primary channel conductance of 26.0 +/- 1.2 pS. It is concluded that inhibition of potassium channel activity depolarizes the plasma membrane, thereby activating L-type, but not T-type, calcium channels. The corresponding influx of calcium serves to trigger secretion of CCK.
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4

Isaev, Dmytro, Karisa Solt, Oksana Gurtovaya, John P. Reeves y Roman Shirokov. "Modulation of the Voltage Sensor of L-type Ca2+ Channels by Intracellular Ca2+". Journal of General Physiology 123, n.º 5 (26 de abril de 2004): 555–71. http://dx.doi.org/10.1085/jgp.200308876.

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Both intracellular calcium and transmembrane voltage cause inactivation, or spontaneous closure, of L-type (CaV1.2) calcium channels. Here we show that long-lasting elevations of intracellular calcium to the concentrations that are expected to be near an open channel (≥100 μM) completely and reversibly blocked calcium current through L-type channels. Although charge movements associated with the opening (ON) motion of the channel's voltage sensor were not altered by high calcium, the closing (OFF) transition was impeded. In two-pulse experiments, the blockade of calcium current and the reduction of gating charge movements available for the second pulse developed in parallel during calcium load. The effect depended steeply on voltage and occurred only after a third of the total gating charge had moved. Based on that, we conclude that the calcium binding site is located either in the channel's central cavity behind the voltage-dependent gate, or it is formed de novo during depolarization through voltage-dependent rearrangements just preceding the opening of the gate. The reduction of the OFF charge was due to the negative shift in the voltage dependence of charge movement, as previously observed for voltage-dependent inactivation. Elevation of intracellular calcium concentration from ∼0.1 to 100–300 μM sped up the conversion of the gating charge into the negatively distributed mode 10–100-fold. Since the “IQ-AA” mutant with disabled calcium/calmodulin regulation of inactivation was affected by intracellular calcium similarly to the wild-type, calcium/calmodulin binding to the “IQ” motif apparently is not involved in the observed changes of voltage-dependent gating. Although calcium influx through the wild-type open channels does not cause a detectable negative shift in the voltage dependence of their charge movement, the shift was readily observable in the Δ1733 carboxyl terminus deletion mutant, which produces fewer nonconducting channels. We propose that the opening movement of the voltage sensor exposes a novel calcium binding site that mediates inactivation.
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5

Yang, Tingting, Min He, Hailiang Zhang, Paula Q. Barrett y Changlong Hu. "L- and T-type calcium channels control aldosterone production from human adrenals". Journal of Endocrinology 244, n.º 1 (enero de 2020): 237–47. http://dx.doi.org/10.1530/joe-19-0259.

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Aldosterone, which plays a key role in the regulation of blood pressure, is produced by zona glomerulosa (ZG) cells of the adrenal cortex. Exaggerated overproduction of aldosterone from ZG cells causes primary hyperaldosteronism. In ZG cells, calcium entry through voltage-gated calcium channels plays a central role in the regulation of aldosterone secretion. Previous studies in animal adrenals and human adrenal adrenocortical cell lines suggest that the T-type but not the L-type calcium channel activity drives aldosterone production. However, recent clinical studies show that somatic mutations in L-type calcium channels are the second most prevalent cause of aldosterone-producing adenoma. Our objective was to define the roles of T and L-type calcium channels in regulating aldosterone secretion from human adrenals. We find that human adrenal ZG cells mainly express T-type CaV3.2/3.3 and L-type CaV1.2/1.3 calcium channels. TTA-P2, a specific inhibitor of T-type calcium channel subtypes, reduced basal aldosterone secretion from acutely prepared slices of human adrenals. Surprisingly, nifedipine, the prototypic inhibitor of L-type calcium channels, also decreased basal aldosterone secretion, suggesting that L-type calcium channels are active under basal conditions. In addition, TTA-P2 or nifedipine also inhibited aldosterone secretion stimulated by angiotensin II- or elevations in extracellular K+. Remarkably, blockade of either L- or T-type calcium channels inhibits basal and stimulated aldosterone production to a similar extent. Low concentrations of TTA-P2 and nifedipine showed additive inhibitory effect on aldosterone secretion. We conclude that T- and L-type calcium channels play equally important roles in controlling aldosterone production from human adrenals.
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Liu, Xiaoyu, Tingting Yang, Langxi Miao, Yan-Ai Mei y Changlong Hu. "Leukotriene B4 Inhibits L-Type Calcium Channels via p38 Signaling Pathway in Vascular Smooth Muscle Cells". Cellular Physiology and Biochemistry 37, n.º 5 (2015): 1903–13. http://dx.doi.org/10.1159/000438551.

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Background/Aims: Arachidonic acid (AA) and its metabolites are important endogenous lipid messengers. In this study, we test the effect of Leukotriene B4 (LTB4), a 5-lipoxygenase metabolite of AA, on L-type calcium channels in A7r5 rat aortic vascular smooth muscle cells. Methods: L-type calcium channel currents were recorded by a patch-clamp technique. The mRNA expression of CaV1.2 was determined by Real-time RT-PCR. The protein expression of CaV1.2 and p38 activity was determined by Western blot analysis. Results: LTB4 inhibits L-type channel currents in A7r5 cells in a dose-and time- dependent manner. LTB4 reduced the mRNA/protein expression of CaV1.2 channels in A7r5 cells. BLT1 receptor antagonist LY29311 abrogated the inhibitory effect of LTB4, while BLT2 receptor antagonist LY255283 had no effect. 5Z-7-oxozeaenol and SB203580, which block TAK1 and p38 kinase respectively, abrogated the LTB4 inhibitory effect on L-type calcium channels. LTB4 increased p38 activity in A7r5 cells. Blockage of Src, PI3K, JNK and NF-κB kinase had no effects on LTB4 inhibition of L-type calcium channel currents in A7r5 cells. Conclusion: We conclude that LTB4 inhibits L-type calcium channels through BLT1-TAk1-p38 signaling pathway. The LTB4 inhibitory effect on L-type calcium channels may be involved in its pathological processes such as atherosclerosis.
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7

Yarotskyy, Viktor, Guofeng Gao, Blaise Z. Peterson y Keith S. Elmslie. "Domain III regulates N-type (CaV2.2) calcium channel closing kinetics". Journal of Neurophysiology 107, n.º 7 (1 de abril de 2012): 1942–51. http://dx.doi.org/10.1152/jn.00993.2011.

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CaV2.2 (N-type) and CaV1.2 (L-type) calcium channels gate differently in response to membrane depolarization, which is critical to the unique physiological functions mediated by these channels. We wondered if the source for these differences could be identified. As a first step, we examined the effect of domain exchange between N-type and L-type channels on activation-deactivation kinetics, which were significantly different between these channels. Kinetic analysis of chimeric channels revealed N-channel-like deactivation for all chimeric channels containing N-channel domain III, while activation appeared to be a more distributed function across domains. This led us to hypothesize that domain III was an important regulator of N-channel closing. This idea was further examined with R-roscovitine, which is a trisubstituted purine that slows N-channel deactivation by exclusively binding to activated N-channels. L-channels lack this response to roscovitine, which allowed us to use N-L chimeras to test the role of domain III in roscovitine modulation of N-channel deactivation. In support of our hypothesis, all chimeric channels containing the N-channel domain III responded to roscovitine with slowed deactivation, while those chimeric channels with L-channel domain III did not. Thus a combination of kinetic and pharmacological evidence supports the hypothesis that domain III is an important regulator of N-channel closing. Our results support specialization of gating functions among calcium channel domains.
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8

Durante, P., C. G. Cardenas, J. A. Whittaker, S. T. Kitai y R. S. Scroggs. "Low-Threshold L-type Calcium Channels in Rat Dopamine Neurons". Journal of Neurophysiology 91, n.º 3 (marzo de 2004): 1450–54. http://dx.doi.org/10.1152/jn.01015.2003.

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Ca2+ channel subtypes expressed by dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc) were studied using whole cell patch-clamp recordings and blockers selective for different channel types (L, N, and P/Q). Nimodipine (Nim, 2 μM), ω-conotoxin GVIA (Ctx, 1 μM), or ω-agatoxin IVA (Atx, 50 nM) blocked 27, 36, and 37% of peak whole cell Ca2+ channel current, respectively, indicating the presence of L-, N-, and P-type channels. Nim blocked approximately twice as much Ca2+ channel current near activation threshold compared with Ctx or Atx, suggesting that small depolarizations preferentially opened L-type versus N- or P-type Ca2+ channels. N- and L-channels in DA neurons opened over a significantly more negative voltage range than those in rat dorsal root ganglion cells, recorded from using identical conditions. These data provide an explanation as to why Ca2+-dependent spontaneous oscillatory potentials and rhythmic firing in DA neurons are blocked by L-channel but not N-channel antagonists and suggest that pharmacologically similar Ca2+ channels may exhibit different thresholds for activation in different types of neurons.
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9

Büschges, A., M. A. Wikström, S. Grillner y A. El Manira. "Roles of High-Voltage–Activated Calcium Channel Subtypes in a Vertebrate Spinal Locomotor Network". Journal of Neurophysiology 84, n.º 6 (1 de diciembre de 2000): 2758–66. http://dx.doi.org/10.1152/jn.2000.84.6.2758.

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Lamprey spinal cord neurons possess N-, L-, and P/Q-type high-voltage–activated (HVA) calcium channels. We have analyzed the role of the different HVA calcium channels subtypes in the overall functioning of the spinal locomotor network by monitoring the influence of their specific agonists and antagonists on synaptic transmission and on N-methyl-d-aspartate (NMDA)–elicited fictive locomotion. The N-type calcium channel blocker ω-conotoxin GVIA (ω-CgTx) depressed synaptic transmission from excitatory and inhibitory interneurons. Blocking L-type and P/Q-type calcium channels with nimodipine and ω-agatoxin, respectively, did not affect synaptic transmission. Application of ω-CgTx initially decreased the frequency of the locomotor rhythm, increased the burst duration, and subsequently increased the coefficient of variation and disrupted the motor pattern. These effects were accompanied by a depression of the synaptic drive between neurons in the locomotor network. Blockade of L-type channels by nimodipine also decreased the frequency and increased the duration of the locomotor bursts. Conversely, potentiation of L-type channels increased the frequency of the locomotor activity and decreased the duration of the ventral root bursts. In contrast to blockade of N-type channels, blockade or potentiation of L-type calcium channels had no effect on the stability of the locomotor pattern. The P/Q-type calcium channel blocker ω-agatoxin IVA had little effect on the locomotor frequency or burst duration. The results indicate that rhythm generation in the spinal locomotor network of the lamprey relies on calcium influx through L-type and N-type calcium channels.
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Rosenberg, R. L., P. Hess y R. W. Tsien. "Cardiac calcium channels in planar lipid bilayers. L-type channels and calcium-permeable channels open at negative membrane potentials." Journal of General Physiology 92, n.º 1 (1 de julio de 1988): 27–54. http://dx.doi.org/10.1085/jgp.92.1.27.

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Planar lipid bilayer recordings were used to study Ca channels from bovine cardiac sarcolemmal membranes. Ca channel activity was recorded in the absence of nucleotides or soluble enzymes, over a range of membrane potentials and ionic conditions that cannot be achieved in intact cells. The dihydropyridine-sensitive L-type Ca channel, studied in the presence of Bay K 8644, was identified by a detailed comparison of its properties in artificial membranes and in intact cells. L-type Ca channels in bilayers showed voltage dependence of channel activation and inactivation, open and closed times, and single-channel conductances in Ba2+ and Ca2+ very similar to those found in cell-attached patch recordings. Open channels were blocked by micromolar concentrations of external Cd2+. In this cell-free system, channel activity tended to decrease during the course of an experiment, reminiscent of Ca2+ channel "rundown" in whole-cell and excised-patch recordings. A purely voltage-dependent component of inactivation was observed in the absence of Ca2+ stores or changes in intracellular Ca2+. Millimolar internal Ca2+ reduced unitary Ba2+ influx but did not greatly increase the rate or extent of inactivation or the rate of channel rundown. In symmetrical Ba2+ solutions, unitary conductance saturated as the Ba2+ concentration was increased up to 500 mM. The bilayer recordings also revealed activity of a novel Ca2+-permeable channel, termed "B-type" because it may contribute a steady background current at negative membrane potentials, which is distinct from L-type or T-type Ca channels previously reported. Unlike L-type channels, B-type channels have a small unitary Ba2+ conductance (7 pS), but do not discriminate between Ba2+ and Ca2+, show no obvious sensitivity to Bay K 8644, and do not run down. Unlike either L- or T-type channels, B-type channels did not require a depolarization for activation and displayed mean open times of greater than 100 ms.
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Tesis sobre el tema "L-typa calcium channels"

1

Peterson, Blaise. "Molecular determinants of dihydropyridine binding on L-type calcium channels /". Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6269.

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Wang, Ming Chuan. "Structural studies of L-type voltage-gated calcium channels". Thesis, University of Manchester, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525174.

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Cifelli, Carlo. "Impairment of force development in K(ATP) channel deficient skeletal muscle involves calcium ion influx through L-type calcium ion channels". Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27342.

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ATP-sensitive potassium (KATP) channels link membrane excitability to metabolism. They are regulated by intracellular nucleotides and other factors, and have been shown to play a role in development of skeletal muscle force, but controversy surrounds their role during fatigue. The aim of this research project was to determine the role of KATP channel under conditions that allow for better assessment of changes in force during fatigue, by virtue of using a smaller whole muscle model less subject to anoxia. Thus, the first objective was to determine the effect of the loss of KATP channel activity on force during fatigue in small FDB muscle bundles. KATP channel deficient fibers had faster and greater decreases in peak tetanic force during fatigue, developed greater resting tension, and had lower force recovery following fatigue compared to control wild type muscles. The second objective was to determine whether the functional impairment in skeletal muscle without KATP channel activity was due to an increase in Ca 2+ influx. When [Ca2+]e was reduced or L-type Ca2+ channels partially blocked, Kir6.2-/- FDB muscle had slower fatigue development, less resting tension, and had an improved force recovery. A novel phenomenon was observed while studying the effect of KATP channel activity in vitro. During a second bout of fatigue the decrease in peak tension was significantly lower than the decrease during the first bout of fatigue. Furthermore, the deleterious effects of the loss of KATP channel activity during an initial fatigue were absent during the second fatigue in FDB exposed to glibenclamide. It is concluded (i) that the KATP channel is important to prevent impairment of function during fatigue, (ii) that this impairment of function is due to an increase in Ca2+ influx through L-type Ca2+ channels, causing Ca2+ overload, and (iii) that fatigue resistance increases while the dependency on the KATP channel to prevent function impairment and fiber damage decreases following one fatigue bout at 37°C; a phenomenon here termed fatigue pre-conditioning.
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4

Xu, Man. "Functional roles of L-type calcium channels in murine embryonic hearts". [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=970967667.

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5

Shao, Ying. "Molecular natures of L-type CAv1.2 (alpha1C) and T-type CAv3.2 (alpha1H) voltage sensitive calcium channels (VSCCs) in mouse osteoblasts and mouse bones". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 169 p, 2005. http://proquest.umi.com/pqdweb?did=954050631&sid=5&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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6

Crump, Shawn M. "THE CARDIAC L-TYPE CALCIUM CHANNEL DISTAL CARBOXYL- TERMINUS AUTO-INHIBITION IS REGULATED BY CALCIUM". UKnowledge, 2012. http://uknowledge.uky.edu/physiology_etds/5.

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The L-type calcium channel (LTCC) provides trigger Ca2+ for sarcoplasmic reticulum Ca2+-release and LTCC function is influenced by interacting proteins including the LTCC Distal Carboxyl-terminus (DCT) and calmodulin. DCT is proteolytically cleaved, and re-associates with the LTCC complex to regulate calcium channel function. DCT reduces LTCC barium current (IBa,L) in reconstituted channel complexes, yet the contribution of DCT to ICa,L in cardiomyocyte systems is unexplored. This study tests the hypothesis that DCT attenuates cardiomyocyte ICa,L. We measured LTCC current and Ca2+ transients with DCT co-expressed in murine cardiomyocytes. We also heterologously co-expressed DCT and CaV1.2 constructs with truncations corresponding to the predicted proteolytic cleavage site, CaV1.2Δ1801, and a shorter deletion corresponding to well-studied construct, CaV1.2Δ1733. DCT inhibited IBa,L in cardiomyocytes, and in HEK 293 cells expressing CaV1.2Δ1801 and CaV1.2Δ1733. Ca2+-CaM relieved DCT block in cardiomyocytes and HEK cells. The selective block of IBa,L combined with Ca2+-CaM effects suggested that DCT-mediated blockade may be relieved under conditions of elevated Ca2+. We therefore tested the hypothesis that DCT block is dynamic, increasing under relatively low Ca2+, and show that DCT reduced diastolic Ca2+ at low stimulation frequencies but spared high frequency Ca2+-entry. DCT reduction of diastolic Ca2+ and relief of block at high pacing frequencies, and under conditions of supraphysiological bath Ca2+ suggests that a physiological function of DCT is to increase the dynamic range of Ca2+ transients in response to elevated pacing frequencies. Our data motivates the new hypothesis that DCT is a native reverse use-dependent inhibitor of LTCC current.
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7

Byse, Miranda Jean. "THE ROLE OF THE L-TYPE CALCIUM CHANNEL AND ITS CARBOXYL-TERMINUS". UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/20.

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In the heart, the primary role of the L-type calcium channel (LTCC) CaV1.2 is to conduct calcium into cardiomyocytes and initiate contraction. However, part of the CaV1.2 channel itself, the cleaved carboxyl-terminus (CCt) can also localize to the nucleus and regulate gene transcription. Therefore, the goal of this dissertation project was to determine the role and regulation of CCt in the embryonic and adult heart. The global hypothesis of my dissertation project is that CCt localizes to the nucleus in embryonic and adult cardiomyocytes via a calcium-mediated mechanism and regulates transcription. A model of pharmacological LTCC block-induced perturbation of murine embryonic heart development was first utilized to study the role of CCt. Pharmacological block at embryonic day 10 perturbed cardiogenesis and increased CaV1.2 expression. This result was not mimicked by removal of extracellular calcium or inhibition of calcium release from the sarcoplasmic reticulum. Co-currently, pharmacological block decreased CCt nuclear localization in embryonic cardiomyocytes. At the transcriptional level, CCt suppressed the CaV1.2 promoter. This indicated that the observed upregulation of CaV1.2 induced by pharmacological block may be caused by nuclear localization of the transcriptional repressor, CCt. Therefore, the conclusion was made that pharmacological LTCC block perturbed embryonic cardiogenesis by decreasing nuclear localization of the transcription factor CCt; implying a role for CCt in embryonic heart development. Next, CCt regulation was studied in the adult heart. Similar to the embryonic heart, pharmacological LTCC block decreased nuclear localization of CCt. Inhibition of the calcium activated phosphatase calcineurin also decreased CCt nuclear localization. To determine a role for CCt in the adult heart, CCt nuclear localization was measured in response to hypertrophic stimuli. Serum-induced cardiomyocyte hypertrophy significantly increased nuclear localization of CCt. In conclusion, this dissertation supports the hypothesis that CCt localizes to the nucleus in embryonic and adult cardiomyocytes, and that this regulation is mediated by calcium entry into the cardiomyocyte. Furthermore, data from this dissertation suggests that CCt nuclear localization may play an important role in embryonic heart development and adult cardiac hypertrophy.
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8

Pang, Chunyan. "REGULATION OF L-TYPE VOLTAGE-DEPENDNET CALCIUM CHANNELS BY THE REM GTPASE". UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_diss/656.

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The Rem, Rem2, Rad, and Gem/Kir GTPases, comprise a novel subfamily of the small Ras-related GTP-binding proteins known as the RGK GTPases, and have been shown to function as potent negative regulators of high voltage-activated (HVA) Ca2+ channels upon overexpression. HVA Ca2+ channels modulate Ca2+ influx in response to membrane depolarization to regulate a wide variety of cellular functions and they minimally consist of a pore-forming α1 subunit, an intracellular β subunit, and a transmembrane complex α2/δ subunit. While the mechanisms underlying RGK-mediated Ca2+ channel regulation remain poorly defined, it appears that both membrane localization and the binding of accessory Ca2+ channel β subunits (CaVβ) are required for suppression of Ca2+ channel currents. We identified a direct interaction between Rem and the L-type Cavα1 C-terminus (CCT), but not the CCT from CaV3.2 T-type channels. Deletion mapping studies suggest that the conserved CB-IQ domain is required for Rem:CCT association, a region known to contribute to both Ca2+-dependent channel inactivation and facilitation through interactions of Ca2+-bound calmodulin (CaM) with the proximal CCT. Furthermore, both Rem2 and Rad GTPases display similar patterns of CCT binding, suggesting that CCT represents a common binding partner for all RGK proteins. While previous studies have found that association of the Rem C-terminus with the plasma membrane is required for channel inhibition, it is not required for CaVβ- subunit binding. However, Rem:CCT association is well correlated with the plasma membrane localization of Rem and more importantly, Rem-mediated channel inhibition upon overexpression. Moreover, co-expression of the proximal CB-IQ containing region of CCT (residues 1507-1669) in HIT-T15 cells partially relieves Rem blockade of ionic current. Interestingly, Ca2+/CaM disrupts Rem:CCT association in vitro. Moreover, CaM overexpression partially relieves Rem-mediated L-type Ca2+ channel inhibition and Rem overexpression alters the kinetics of calcium-dependent inactivation. Together, these data suggest that the association of Rem with the CCT represents a crucial molecular determinant for Rem-mediated L-type Ca2+ channel regulation and provides new insights into this novel channel regulatory process. These studies also suggest that instead of acting as complete Ca2+ channel blockers, RGK proteins may function as endogenous regulators for the channel inactivation machinery.
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9

Milholland, Rebecca. "L-type calcium channels mediate nicotinic acetylcholine receptor aggregation on cultured myotubes". Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/280370.

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In this dissertation, I have presented new information on several aspects of the signaling pathway responsible for the clustering of AChRs on muscle cells. First, I have shown that activation of L-CaChs is both necessary for agrin induced clustering of AChRs and sufficient to stimulate AChR clustering even in the absence of agrin. Additionally, I have shown that activation of AChRs causes their own clustering by influencing the activity of L-CaChs. I have also shown that neither AChRs nor L-CaChs play a role in MuSK activation or AChR beta subunit phosphorylation suggesting that the role of AChR and L-CaCh is downstream of MuSK activation and phosphorylation of the AChR beta subunit in the signaling cascade that leads to the aggregation of AChRs. Finally, I have shown that calcium induced clustering and phosphorylation of AChRs require LCaCh activation. These data suggested that although L-CaCh activation is insufficient to cause AChR beta subunit phosphorylation L-CaCh may modulate an intermediate step between MuSK activation and AChR phosphorylation. These data therefore support the hypothesis that L-CaCh activation delivers extracellular calcium to the intracellular machinery that regulates AChR clustering. Furthermore, these data establish the position of L-CaChs in the signaling hierarchy responsible for AChR clustering as being downstream of or parallel to both MuSK activation and AChR phosphorylation in the signaling cascade behind AChR clustering. The data presented in this paper begin to provide an integrated view of NMJ formation in which neuromuscular transmission, calcium signaling, and signaling cascades mediated by neurotrophic factors act in concert to regulate the localization of synaptic molecules to junctional regions of the muscle fiber. Many questions remain, however, regarding the events downstream of MuSK and L-CaCh activation.
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Waite, Sarah. "Regulation of myometrial contractility : defining the contribution of the MaxiK potassium channel and the L- and T-type calcium channels". Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/11621/.

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This thesis describes a comprehensive study investigating the roles of the MaxiK potassium channel (KCNMA1), L-Type calcium channel (CACNA1C) and T-Type calcium channel (CACNA1G) in the maintenance of quiescence (relaxed myometrium), the preparation for parturition (non-contracting myometrium) and the regulation of the co-ordinated contractions characteristic of parturition itself (contracting myometrium). The role of these channels was investigated using primary human myometrial cell cultures under relaxed, non-contracting and contracting conditions. Protein studies revealed changes in both the amount and channel isoforms expressed between the different conditions. Protein-protein interaction studies revealed that the KCNMA1 and CACNA1C associated with Caveolin-1, Gαs and β2-Adrenergic Receptor. RNA studies revealed that the different incubation conditions modified expression of total channel mRNA and that of various splice variants. Previous research has demonstrated that the CACNA1C channel C-terminus can function as a transcription factor termed CCAT. Within this thesis inmmunohistochemistry staining and protein localisation studies revealed nuclear localisation of both the CACNA1C and KCNMA1 C-terminii. Therefore, genomic studies were undertaken utilising the ChIP assay, coupled with ChIP sequencing, to study the role of the KCNMA1 channel as a transcription factor. Chip-sequencing data files were then analysed using Galaxy, an open access web-based platform. Peak calling generated 47 peaks, 21 were successfully mapped to known genes, including RB1, JPH2 and MAP3K7. Motif discovery was then undertaken for both the KCNMA1 protein utilising GYM and the successfully mapped peaks using the Panoptic Motif Search Tool. A helix-turn-helix motif was discovered in the C-terminal region of the KCNMA1 protein and ten putative transcription factor binding motifs were discovered within the peak regions. The significance of these findings is discussed.
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Libros sobre el tema "L-typa calcium channels"

1

Tytgat, Jan. Comparison between cardiac L- and T-type calcium channels: An electro-physiological and pharmacological study. Leuven: Leuven University Press, 1990.

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Kulbatski, Iris. L-type calcium channels and NGF in regenerating rat sympathetic neurons. Ottawa: National Library of Canada, 2002.

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Henckels, Kathryn. Mid-channel proteolysis of the L-type voltage gated calcium channel and the potential role of amyloid-β precursor protein. [New York, N.Y.?]: [publisher not identified], 2014.

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Sikora, Lindsey. The effects of the L-type calcium channel antagonist nimodipine on learning and memory following low and high concentrations of ethanol consumption. Sudbury, Ont: Laurentian University, 2005.

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Oudit, Gavin Y. Role of L-type Ca2+ channel and oxidative stress in the pathogenesis of iron-overload cardiomyopathy: Calcium channel blockers and taurine as potential therapies. 2005.

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Capítulos de libros sobre el tema "L-typa calcium channels"

1

Triggle, David J. "Pharmacology of Cav1 (L-Type) Channels". En Calcium Channel Pharmacology, 21–72. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9254-3_2.

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Koschak, Alexandra, Alexandra Pinggera, Klaus Schicker y Jörg Striessnig. "Role of L-Type Ca2+ Channels in Sensory Cells". En Pathologies of Calcium Channels, 47–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_3.

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Matthes, Jan y Stefan Herzig. "Auxiliary β-Subunits of L-Type Ca2+ Channels in Heart Failure". En Pathologies of Calcium Channels, 255–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_14.

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Koschak, Alexandra y Amy Lee. "Cav1 L-Type Calcium Channels in the Auditory and Visual Systems". En Voltage-Gated Calcium Channels, 475–89. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08881-0_17.

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Ruan, Yanfei, Raffaella Bloise, Carlo Napolitano y Silvia G. Priori. "L-Type Calcium Channel Disease". En Electrical Diseases of the Heart, 209–17. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4881-4_12.

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Davenport, Andrew, Todd W. Costantini, Raul Coimbra, Marc M. Sedwitz, A. Brent Eastman, David V. Feliciano, David V. Feliciano et al. "Voltage-Sensitive Calcium Channels (L-type)". En Encyclopedia of Intensive Care Medicine, 2458. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3372.

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Artalejo, C. R., M. G. López, C. F. Castillo, M. A. Moro y A. G. García. "L-Type Calcium Channels and Adrenomedullary Secretion". En The Calcium Channel: Structure, Function and Implications, 347–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73914-9_29.

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Hofmann, Franz, Norbert Klugbauer, Lubica Lacinová, Claudia Seisenberger, Angela Schuster y Andrea Welling. "Interaction of the L-Type Calcium Channel with Calcium Channel Blockers". En Molecular and Cellular Mechanisms of Cardiovascular Regulation, 231–42. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-65952-5_18.

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Hofmann, Franz y Martin Biel. "L-type calcium channel structure and function". En Developments in Cardiovascular Medicine, 63–69. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-3990-8_6.

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Pietrobon, Daniela, Lia Forti y Peter Hess. "Voltage-Dependent Modal Gating in Cardiac and Neuronal L-type Calcium Channels". En Intracellular Regulation of Ion Channels, 173–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84628-1_19.

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Actas de conferencias sobre el tema "L-typa calcium channels"

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KAKU, TOSHIHIKO, HIDEAKI OZAKI, SATOSHI ISHII, TAKAO SHIMIZU y KATSUSHIGE ONO. "PLATELET ACTIVATING FACTOR AFFECTS INTRACELLULAR CALCIUM CONCENTRATION BY MODULATING L-TYPE CALCIUM CHANNEL". En Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0022.

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Gupta, Nitika, Liam F. McCormick, Ohm Prakash, Lu-Yun Lian, Caroline Dart y Nordine Helassa. "BS12 Calmodulin mutations associated with long QT syndrome impair L-type calcium channel regulation". En British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.192.

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Jun He, Wei Zhou, Shaoqun Zeng y Qingming Luo. "L-type calcium channels mediate synchronized spontaneous Ca2+spikes in cultured cortical networks". En 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616793.

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Dias, Thales Augusto Oliveira y Silvia Graciela Ruginsk Leitão. "Participation of calcium channels in the action of angiotensin II in astrocytes". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.299.

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Background: The renin-angiotensin-aldosterone system is the main regulator of blood pressure and blood volume, with most effects being mediated by angiotensin II (Ang-II) - responsible, in the central nervous system, for actions such as thirst and sodium appetite. Astrocytes are believed to mediate such a response, as they express receptors for Ang-II and respond directly to dehydration with impacting morphological changes in the synaptic microenvironment. Many of its functions involve L-type calcium channels (LTCCs). Objectives: Evaluate the participation of LTCCs in the effects induced by AngII in cultured hypothalamic astrocytes. Methods: The effect of incubation with verapamil on the morphological responses induced by Ang-II was evaluated in hypothalamic astrocyte culture, by analyzing the expression of the cytoskeletal protein GFAP and the cell viability by the MTT assay, by immunofluorescence. Results: Incubation with Ang-II reduced the cell area considerably due to GFAP expression in relation to the control group (DMEM p<0.001), indicating that the results observed on GFAP expression did not result from cell death. Conclusion: Incubation with Ang-II alters the astrocyte morphology, reducing its area, effect at least in part, blocked by the action of Verapamil, indicating the participation of LTCCs in the mediation of this process.
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Sher, Anna, Ken Wang, Andrew Wathen, Gary Mirams, David Abramson y David Gavaghan. "A Local Sensitivity Analysis Method for Developing Biological Models with Identifiable Parameters: Application to L-type Calcium Channel Modelling". En 2010 IEEE 6th International Conference on E Science (e-Science). IEEE, 2010. http://dx.doi.org/10.1109/escience.2010.56.

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Shen, "Yumin, Na Zhao, Zhipeng Cai, Chengyu Liu y Jianqing Li". "N2091S Mutation in L-type Calcium Channel Promotes Action Potential Alternans in M Cells of Human Ventricle: A Simulation Study". En 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.143.

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Felicia, Suciu, Arcuș Mariana, Adrian Cosmin, Bucur Laura, Popescu Antoanela y Badea Victoria. "STUDIES ON THE MORPHO-ANATOMICAL PARTICULARITIES OF LYSIMACHIA NUMMULARIA L." En GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/25.

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"The objective of the study was the histo-anatomical analysis of the root, stem and leaf belonging to the species Lysimachia nummularia L. from the Primulaceae family. The plant is native to Europe, but has been introduced to North America, where it is considered an invasive species in some areas. It aggressively spreads in favourable conditions, such as low wet ground or near ponds. It is moderately difficult to remove by hand pulling. Any tiny piece left behind will regrow. The research results led to the following assessments: root with primary structure and beginning of secondary structure, the presence of calcium oxalate druze in the bark, endoderm and primary type conducting bundles. The results of the study also demonstrated the existence of the stem with four prominent ribs, a meatic-type bark with small secretory channels and a central cylinder with a secondary structure. Another element studied from a histo-anatomical point of view; leaf with dorsi-ventral bifacial structure, with heterogeneous asymmetrical structure, collateral free-woody bundle, without periectors. From the morpho-anatomical data described, it can be concluded that the species Lysimachia nummularia L. belongs to the family Primulaceae and is related to other species of the genus Lysimachia."
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