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Artykuły w czasopismach na temat „Influx de calcium”

Autor: Grafiati

Data publikacji: 2 listopada 2024

Data aktualizacji: 31 lipca 2025

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1

King, Leslie B., and Bruce D. Freedman. "B-lymphocyte calcium inFlux." Immunological Reviews 231, no. 1 (2009): 265–77. http://dx.doi.org/10.1111/j.1600-065x.2009.00822.x.

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Neher, Erwin. "Controls on calcium influx." Nature 355, no. 6358 (1992): 298–99. http://dx.doi.org/10.1038/355298a0.

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McCarthy, Nicola. "Calcium influx is moving." Nature Reviews Cancer 9, no. 4 (2009): 230–31. http://dx.doi.org/10.1038/nrc2629.

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GIBBONS, SIMON J., JAMES R. BRORSON, DAVID BLEAKMAN, PAUL S. CHARD, and RICHARD J. MILLER. "Calcium Influx and Neurodegeneration." Annals of the New York Academy of Sciences 679, no. 1 Markers of Ne (1993): 22–33. http://dx.doi.org/10.1111/j.1749-6632.1993.tb18286.x.

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Vostal, J. G., and J. C. Fratantoni. "Econazole inhibits thapsigargin-induced platelet calcium influx by mechanisms other than cytochrome P-450 inhibition." Biochemical Journal 295, no. 2 (1993): 525–29. http://dx.doi.org/10.1042/bj2950525.

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Cytochrome P-450 has been suggested as a mediator of the signal between depleted platelet calcium stores and an increase in plasma membrane permeability to calcium which follows depletion of the stores. This hypothesis is based on the observations that inhibitors of cytochrome P-450, such as the imidazole antifungal agents, also inhibit influx of a calcium surrogate (manganese) into calcium-depleted platelets. We tested the effects of econazole and of a cytochrome P-450 inhibitor, carbon monoxide (CO), on thapsigargin (TG)-induced platelet 45Ca2+ influx. TG specifically depletes internal calci

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6

Ramagopal, M. V., and S. J. Mustafa. "Effect of adenosine and its analogues on calcium influx in coronary artery." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 6 (1988): H1492—H1498. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1492.

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In the present study, we have investigated the changes in calcium influx during the relaxing responses to adenosine and its analogues. Calcium-45 influx was measured in bovine coronary artery rings in the presence of prostaglandin F2 alpha (10(-5) M) and KCl (50 and 100 mM). Prostaglandin F2 alpha and KCl caused increases in calcium influx. Prostaglandin F2 alpha produced a further contraction when added to rings maximally contracted with KCl (100 mM or higher), suggesting two different mechanisms for prostaglandin F2 alpha- and KCl-induced contractions. Similarly, a greater calcium influx was

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7

Davis, Michael J., and Neeraj R. Sharma. "Calcium-Release-Activated Calcium Influx in Endothelium." Journal of Vascular Research 34, no. 3 (1997): 186–95. http://dx.doi.org/10.1159/000159222.

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8

Capiod, Thierry. "Cell proliferation, calcium influx and calcium channels." Biochimie 93, no. 12 (2011): 2075–79. http://dx.doi.org/10.1016/j.biochi.2011.07.015.

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9

Chen, Huanmian, and Nevin A. Lambert. "Inhibition of Dendritic Calcium Influx by Activation of G-Protein–Coupled Receptors in the Hippocampus." Journal of Neurophysiology 78, no. 6 (1997): 3484–88. http://dx.doi.org/10.1152/jn.1997.78.6.3484.

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Chen, Huanmian and Nevin A. Lambert. Inhibition of dendritic calcium influx by activation of G-protein–coupled receptors in the hippocampus. J. Neurophysiol. 78: 3484–3488, 1997. Gi proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein–coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in den

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10

Wang, Z., M. Estacion, and L. J. Mordan. "Ca2+ influx via T-type channels modulates PDGF-induced replication of mouse fibroblasts." American Journal of Physiology-Cell Physiology 265, no. 5 (1993): C1239—C1246. http://dx.doi.org/10.1152/ajpcell.1993.265.5.c1239.

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The role of low-threshold voltage-gated calcium channels (VGCC) in modulating extracellular calcium influx and proliferation was investigated in platelet-derived growth factor (PDGF)-stimulated C3H/10T1/2 mouse fibroblasts. Previous studies demonstrated that cell cycle progression after PDGF stimulation was dependent on extracellular calcium influx producing a sustained increase in the intracellular calcium concentration. In this study, PDGF-induced calcium influx, the sustained intracellular calcium increase, and progression to S phase were inhibited by nordihydroguariaretic acid (NDGA), an i

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11

Kwon, Min Seong, Chun Shik Park, Kyeong-rock Choi, et al. "Calreticulin Couples Calcium Release and Calcium Influx in Integrin-mediated Calcium Signaling." Molecular Biology of the Cell 11, no. 4 (2000): 1433–43. http://dx.doi.org/10.1091/mbc.11.4.1433.

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The engagement of integrin α7 in E63 skeletal muscle cells by laminin or anti-α7 antibodies triggered transient elevations in the intracellular free Ca2+concentration that resulted from both inositol triphosphate-evoked Ca2+release from intracellular stores and extracellular Ca2+influx through voltage-gated, L-type Ca2+channels. The extracellular domain of integrin α7 was found to associate with both ectocalreticulin and dihydropyridine receptor on the cell surface. Calreticulin appears to also associate with cytoplasmic domain of integrin α7 in a manner highly dependent on the cytosolic Ca2+c

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12

O'Neil, R. G., and L. Leng. "Osmo-mechanically sensitive phosphatidylinositol signaling regulates a Ca2+ influx channel in renal epithelial cells." American Journal of Physiology-Renal Physiology 273, no. 1 (1997): F120—F128. http://dx.doi.org/10.1152/ajprenal.1997.273.1.f120.

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Regulation of dihydropyridine (nifedipine)-sensitive calcium influx was studied in rabbit culture proximal tubule cells using the fura 2 fluorescence ratio technique. "Osmo-mechanically induced" swelling of cells by exposure to hypotonic medium (220 mosmol/kgH2O) caused a rapid rise in intracellular calcium that was predominantly due to influx of calcium via both dihydropyridine-sensitive (nifedipine-sensitive) and -insensitive calcium influx pathways. The dihydropyridine-sensitive pathway was regulated, in part, by the phosphatidylinositol signaling pathway. Inhibition of phospholipase C by t

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13

Wang, Chunmin, and Zoltan Machaty. "Calcium influx in mammalian eggs." REPRODUCTION 145, no. 4 (2013): R97—R105. http://dx.doi.org/10.1530/rep-12-0496.

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Calcium (Ca2+) signals are involved in the regulation of oocyte maturation and play a critical role during fertilization. In the egg, Ca2+is stored in the lumen of the endoplasmic reticulum and a signal is generated when the stored Ca2+is released through specialized channels in the membrane of the endoplasmic reticulum to elevate the free Ca2+concentration in the cytoplasm. Extracellular Ca2+is also important, indicated by the fact that the mobilization of luminal Ca2+is typically followed by Ca2+entry across the plasma membrane. The transmembrane Ca2+flux replenishes the endoplasmic reticulu

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14

Robinson, Lisbeth C., and Jonathan S. Marchant. "Calcium Influx: Beyond ‘Current’ Biology." Current Biology 16, no. 14 (2006): R548—R550. http://dx.doi.org/10.1016/j.cub.2006.06.036.

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Parekh, A. B., and R. Penner. "Store depletion and calcium influx." Physiological Reviews 77, no. 4 (1997): 901–30. http://dx.doi.org/10.1152/physrev.1997.77.4.901.

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Calcium influx in nonexcitable cells regulates such diverse processes as exocytosis, contraction, enzyme control, gene regulation, cell proliferation, and apoptosis. The dominant Ca2+ entry pathway in these cells is the store-operated one, in which Ca2+ entry is governed by the Ca2+ content of the agonist-sensitive intracellular Ca2+ stores. Only recently has a Ca2+ current been described that is activated by store depletion. The properties of this new current, called Ca2+ release-activated Ca2+ current (ICRAC), have been investigated in detail using the patch-clamp technique. Despite intense

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16

Turner, P. R., P. Y. Fong, W. F. Denetclaw, and R. A. Steinhardt. "Increased calcium influx in dystrophic muscle." Journal of Cell Biology 115, no. 6 (1991): 1701–12. http://dx.doi.org/10.1083/jcb.115.6.1701.

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We examined pathways which might result in the elevated resting free calcium [( Ca2+]i) levels observed in dystrophic mouse (mdx) skeletal muscle fibers and myotubes and human Duchenne muscular dystrophy myotubes. We found that mdx fibers, loaded with the calcium indicator fura-2, were less able to regulate [Ca2+]i levels in the region near the sarcolemma. Increased calcium influx or decreased efflux could lead to elevated [Ca2+]i levels. Calcium transient decay times were identical in normal and mdx fibers if resting [Ca2+]i levels were similar, suggesting that calcium-sequestering mechanisms

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17

Putney, James W., and Gary S. Bird. "Cytoplasmic calcium oscillations and store-operated calcium influx." Journal of Physiology 586, no. 13 (2008): 3055–59. http://dx.doi.org/10.1113/jphysiol.2008.153221.

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18

Baldridge, William H., Dmitri E. Kurennyi, and Steven Barnes. "Calcium-Sensitive Calcium Influx in Photoreceptor Inner Segments." Journal of Neurophysiology 79, no. 6 (1998): 3012–18. http://dx.doi.org/10.1152/jn.1998.79.6.3012.

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Baldridge, William H., Dmitri E. Kurennyi, and Steven Barnes. Calcium-sensitive calcium influx in photoreceptor inner segments. J. Neurophysiol. 79: 3012–3018, 1998. The effect of external calcium concentration ([Ca2+]o) on membrane potential–dependent calcium signals in isolated tiger salamander rod and cone photoreceptor inner segments was investigated with patch-clamp and calcium imaging techniques. Mild depolarizations led to increases in intracellular Ca2+ levels ([Ca2+]i) that were smaller when [Ca2+]o was elevated to 10 mM than when it was 3 mM, even though maximum Ca2+ conductance incr

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19

Penner, Reinhold, Cristina Fasolato, and Markus Hoth. "Calcium influx and its control by calcium release." Current Opinion in Neurobiology 3, no. 3 (1993): 368–74. http://dx.doi.org/10.1016/0959-4388(93)90130-q.

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BOSE, Diptiman D., Roshanak RAHIMIAN, and David W. THOMAS. "Activation of ryanodine receptors induces calcium influx in a neuroblastoma cell line lacking calcium influx factor activity." Biochemical Journal 386, no. 2 (2005): 291–96. http://dx.doi.org/10.1042/bj20040900.

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We have further characterized the Ca2+ signalling properties of the NG115-401L (or 401L) neuroblastoma cell line, which has served as an important cell line for investigating SOC (store-operated channel) influx pathways. These cells possess an unusual Ca2+ signalling phenotype characterized by the absence of Ca2+ influx when Ca2+ stores are depleted by inhibitors of SERCA (sarcoplasmic/endoplasmic reticulum Ca2+-ATPase). Previous studies found that Ca2+-store depletion does not produce a CIF (Ca2+ influx factor) activity in 401L cells. These observations have prompted the question whether 401L

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21

Schiebinger, R. J., C. M. Joseph, Y. Li, and E. J. Cragoe. "Mechanism of hyperosmolality stimulation of ANP secretion: its dependency on calcium and sodium." American Journal of Physiology-Endocrinology and Metabolism 268, no. 3 (1995): E476—E483. http://dx.doi.org/10.1152/ajpendo.1995.268.3.e476.

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The calcium dependency of hyperosmolality stimulation of atrial natriuretic peptide (ANP) secretion was determined using isolated superfused nonbeating rat left atrium. Increasing osmolality by 65, 85, and 100 mosmol/kgH2O by superfusion with sucrose produced a peak rise in ANP secretion of 1.8-, 2.0-, and 2.7-fold. To determine whether calcium influx played a role in osmolality (osm)-stimulated ANP secretion, atria were superfused with 2 mM lanthanum, a calcium antagonist. Lanthanum inhibited by 85% the response to a 100 mosmol/kgH2O increase in osm. The voltage-dependent calcium channel bloc

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22

Zweifach, Adam. "Target-Cell Contact Activates a Highly Selective Capacitative Calcium Entry Pathway in Cytotoxic T Lymphocytes." Journal of Cell Biology 148, no. 3 (2000): 603–14. http://dx.doi.org/10.1083/jcb.148.3.603.

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Calcium influx is critical for T cell activation. Evidence has been presented that T cell receptor–stimulated calcium influx in helper T lymphocytes occurs via channels activated as a consequence of depletion of intracellular calcium stores, a mechanism known as capacitative Ca2+ entry (CCE). However, two key questions have not been addressed. First, the mechanism of calcium influx in cytotoxic T cells has not been examined. While the T cell receptor–mediated early signals in helper and cytotoxic T cells are similar, the physiology of the cells is strikingly different, raising the possibility

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23

Papa, Arianne, Jared Kushner, and Steven O. Marx. "Adrenergic Regulation of Calcium Channels in the Heart." Annual Review of Physiology 84, no. 1 (2022): 285–306. http://dx.doi.org/10.1146/annurev-physiol-060121-041653.

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Each heartbeat is initiated by the action potential, an electrical signal that depolarizes the plasma membrane and activates a cycle of calcium influx via voltage-gated calcium channels, calcium release via ryanodine receptors, and calcium reuptake and efflux via calcium-ATPase pumps and sodium-calcium exchangers. Agonists of the sympathetic nervous system bind to adrenergic receptors in cardiomyocytes, which, via cascading signal transduction pathways and protein kinase A (PKA), increase the heart rate (chronotropy), the strength of myocardial contraction (inotropy), and the rate of myocardia

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24

Schiebinger, R. J., L. M. Braley, A. Menachery, and G. H. Williams. "Unique calcium dependencies of the activating mechanism of the early and late aldosterone biosynthetic pathways in the rat." Journal of Endocrinology 110, no. 2 (1986): 315–25. http://dx.doi.org/10.1677/joe.0.1100315.

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ABSTRACT This study compared the extracellular calcium dependency and the enzymatic locus of that dependency for N6,O2′-dibutyryl cyclic AMP (dbcAMP)-, angiotensin II- and potassium-stimulated aldosterone secretion in dispersed rat glomerulosa cells. The need for extracellular calcium, calcium influx, and specifically for calcium influx through the calcium channel was examined. dbcAMP, angiotensin II and potassium, in the presence of calcium (3·5 mmol/l), significantly (P < 0·01) increased aldosterone output by at least 1·5-fold. Yet in the absence of extracellular calcium or in the presenc

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Bialecki, R. A., T. J. Kulik, and W. S. Colucci. "Stretching increases calcium influx and efflux in cultured pulmonary arterial smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 263, no. 5 (1992): L602—L606. http://dx.doi.org/10.1152/ajplung.1992.263.5.l602.

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To determine the effect of a single static stretch on calcium fluxes in cultured pulmonary arterial smooth muscle cells (PASMC), calcium influx and efflux were evaluated in PASMC on a collagen-coated silicone membrane using 45Ca2+ as a tracer. A single 20% linear stretch of the silicone membrane of 1 min in duration increased calcium uptake by 71%. This effect was partially inhibited by verapamil or gadolinium, but was not altered by staurosporine, pertussis toxin, or removal of extracellular sodium. Stretch-stimulated calcium uptake attenuated over time, such that uptake during the last minut

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Bong, Alice Hui Li, Trinh Hua, Choon Leng So, et al. "AKT Regulation of ORAI1-Mediated Calcium Influx in Breast Cancer Cells." Cancers 14, no. 19 (2022): 4794. http://dx.doi.org/10.3390/cancers14194794.

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Although breast cancer cells often exhibit both abnormal AKT signaling and calcium signaling, the association between these two pathways is unclear. Using a combination of pharmacological tools, siRNA and CRISPR/Cas9 gene silencing techniques, we investigated the association between PTEN, AKT phosphorylation and calcium signaling in a basal breast cancer cell line. We found that siRNA-mediated PTEN silencing promotes AKT phosphorylation and calcium influx in MDA-MB-231 cells. This increase in AKT phosphorylation and calcium influx was phenocopied by the pharmacological AKT activator, SC79. The

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Spungin, B., and H. Breitbart. "Calcium mobilization and influx during sperm exocytosis." Journal of Cell Science 109, no. 7 (1996): 1947–55. http://dx.doi.org/10.1242/jcs.109.7.1947.

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We have previously shown that two intracellular events which occur during capacitation of bovine sperm are the formation of actin filaments on the plasma and outer acrosomal membranes and the attachment of a PIP2-specific phospholipase C (PLC) to this membrane bound F-actin. This PLC plays an essential role in sperm exocytosis (acrosome reaction). In the present report, we further elucidated the role of this PLC using a PIP2-specific PLC of bacterial origin. This PLC is different from the endogenous sperm PLC in that it is calcium independent and not inhibited by neomycin. Here we report using

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Zhang, Chuan-Li, J. Adam Wilson, Justin Williams, and Shing Yan Chiu. "Action Potentials Induce Uniform Calcium Influx in Mammalian Myelinated Optic Nerves." Journal of Neurophysiology 96, no. 2 (2006): 695–709. http://dx.doi.org/10.1152/jn.00083.2006.

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The myelin sheath enables saltatory conduction by demarcating the axon into a narrow nodal region for excitation and an extended, insulated internodal region for efficient spread of passive current. This anatomical demarcation produces a dramatic heterogeneity in ionic fluxes during excitation, a classical example being the restriction of Na influx at the node. Recent studies have revealed that action potentials also induce calcium influx into myelinated axons of mammalian optic nerves. Does calcium influx in myelinated axons show spatial heterogeneity during nerve excitation? To address this,

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Siesjo, BK. "Calcium, Excitotoxins, and Brain Damage." Physiology 5, no. 3 (1990): 120–25. http://dx.doi.org/10.1152/physiologyonline.1990.5.3.120.

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Cellular energy failure and loss of calcium homeostasis are important mediators of ischemic brain damage. The role of influx/release has been reemphasized, and excitatory amino acids have been identified as mediators of enhanced calcium influx.

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Schweda, Frank, Günter A. J. Riegger, Armin Kurtz, and Bernhard K. Krämer. "Store-operated calcium influx inhibits renin secretion." American Journal of Physiology-Renal Physiology 279, no. 1 (2000): F170—F176. http://dx.doi.org/10.1152/ajprenal.2000.279.1.f170.

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On the basis of evidence that changes in the extracellular concentration of calcium effectively modulate renin secretion from renal juxtaglomerular cells, our study aimed to determine the effect of calcium influx activated by depletion of intracellular calcium stores on renin secretion. For this purpose we characterized the effects of the endoplasmatic Ca2+-ATPase inhibitors thapsigargin (300 nM) and cyclopiazonic acid (20 μM) on renin secretion from isolated perfused rat kidneys. We found that Ca2+-ATPase inhibition caused a potent inhibition of basal renin secretion as well as renin secretio

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Vyshedskiy, Andrey, and Jen-Wei Lin. "Presynaptic Ca2+ Influx at the Inhibitor of the Crayfish Neuromuscular Junction: A Photometric Study at a High Time Resolution." Journal of Neurophysiology 83, no. 1 (2000): 552–62. http://dx.doi.org/10.1152/jn.2000.83.1.552.

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Presynaptic calcium influx at the inhibitor of the crayfish neuromuscular junction was investigated by measuring fluorescence transients generated by calcium-sensitive dyes. This approach allowed us to correlate presynaptic calcium influx with transmitter release at a high time resolution. Systematic testing of the calcium indicators showed that only low-affinity dyes, with affinities in the range of micromolar, should be used to avoid saturation of dye binding and interference with transmitter release. Presynaptic calcium influx was regulated by slowly increasing the duration of the action po

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Ahmadpour, Noushin, Meher Kantroo, and Jillian L. Stobart. "Extracellular Calcium Influx Pathways in Astrocyte Calcium Microdomain Physiology." Biomolecules 11, no. 10 (2021): 1467. http://dx.doi.org/10.3390/biom11101467.

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Astrocytes are complex glial cells that play many essential roles in the brain, including the fine-tuning of synaptic activity and blood flow. These roles are linked to fluctuations in intracellular Ca2+ within astrocytes. Recent advances in imaging techniques have identified localized Ca2+ transients within the fine processes of the astrocytic structure, which we term microdomain Ca2+ events. These Ca2+ transients are very diverse and occur under different conditions, including in the presence or absence of surrounding circuit activity. This complexity suggests that different signalling mecha

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Cui, Jiangjun, Jaap A. Kaandorp, Olufisayo O. Ositelu, et al. "Simulating calcium influx and free calcium concentrations in yeast." Cell Calcium 45, no. 2 (2009): 123–32. http://dx.doi.org/10.1016/j.ceca.2008.07.005.

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Jones, Bertina F., Rebecca R. Boyles, Sung-Yong Hwang, Gary S. Bird, and James W. Putney. "Calcium influx mechanisms underlying calcium oscillations in rat hepatocytes." Hepatology 48, no. 4 (2008): 1273–81. http://dx.doi.org/10.1002/hep.22461.

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Grusak, Michael A., Brian W. Stephens, and Donald J. Merhaut. "Influence of Whole-plant Net Calcium Influx and Partitioning on Calcium Concentration in Snap Bean Pods." Journal of the American Society for Horticultural Science 121, no. 4 (1996): 656–59. http://dx.doi.org/10.21273/jashs.121.4.656.

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Snap beans (Phaseolus vulgaris L.) are a food source that can contribute to dietary Ca requirements in humans. Factors which might enhance the concentration of Ca in snap bean pods have been investigated by measuring whole-plant net Ca influx, whole-plant Ca partitioning, and various growth parameters in two snap bean cultivars—Hystyle and Labrador—that differ in pod Ca concentration. Plants were grown hydroponically under controlled environmental conditions while being provided adequate quantities of Ca. The concentration of Ca in pods (dry weight basis) was 52% higher in `Hystyle', relative

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Parker, J. C. "Diamide stimulates calcium-sodium exchange in dog red blood cells." American Journal of Physiology-Cell Physiology 253, no. 4 (1987): C580—C587. http://dx.doi.org/10.1152/ajpcell.1987.253.4.c580.

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Calcium influx can be stimulated in dog red blood cells by preexposure to diamide under certain conditions. Diamide-activated calcium influx resembles swelling-induced Ca2+-Na+ exchange in several respects. These include saturation of calcium influx at external calcium levels greater than 0.5 mM, suppression of calcium influx by external sodium, and inhibition by quinidine. The ability of diamide to stimulate this transport pathway depends critically on the ionic composition of the medium in which the cells are bathed at the time of diamide exposure. The effect is greatest if the diamide prein

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37

Reid, Robert J., and F. Andrew Smith. "Regulation of Calcium Influx in Chara." Plant Physiology 100, no. 2 (1992): 637–43. http://dx.doi.org/10.1104/pp.100.2.637.

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Foresta, C. "Calcium influx pathways in human spermatozoa." Molecular Human Reproduction 3, no. 1 (1997): 1–4. http://dx.doi.org/10.1093/molehr/3.1.1.

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Putney, James W., and Takuro Tomita. "Phospholipase C signaling and calcium influx." Advances in Biological Regulation 52, no. 1 (2012): 152–64. http://dx.doi.org/10.1016/j.advenzreg.2011.09.005.

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Chu, Xin, Joseph Y. Cheung, Dwayne L. Barber, et al. "Erythropoietin Modulates Calcium Influx through TRPC2." Journal of Biological Chemistry 277, no. 37 (2002): 34375–82. http://dx.doi.org/10.1074/jbc.m205541200.

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Adapala, Ravi K., Phani K. Talasila, Ian N. Bratz та ін. "PKCα mediates acetylcholine-induced activation of TRPV4-dependent calcium influx in endothelial cells". American Journal of Physiology-Heart and Circulatory Physiology 301, № 3 (2011): H757—H765. http://dx.doi.org/10.1152/ajpheart.00142.2011.

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Transient receptor potential vanilloid channel 4 (TRPV4) is a polymodally activated nonselective cationic channel implicated in the regulation of vasodilation and hypertension. We and others have recently shown that cyclic stretch and shear stress activate TRPV4-mediated calcium influx in endothelial cells (EC). In addition to the mechanical forces, acetylcholine (ACh) was shown to activate TRPV4-mediated calcium influx in endothelial cells, which is important for nitric oxide-dependent vasodilation. However, the molecular mechanism through which ACh activates TRPV4 is not known. Here, we show

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Morgan, Sherif H., Md Abdul Kader, and Sylvia Lindberg. "Cytosolic Sodium Influx in Mesophyll Protoplasts of Arabidopsis thaliana, wt, sos1:1 and nhx1 Differs and Induces Different Calcium Changes." Plants 11, no. 24 (2022): 3439. http://dx.doi.org/10.3390/plants11243439.

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The sodium influx into the cytosol of mesophyll protoplasts from Arabidopsis thaliana cv. Columbia, wild type, was compared with the influx into sos1-1 and nhx1 genotypes, which lack the Na+/H+ antiporter in the plasma membrane and tonoplast, respectively. Changes in cytosolic sodium and calcium concentrations upon a 100 mM NaCl addition were detected by use of epifluorescence microscopy and the sodium-specific fluorescent dye SBFI, AM, and calcium sensitive Fura 2, AM, respectively. There was a smaller and mainly transient influx of Na+ in the cytosol of the wild type compared with the sos1-1

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Dang, An K., Nathan L. Chaplin, Dilyara A. Murtazina, Ulrich Boehm, Colin M. Clay, and Gregory C. Amberg. "Subplasmalemmal hydrogen peroxide triggers calcium influx in gonadotropes." Journal of Biological Chemistry 293, no. 41 (2018): 16028–42. http://dx.doi.org/10.1074/jbc.ra118.001830.

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Gonadotropin-releasing hormone (GnRH) stimulation of its eponymous receptor on the surface of endocrine anterior pituitary gonadotrope cells (gonadotropes) initiates multiple signaling cascades that culminate in the secretion of luteinizing and follicle-stimulating hormones, which have critical roles in fertility and reproduction. Enhanced luteinizing hormone biosynthesis, a necessary event for ovulation, requires a signaling pathway characterized by calcium influx through L-type calcium channels and subsequent activation of the mitogen-activated protein kinase extracellular signal-regulated k

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Wachowiak, Matt, John P. McGann, Philip M. Heyward, Zuoyi Shao, Adam C. Puche, and Michael T. Shipley. "Inhibition of Olfactory Receptor Neuron Input to Olfactory Bulb Glomeruli Mediated by Suppression of Presynaptic Calcium Influx." Journal of Neurophysiology 94, no. 4 (2005): 2700–2712. http://dx.doi.org/10.1152/jn.00286.2005.

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We investigated the cellular mechanism underlying presynaptic regulation of olfactory receptor neuron (ORN) input to the mouse olfactory bulb using optical-imaging techniques that selectively report activity in the ORN presynaptic terminal. First, we loaded ORNs with calcium-sensitive dye and imaged stimulus-evoked calcium influx in a slice preparation. Single olfactory nerve shocks evoked rapid fluorescence increases that were largely blocked by the N-type calcium channel blocker ω-conotoxin GVIA. Paired shocks revealed a long-lasting suppression of calcium influx with ∼40% suppression at 400

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Church, D. J., V. van der Bent, M. B. Vallotton, A. M. Capponi, and U. Lang. "Calcium influx in platelet activating factor-induced atrial natriuretic peptide release in rat cardiomyocytes." American Journal of Physiology-Endocrinology and Metabolism 266, no. 3 (1994): E403—E409. http://dx.doi.org/10.1152/ajpendo.1994.266.3.e403.

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Atrial natriuretic peptide (ANP) is released from the myocardium after the activation of protein kinase C and/or ischemia, events that are associated with an increase in platelet activating factor (PAF) production in this tissue. In this study we demonstrate that PAF, but not lyso-PAF, induces a concentration-dependent increase in ANP secretion in spontaneously beating neonatal rat cardiomyocytes, a response associated with increases in cellular adenosine 3',5'-cyclic monophosphate (cAMP) formation, calcium influx, and the mobilization of calcium from intracellular stores. cAMP formation and c

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Borst, J. G. G., and B. Sakmann. "Effect of changes in action potential shape on calcium currents and transmitter release in a calyx–type synapse of the rat auditory brainstem." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (1999): 347–55. http://dx.doi.org/10.1098/rstb.1999.0386.

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We studied the relation between the size of presynaptic calcium influx and transmitter release by making simultaneous voltage clamp recordings from presynaptic terminals, the calyces of Held and postsynaptic cells, the principal cells of the medial nucleus of the trapezoid body, in slices of the rat brainstem. Calyces were voltage clamped with different action potential waveforms. The amplitude of the excitatory postsynaptic currents depended supralinearly on the size of the calcium influx, in the absence of changes in the time–course of the calcium influx. This result is in agreement with the

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Gillo, B., YS Ma, and AR Marks. "Calcium influx in induced differentiation of murine erythroleukemia cells." Blood 81, no. 3 (1993): 783–92. http://dx.doi.org/10.1182/blood.v81.3.783.783.

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Abstract Murine erythroleukemia cells (MELC) have served as a model for examining the regulation of erythroid differentiation. However, the role of Ca2+ in the signal transduction pathways regulating differentiation remains unclear. To begin to address this uncertainty we have characterized the regulation of cytoplasmic Ca2+ and the possible role of calcium channels during induced differentiation in MELC. MELC can be induced to terminal differentiation using the polar/apolar compound hexamethylene bisacetamide (HMBA). We found that HMBA stimulated Ca2+ influx within 3 to 6 minutes and that Ca2

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Gillo, B., YS Ma, and AR Marks. "Calcium influx in induced differentiation of murine erythroleukemia cells." Blood 81, no. 3 (1993): 783–92. http://dx.doi.org/10.1182/blood.v81.3.783.bloodjournal813783.

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Murine erythroleukemia cells (MELC) have served as a model for examining the regulation of erythroid differentiation. However, the role of Ca2+ in the signal transduction pathways regulating differentiation remains unclear. To begin to address this uncertainty we have characterized the regulation of cytoplasmic Ca2+ and the possible role of calcium channels during induced differentiation in MELC. MELC can be induced to terminal differentiation using the polar/apolar compound hexamethylene bisacetamide (HMBA). We found that HMBA stimulated Ca2+ influx within 3 to 6 minutes and that Ca2+ entry w

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Sadras, Francisco, Teneale A. Stewart, Mélanie Robitaille, et al. "Altered Calcium Influx Pathways in Cancer-Associated Fibroblasts." Biomedicines 9, no. 6 (2021): 680. http://dx.doi.org/10.3390/biomedicines9060680.

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Cancer-associated fibroblasts (CAFs) represent an important component of the tumour microenvironment and are implicated in disease progression. Two outstanding questions in cancer biology are how CAFs arise and how they might be targeted therapeutically. The calcium signal also has an important role in tumorigenesis. To date, the role of calcium signalling pathways in the induction of the CAF phenotype remains unexplored. A CAF model was generated through exogenous transforming growth factor beta 1 (TGFβ1) stimulation of the normal human mammary fibroblast cell line, HMF3S (HMF3S-CAF), and cha

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Weber, Lynn P., Wing L. Chow, Janice Moshenko, Slavica Belsher, and Kathleen M. MacLeod. "Pharmacological investigation of signaling mechanisms contributing to phasic and tonic components of the contractile response of rat arteries to noradrenaline." Canadian Journal of Physiology and Pharmacology 73, no. 5 (1995): 594–601. http://dx.doi.org/10.1139/y95-075.

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The mechanisms contributing to the contractile responses to two different concentrations of noradrenaline (NA) in rat aorta and mesenteric artery were compared using nifedipine, which inhibits calcium influx through dihydropyridine-sensitive channels, ryanodine, which depletes intracellular calcium stores, and calphostin C, which inhibits protein kinase C (PKC). Both submaximal and maximal concentrations of NA induced a biphasic response in aorta and mesenteric artery, with an early fast phase and a later sustained tonic component. Calcium release from intracellular stores contributed to the p

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