Journal articles: 'Influx de calcium'

1

King, Leslie B., and Bruce D. Freedman. "B-lymphocyte calcium inFlux." Immunological Reviews 231, no. 1 (September 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 (January 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 (March 12, 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 (May 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 (October 15, 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 calcium stores and activates store-regulated calcium influx. Econazole blocked 45Ca2+ influx when it was added before TG (IC50 11 microM). Econazole at a concentration (20 microM) that inhibited 83% of TG-induced calcium influx was not inhibitory to TG-induced calcium efflux from 45Ca(2+)-loaded platelets, and did not affect calcium fluxes in resting platelets. This econazole concentration was also inhibitory to calcium influx even when it was added after the stores had been calcium-depleted by EGTA and TG for 15 min and the signal to increase calcium influx had already been generated. Inhibition of cytochrome P-450 with CO bubbled through platelet suspensions did not change calcium influx in resting cells and potentiated TG-induced calcium influx (160% of control calcium accumulation at 20 min). This effect appeared to be concentration-dependent, such that a 5 min exposure to CO produced a greater influx potentiation than a 3 min exposure. These observations indicate that (1) cytochrome P-450 does not mediate store-regulated calcium influx, and (2) econazole probably inhibits store-regulated calcium influx by an alternative mechanism, such as interaction with plasma membrane calcium channels.

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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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7

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

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8

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 (December 1, 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 observed when prostaglandin F2 alpha was mixed with KCl (50 or 100 mM). At all the concentrations tested, adenosine and its analogues [5'-(N-ethyl-carboxamidoadenosine, NECA; N6-(L-2-phenylisopropyl)adenosine, L-PIA] significantly inhibited prostaglandin F2 alpha-induced increases in calcium influx. However, only higher concentrations of adenosine, NECA, and L-PIA inhibited 100 mM KCl-induced calcium influx. Previous treatment with 8-phenyltheophylline blocked the inhibitory actions of adenosine, NECA, and L-PIA on calcium influx. The inhibition of calcium influx by adenosine, NECA, and L-PIA correlated well with their relaxing ability in the presence of prostaglandin F2 alpha. The data suggest that prostaglandin F2 alpha-induced calcium influx was more sensitive to the action of adenosine and its analogues than the calcium influx induced by high K+ depolarization.

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Wang, Chunmin, and Zoltan Machaty. "Calcium influx in mammalian eggs." REPRODUCTION 145, no. 4 (April 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 reticulum, and thus, it is essential to sustain prolonged Ca2+signals. It also seems to be responsible for the stimulation of important signaling cascades required for complete egg activation. Characterization of the pathway that mediates Ca2+entry implies that its major components include STIM1, a protein that senses the filling status of the stores, and ORAI1, a channel protein located in the plasma membrane. Defining the mechanism and functions of Ca2+entry will not only lead to a better understanding of egg physiology but may also help improving the efficiency of a number of assisted reproductive technologies.

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

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11

Parekh, A. B., and R. Penner. "Store depletion and calcium influx." Physiological Reviews 77, no. 4 (October 1, 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 research, the nature of the signal that couples Ca2+ store content to the Ca2+ channels in the plasma membrane has remained elusive. Although ICRAC appears to be the most effective and widespread influx pathway, other store-operated currents have also been observed. Although the Ca2+ release-activated Ca2+ channel has not yet been cloned, evidence continues to accumulate that the Drosophila trp gene might encode a store-operated Ca2+ channel. In this review, we describe the historical development of the field of Ca2+ signaling and the discovery of store-operated Ca2+ currents. We focus on the electrophysiological properties of the prototype store-operated current ICRAC, discuss the regulatory mechanisms that control it, and finally consider recent advances toward the identification of molecular mechanisms involved in this ubiquitous and important Ca2+ entry pathway.

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12

Kwon, Min Seong, Chun Shik Park, Kyeong-rock Choi, Chul-Seung Park, Joohong Ahnn, Jae Il Kim, Soo Hyun Eom, Stephen J. Kaufman, and Woo Keun Song. "Calreticulin Couples Calcium Release and Calcium Influx in Integrin-mediated Calcium Signaling." Molecular Biology of the Cell 11, no. 4 (April 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+concentration. It appeared that intracellular Ca2+release was a prerequisite for Ca2+influx and that calreticulin associated with the integrin cytoplasmic domain mediated the coupling of between the Ca2+release and Ca2+influx. These findings suggest that calreticulin serves as a cytosolic activator of integrin and a signal transducer between integrins and Ca2+channels on the cell surface.

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13

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 (December 1, 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 dendrites; 2) hyperpolarization resulting from K+ channel activation would deinactivate low-threshold, T-type calcium channels on dendrites, increasing calcium influx mediated by these channels; and 3) activation of these receptors would inhibit propagation of action potentials into dendrites, and thus indirectly decrease calcium influx. Activation of adenosine receptors, which couple to Gi proteins, inhibited calcium influx in cell bodies and proximal dendrites without inhibiting action-potential propagation into the proximal dendrites. Inhibition of dendritic calcium influx was not changed in the presence of 50 μM nickel, which preferentially blocks T-type channels, suggesting influx through these channels is not increased by activation of G-proteins. Adenosine inhibited propagation of action potentials into the distal branches of pyramidal neuron dendrites, leading to a three- to fourfold greater inhibition of calcium influx in the distal dendrites than in the soma or proximal dendrites. These results suggest that voltage-gated calcium channels are inhibited in pyramidal neuron dendrites, as they are in cell bodies and terminals and thatG-protein–mediated inhibition of action-potential propagation can contribute substantially to inhibition of dendritic calcium influx.

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14

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 (November 1, 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 inhibitor of calcium influx through VGCC. With the use of the whole cell patch-clamp technique to measure calcium currents, NDGA inhibited inward calcium current through low-threshold VGCC, the only VGCC expressed in C3H/10T1/2 fibroblasts. The inhibitory effects of NDGA on calcium influx and cell proliferation each had a mean inhibitory dose of 2-3 microM. Although NDGA also effectively inhibits cyclooxygenase and lipoxygenase, the addition of prostaglandins or leukotrienes could not reverse this inhibition nor could it be replicated by other antioxidants. These data support the hypothesis that low-threshold VGCC can mediate extracellular calcium influx on the stimulation of cell proliferation by PDGF.

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15

Putney, James W., and Gary S. Bird. "Cytoplasmic calcium oscillations and store-operated calcium influx." Journal of Physiology 586, no. 13 (June 28, 2008): 3055–59. http://dx.doi.org/10.1113/jphysiol.2008.153221.

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16

Baldridge, William H., Dmitri E. Kurennyi, and Steven Barnes. "Calcium-Sensitive Calcium Influx in Photoreceptor Inner Segments." Journal of Neurophysiology 79, no. 6 (June 1, 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 increased 30% with the increase in [Ca2+]o. When external calcium was lowered to 1 mM [Ca2+]o, maximum Ca2+ conductance was reduced, as expected, but the mild depolarization-induced increase in [Ca2+]i was larger than in 3 mM [Ca2+]o. In contrast, when photoreceptors were strongly depolarized, the increase in [Ca2+]i was less when [Ca2+]o was reduced. An explanation for these observations comes from an assessment of Ca2+ channel gating in voltage-clamped photoreceptors under changing conditions of [Ca2+]o. Although Ca2+ conductance increased with increasing [Ca2+]o, surface charge effects dictated large shifts in the voltage dependence of Ca2+ channel gating. Relative to the control condition (3 mM [Ca2+]o), 10 mM [Ca2+]o shifted Ca2+ channel activation 8 mV positive, reducing channel open probability over a broad range of potentials. Reducing [Ca2+]o to 1 mM reduced Ca2+ conductance but shifted Ca2+ channel activation negative by 6 mV. Thus the intracellular calcium signals reflect a balance between competing changes in gating and permeation of Ca2+ channels mediated by [Ca2+]o. In mildly depolarized cells, the [Ca2+]o-induced changes in Ca2+ channel activation proved stronger than the [Ca2+]o-induced changes in conductance. In response to the larger depolarizations caused by 80 mM [K+]o, the opposite is true, with conductance changes dominating the effects on channel activation.

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17

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

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18

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 (July 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 treatment with 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (NCDC), inhibition of protein kinase C (PKC) by staurosporine, or long-term (24 h) treatment with phorbol 12-myristate 13-acetate (PMA) to downregulate PKC abolished most of the osmo-induced, dihydropyridine-sensitive calcium influx signal. Short-term (seconds) PMA treatment to activate PKC produced a marked stimulation of both dihydropyridine-sensitive and -insensitive calcium influx in isotonic (2- to 3-fold stimulation) and hypotonic (5-fold stimulation) conditions. In contrast, elevation of adenosine 3',5'-cyclic monophosphate (cAMP) by treatment with forskolin or inhibition of protein kinase A (PKA) by treatment with the cAMP analog, Rp-8-CPT-cAMPS (the Rp diastereoisomer of adenosine 3',5'-cyclic monophosphothionate), had little or no influence on calcium influx, including dihydropyridine-sensitive calcium influx. It is concluded that osmo-mechanical stress activates a dihyropyridine-sensitive calcium influx pathway that is predominantly regulated via the phosphatidylinositol signaling pathway and PKC and not through the cAMP/PKA signaling pathway.

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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 (December 15, 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 are not altered in dystrophic muscle, but are slowed by the higher resting [Ca2+]i. The defect appears to be specific for calcium since resting free sodium levels and sodium influx rates in the absence of Na+/K(+)-ATPase activity were identical in normal and dystrophic cells when measured with sodium-binding benzofuran isophthalate. Calcium leak channels, whose opening probabilities (Po) were voltage independent, could be the major calcium influx pathway at rest. We have shown previously that calcium leak channel Po is significantly higher in dystrophic myotubes. These leak channels were selective for calcium over sodium under physiological conditions. Agents that increased leak channel activity also increased [Ca2+]i in fibers and myotubes. These results suggest that increased calcium influx, as a result of increased leak channel activity, could result in the elevated [Ca2+]i in dystrophic muscle.

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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 (February 22, 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 cells possess the signalling machinery that permits non-voltage-gated Ca2+ influx to occur. We tested the hypothesis that ryanodine-sensitive Ca2+ pools and activation of RyRs (ryanodine receptors) constitute a signalling pathway capable of inducing Ca2+ influx in 401L cells. We found that 401L cells express mRNA for RyR1 and RyR2 and that RyR activators induced Ca2+ release. Activation of RyRs robustly couples with Ca2+ influx responses in 401L cells, in sharp contrast with absence of Ca2+ influx when cells are treated with SERCA inhibitors. Thus it is clear that 401L cells, despite lacking depletion-induced Ca2+ influx pathways, express the functional components of a Ca2+ influx pathway under the control of RyR function. These findings further support the importance of the 401L cell line as an important cell phenotype for deciphering Ca2+ influx regulation.

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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 (March 1, 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 blocker isradipine had no effect on osm-stimulated ANP secretion, suggesting that calcium influx via voltage-dependent calcium channels was not playing a significant role. Likewise, depleting sarcoplasmic reticulum calcium with 1 microM ryanodine did not block the response to osm, suggesting that calcium influx was not adequate to induce consequential release of calcium from the sarcoplasmic reticulum. To determine whether calcium influx was via Na(+)-Ca2+ exchange, we determined the sodium dependency of osm-stimulated ANP secretion. Replacement of sodium with lithium or choline blocked the secretory response to 100 mosmol/kgH2O. We conclude that osm-stimulated ANP secretion is calcium and sodium dependent. Calcium influx via Na(+)-Ca2+ exchange is highly implicated as the mechanism of cellular calcium entry.

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Zweifach, Adam. "Target-Cell Contact Activates a Highly Selective Capacitative Calcium Entry Pathway in Cytotoxic T Lymphocytes." Journal of Cell Biology 148, no. 3 (February 7, 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 that the mechanism of calcium influx is also different. Second, contact of T cells with antigen-presenting cells or targets involves a host of intercellular interactions in addition to those between antigen–MHC and the T cell receptor. The possibility that calcium influx pathways in addition to those activated via the T cell receptor may be activated by contact with relevant cells has not been addressed. We have used imaging techniques to show that target-cell–stimulated calcium influx in CTLs occurs primarily through CCE. We investigated the permeability of the CTL influx pathway for divalent cations, and compared it to the permeability of CCE in Jurkat human leukemic T cells. CCE in CTLs shows a similar ability to discriminate between calcium, barium, and strontium as CCE in Jurkat human leukemic T lymphocytes, where CCE is likely to mediated by Ca2+ release–activated Ca2+ current (CRAC) channels, suggesting that CRAC channels also underlie CCE in CTLs. These results are the first determination of the mechanism of calcium influx in cytotoxic T cells and the first demonstration that cell contact–mediated calcium signals in T cells occur via depletion-activated channels.

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Papa, Arianne, Jared Kushner, and Steven O. Marx. "Adrenergic Regulation of Calcium Channels in the Heart." Annual Review of Physiology 84, no. 1 (February 10, 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 myocardial relaxation (lusitropy). These effects correlate with increased intracellular concentration of calcium, which is required for the augmentation of cardiomyocyte contraction. Despite extensive investigations, the molecular mechanisms underlying sympathetic nervous system regulation of calcium influx in cardiomyocytes have remained elusive over the last 40 years. Recent studies have uncovered the mechanisms underlying this fundamental biologic process, namely that PKA phosphorylates a calcium channel inhibitor, Rad, thereby releasing inhibition and increasing calcium influx. Here, we describe an updated model for how signals from adrenergic agonists are transduced to stimulate calcium influx and contractility in the heart.

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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 (August 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 presence of lanthanum (an inhibitor of calcium influx by most mechanisms) all three stimuli failed to increase aldosterone secretion. Nifedipine, a dihydropyridine calcium channel antagonist, significantly (P < 0·01) reduced angiotensin II- and potassium-stimulated aldosterone secretion, but had no effect on dbcAMP-stimulated aldosterone secretion (100 ± 14 vs 105 ± 19 pmol/106 cells). Likewise nitrendipine failed to inhibit ACTH-stimulated aldosterone secretion. Angiotension II and potassium activation of both the early aldosterone biosynthetic pathway (as reflected by pregnenolone production in the presence of cyanoketone) and also its late pathway (as reflected by the conversion of exogenous corticosterone to aldosterone in the presence of cyanoketone) were significantly (P < 0·01) inhibited by lanthanum, nifedipine and by reducing the extracellular calcium concentration. However, with dbcAMP stimulation, none of these manipulations modified pregnenolone production. Late pathway activation by dbcAMP was inhibited by lanthanum and a reduction in extracellular calcium, but not by nifedipine. These observations suggest that: (1) the extracellular calcium dependency of dbcAMP-, angiotensin II- and potassium-stimulated aldosterone secretion reflects a need for calcium influx; (2) with dbcAMP stimulation, activation of the late pathway is dependent on calcium influx by a calcium channel-independent mechanism, whereas activation of the early pathway is not dependent on extracellular calcium or calcium influx and (3) activation of both the early and late pathway by angiotensin II and potassium is dependent on calcium influx by a calcium channel-dependent mechanism. Therefore, we conclude that the mechanism of activation of the early aldosterone biosynthetic pathway by dbcAMP is different from angiotensin II or potassium and early pathway activation is distinct from that of late pathway activation with dbcAMP stimulation. J. Endocr. (1986) 110, 315–325

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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 (October 6, 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 mechanisms mediate microdomain events which may then encode specific astrocyte functions from the modulation of synapses up to brain circuits and behaviour. Several recent studies have shown that a subset of astrocyte microdomain Ca2+ events occur rapidly following local neuronal circuit activity. In this review, we consider the physiological relevance of microdomain astrocyte Ca2+ signalling within brain circuits and outline possible pathways of extracellular Ca2+ influx through ionotropic receptors and other Ca2+ ion channels, which may contribute to astrocyte microdomain events with potentially fast dynamics.

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Cui, Jiangjun, Jaap A. Kaandorp, Olufisayo O. Ositelu, Veronica Beaudry, Alicia Knight, Yves F. Nanfack, and Kyle W. Cunningham. "Simulating calcium influx and free calcium concentrations in yeast." Cell Calcium 45, no. 2 (February 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 (June 9, 2008): 1273–81. http://dx.doi.org/10.1002/hep.22461.

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28

Spungin, B., and H. Breitbart. "Calcium mobilization and influx during sperm exocytosis." Journal of Cell Science 109, no. 7 (July 1, 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 bovine sperm that this bacterial PLC can restore actin release from extracted membranes as well as membrane fusion in a cell-free assay when the endogenous PLC is inhibited by neomycin. The sperm PLC requires 2 microM calcium for half maximal activation, while half maximal actin release from extracted plasma membranes occurs at 80 microM. Extracted sperm membranes were examined for calcium pumps and channels. Sperm plasma membranes were found to possess a thapsigargin insensitive calcium pump and calcium channels which are opened by phosphorylation by protein kinase C. The acrosomal membrane possesses a calcium pump which is inhibited by thapsigargin and calcium channels which are opened by cAMP. These observations are discussed in terms of a model of acrosomal exocytosis which involves a calcium rise that occurs in two stages resulting from calcium mobilization from internal stores followed by influx of extracellular calcium.

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Reid, Robert J., and F. Andrew Smith. "Regulation of Calcium Influx in Chara." Plant Physiology 100, no. 2 (October 1, 1992): 637–43. http://dx.doi.org/10.1104/pp.100.2.637.

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30

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

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31

Putney, James W., and Takuro Tomita. "Phospholipase C signaling and calcium influx." Advances in Biological Regulation 52, no. 1 (January 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, Lutz Birnbaumer, Lawrence I. Rothblum, Kathleen Conrad, Virginia Abrasonis, et al. "Erythropoietin Modulates Calcium Influx through TRPC2." Journal of Biological Chemistry 277, no. 37 (July 11, 2002): 34375–82. http://dx.doi.org/10.1074/jbc.m205541200.

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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 (November 1, 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 minute of a 5-min sustained stretch was 46% of that during the first minute of stretch. A single 20% stretch sustained for 6 min caused a 47% increase in calcium efflux, the magnitude of which was linearly related to the degree of cell stretch. Gadolinium and removal of extracellular calcium each partially inhibited stretch-induced calcium efflux. We conclude that a single static stretch of PASMC causes increases in both calcium influx and efflux. Stretch-stimulated calcium influx does not require sodium influx and is mediated in part by a pathway sensitive to both gadolinium and verapamil. Stretch-stimulated calcium efflux is due to both calcium influx via a gadolinium-sensitive pathway and mobilization of intracellular stores. Because calcium is a key cellular second messenger, these effects of stretch on cellular calcium handling may play a role in the regulation of vascular smooth muscle cell phenotype and function.

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Siesjo, BK. "Calcium, Excitotoxins, and Brain Damage." Physiology 5, no. 3 (June 1, 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 (July 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 secretion activated by isoproterenol, bumetanide, and by a fall in the renal perfusion pressure. The inhibitory effect of Ca2+-ATPase inhibition on renin secretion was reversed within seconds by lowering of the extracellular calcium concentration into the submicromolar range but was not affected by lanthanum, gadolinium, flufenamic acid, or amlodipine. These data suggest that calcium influx triggered by release of calcium from internal stores is a powerful mechanism to inhibit renin secretion from juxtaglomerular cells. The store-triggered calcium influx pathway in juxtaglomerular cells is apparently not sensitive to classic blockers of the capacitative calcium entry pathway.

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Bong, Alice Hui Li, Trinh Hua, Choon Leng So, Amelia A. Peters, Mélanie Robitaille, Yin Yi Tan, Sarah J. Roberts-Thomson, and Gregory R. Monteith. "AKT Regulation of ORAI1-Mediated Calcium Influx in Breast Cancer Cells." Cancers 14, no. 19 (September 30, 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 increased calcium influx associated with SC79 is inhibited by silencing AKT2, but not AKT1. This increase in calcium influx is suppressed when the store-operated calcium channel, ORAI1 is silenced. The results from this study open a novel avenue for therapeutic targeting of cancer cells with increased AKT activation. Given the association between ORAI1 and breast cancer, ORAI1 is a possible therapeutic target in cancers with abnormal AKT signaling.

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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 (July 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 to `Labrador', but net Ca influx throughout crop development or total plant Ca content at three stages of development were similar in both cultivars, demonstrating that pod Ca concentration differences were not due to differences in total plant Ca influx. However, `Hystyle' partitioned more total plant Ca to pods, relative to `Labrador'. Calcium flux analysis also revealed that daily rates of whole-plant net Ca influx gradually declined throughout the period of pod growth in both cultivars; this decline was not related to whole-plant water influx. These results suggest that enhancements in whole-plant net Ca influx during pod growth and/or enhancements in the xylem transport of absorbed Ca to developing pods could increase the Ca concentration of snap bean pods.

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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 (August 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, we analyzed spatial profiles of axonal calcium transients during action potentials by selectively staining axons with calcium indicators and subjected the data to theoretical analysis with parameters for axial calcium diffusion empirically determined using photolysis of caged compounds. The results show surprisingly that during action potentials, calcium influx occurs uniformly along an axon of a fully myelinated mouse optic nerve.

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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 (January 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 potential through progressive block of potassium channels. The amplitude of the calcium transient, measured from a cluster of varicosities, was linearly related to the duration of the action potential with a slope of 1.2. Gradual changes in potassium channel block allowed us to estimate the calcium cooperativity of transmitter release over a 10-fold range in presynaptic calcium influx. Calcium cooperativity measured here exhibited one component with an average value of 3.1. Inspection of simultaneously recorded presynaptic calcium transients and inhibitory postsynaptic currents (IPSCs) showed that prolonged action potentials were associated with a slow rising phase of presynaptic calcium transients, which were matched by a slow rate of rise of IPSCs. The close correlation suggests that fluorescence transients provide information on the rate of calcium influx. Because there is an anatomic mismatch between the presynaptic calcium transient, measured from a cluster of varicosities, and IPSC, measured with two-electrode voltage clamp, macropatch recording was used to monitor inhibitory postsynaptic responses from the same cluster of varicosities from which the calcium transient was measured. Inhibitory postsynaptic responses recorded with the macropatch method exhibited a faster rising phase than that recorded with two-electrode voltage clamp. This difference could be attributed to slight asynchrony of transmitter release due to action potential conduction along fine branches. In conclusion, this report shows that fluorescence transients generated by calcium-sensitive dyes can provide insights to the properties of presynaptic calcium influx, and its correlation with transmitter release, at a high time resolution.

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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 (October 1, 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 preincubation is conducted in a hypotonic lithium chloride medium containing at least 1 microM calcium. Stimulation of Ca2+-Na+ exchange is seen at diamide concentrations (0.10-0.33 mM) that are lower than those reported to cause major spectrin cross-linking, glutathione depletion, Ca2+-ATPase inhibition, or ion channel formation. The results suggest that dog red cells have a large latent capacity for Ca2+-Na+ exchange.

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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 (August 28, 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 kinase (ERK). We previously reported that highly localized subplasmalemmal calcium microdomains produced by L-type calcium channels (calcium sparklets) play an essential part in GnRH-dependent ERK activation. Similar to calcium, reactive oxygen species (ROS) are ubiquitous intracellular signaling molecules whose subcellular localization determines their specificity. To investigate the potential influence of oxidant signaling in gonadotropes, here we examined the impact of ROS generation on L-type calcium channel function. Total internal reflection fluorescence (TIRF) microscopy revealed that GnRH induces spatially restricted sites of ROS generation in gonadotrope-derived αT3-1 cells. Furthermore, GnRH-dependent stimulation of L-type calcium channels required intracellular hydrogen peroxide signaling in these cells and in primary mouse gonadotropes. NADPH oxidase and mitochondrial ROS generation were each necessary for GnRH-mediated stimulation of L-type calcium channels. Congruently, GnRH increased oxidation within subplasmalemmal mitochondria, and L-type calcium channel activity correlated strongly with the presence of adjacent mitochondria. Collectively, our results provide compelling evidence that NADPH oxidase activity and mitochondria-derived hydrogen peroxide signaling play a fundamental role in GnRH-dependent stimulation of L-type calcium channels in anterior pituitary gonadotropes.

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Estacion, M., and L. J. Mordan. "Competence induction by PDGF requires sustained calcium influx by a mechanism distinct from storage-dependent calcium influx." Cell Calcium 14, no. 6 (June 1993): 439–54. http://dx.doi.org/10.1016/0143-4160(93)90003-o.

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Adapala, Ravi K., Phani K. Talasila, Ian N. Bratz, David X. Zhang, Makoto Suzuki, J. Gary Meszaros, and Charles K. Thodeti. "PKCα mediates acetylcholine-induced activation of TRPV4-dependent calcium influx in endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 3 (September 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 that ACh-induced calcium influx and endothelial nitric oxide synthase (eNOS) phosphorylation but not calcium release from intracellular stores is inhibited by a specific TRPV4 antagonist, AB-159908. Importantly, activation of store-operated calcium influx was not altered in the TRPV4 null EC, suggesting that TRPV4-dependent calcium influx is mediated through a receptor-operated pathway. Furthermore, we found that ACh treatment activated protein kinase C (PKC) α, and inhibition of PKCα activity by the specific inhibitor Go-6976, or expression of a kinase-dead mutant of PKCα but not PKCε or downregulation of PKCα expression by chronic 12- O-tetradecanoylphorbol-13-acetate treatment, completely abolished ACh-induced calcium influx. Finally, we found that ACh-induced vasodilation was inhibited by the PKCα inhibitor Go-6976 in small mesenteric arteries from wild-type mice, but not in TRPV4 null mice. Taken together, these findings demonstrate, for the first time, that a specific isoform of PKC, PKCα, mediates agonist-induced receptor-mediated TRPV4 activation in endothelial cells.

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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 (December 9, 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 and nhx1 genotypes, in which the influx lasted for a longer time. Sodium chloride addition to the protoplasts’ medium induced a significant increase in cytosolic calcium concentration in the wild type at 1.0 mM external calcium, and to a lesser extent in nhx1, however, it was negligible in the sos1-1 genotype. LiCl inhibited the cytosolic calcium elevation in the wild type. The results suggest that the salt-induced calcium elevation in the cytosol of mesophyll cells depends on an influx from both internal and external stores and occurs in the presence of an intact Na+/H+ antiporter at the plasma membrane. The Arabidopsis SOS1 more effectively regulates sodium homeostasis than NHX1.

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45

Sadras, Francisco, Teneale A. Stewart, Mélanie Robitaille, Amelia A. Peters, Priyakshi Kalita-de Croft, Patsy S. Soon, Jodi M. Saunus, Sunil R. Lakhani, Sarah J. Roberts-Thomson, and Gregory R. Monteith. "Altered Calcium Influx Pathways in Cancer-Associated Fibroblasts." Biomedicines 9, no. 6 (June 16, 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 changes in calcium signalling were investigated. Functional changes in HMF3S-CAF calcium signalling pathways were assessed using a fluorescent indicator, gene expression, gene-silencing and pharmacological approaches. HMF3S-CAF cells demonstrated functionally altered calcium influx pathways with reduced store-operated calcium entry. In support of a calcium signalling switch, two voltage-gated calcium channel (VGCC) family members, CaV1.2 and CaV3.2, were upregulated in HMF3S-CAFs and a subset of patient-derived breast CAFs. Both siRNA-mediated silencing and pharmacological inhibition of CaV1.2 or CaV3.2 significantly impaired CAF activation in HMF3S cells. Our findings show that VGCCs contribute to TGFβ1-mediated induction of HMF3S-CAF cells and both transcriptional interference and pharmacological antagonism of CaV1.2 and CaV3.2 inhibit CAF induction. This suggests a potential therapeutic role for targeting calcium signalling in breast CAFs.

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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 (October 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-ms interstimulus intervals and a recovery time constant of ∼450 ms. Blocking activation of postsynaptic olfactory bulb neurons with APV/CNQX reduced this suppression. The GABAB receptor agonist baclofen inhibited calcium influx, whereas GABAB antagonists reduced paired-pulse suppression without affecting the response to the conditioning pulse. We also imaged transmitter release directly using a mouse line that expresses synaptopHluorin selectively in ORNs. We found that the relationship between calcium influx and transmitter release was superlinear and that paired-pulse suppression of transmitter release was reduced, but not eliminated, by APV/CNQX and GABAB antagonists. These results demonstrate that primary olfactory input to the CNS can be presynaptically regulated by GABAergic interneurons and show that one major intracellular pathway for this regulation is via the suppression of calcium influx through N-type calcium channels in the presynaptic terminal. This mechanism is unique among primary sensory afferents.

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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 (March 1, 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 calcium influx appear to play major roles in PAF-induced ANP secretion in this system, insofar as PAF-induced ANP release was substantially reduced in the presence of the (R)-p-diastereoisomer of adenosine 3',5'-cyclic monophosphorothioate (10 microM), whereas both PAF-induced calcium influx and ANP secretion were abolished in the presence of the calcium channel antagonist nifedipine (0.1 microM). Consistent with these results, N6-2'-O-dibutyryl cAMP (DBcAMP, 10 microM) and/or forskolin (0.1 microM) simultaneously increased cAMP production, calcium influx, and ANP release in these cells, with both DBcAMP- and forskolin-induced ANP secretion being fully abolished in the presence of 0.1 microM nifedipine. Taken together, these results suggest that PAF, DBcAMP, and forskolin promote ANP secretion in spontaneously beating cardiomyocytes via the activation of a cAMP-dependent, nifedipine-sensitive myocardial calcium channel and that calcium influx is a major requirement for cAMP-induced ANP secretion in this system.

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Jaffe, Lionel F. "Stretch-activated calcium channels relay fast calcium waves propagated by calcium-induced calcium influx." Biology of the Cell 99, no. 3 (March 2007): 175–84. http://dx.doi.org/10.1042/bc20060031.

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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 (February 28, 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 view thact at this synapse most vesicles are released by the combined action of multiple calcium channels.

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Menè, Paolo, Anna Teti, Francesco Pugliese, and Giulio A. Cinotti. "Calcium release-activated calcium influx in cultured human mesangial cells." Kidney International 46, no. 1 (July 1994): 122–28. http://dx.doi.org/10.1038/ki.1994.251.

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Journal articles on the topic 'Influx de calcium'

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