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Добірка наукової літератури з теми "Influx de calcium"

Автор: Grafiati

Опубліковано: 2 листопада 2024

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Статті в журналах з теми "Influx de calcium"

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 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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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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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 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 (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 (2006): R548—R550. http://dx.doi.org/10.1016/j.cub.2006.06.036.

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Дисертації з теми "Influx de calcium"

Wang, Fang. "DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?" Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/214814.

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Physiology Ph.D. Cardiovascular disease remains the number one cause or mortally in the western world. Heart failure is the most rapidly growing cardiovascular disease (Hobbs, 2004; Levy, et al., 2002). Heart failure, by definition, is progressive deteriorating function of the heart due to progressive cardiac myocytes loss. Though after decades of endeavor of searching the pathophysiology and treatments for heart failure, it remains highly lethal. Therefore, it is vital to find novel therapies to help treat such chronic disease. Replace the lost cardiomyocyte with new ones could restore cardiac function and reduce mortality. The purpose of this study is to investigate on how TTCCs (T-type calcium channels) affect cardiomyocyte proliferation. In mice after birth, the major TTCC expressed in the heart is Cav3.1/α1G, and therefore we used Cav3.1/α1G transgenic (TG), knockout (-/-) and wild type mice respectively to define the role of TTCC in cardiomyocyte proliferation. In neonatal mouse ventricular myocyte (NMVMs) right after birth, there is almost no TTCC after birth in α1G-/- NMVMs, whereas there are around 35% NMVMs in wild type (WT) show TTCC. On day 7 after birth, there are no T-type calcium currents in both α1G-/- NMVMs and WT NMVMs. Using BrdU, a DNA synthesis marker, we identified plenty of BrdU positive cardiomyocyte during the first seven days after birth. Cardiomyocyte is special due to its double nucleation property. Our cell cycle studies showed that there is significant difference in cell cycle distribution between α1G-/- and WT NMVMs on day seven after birth. Significantly more NMVMs are arrested in G1 phase in α1G-/-, compared to WT NMVMs. Even until 2 month old, there are still significantly more mono-nucleated cardiomyocyte in α1G-/- than in WT. In conclusion, all these evidence showed that blocking T-type calcium channel could partially prevent binucleation from happening and stop cardiomyocytes withdrawal from cell cycle. Mononucleated cardiomyocyte is still able to proliferate. Hence, mononucleated cardiomyocytes in adult still have potential to proliferation because these cardiomyoctes are arrested in their cell-cycle before their terminal differentiation, which could offer a novel approach for cardiac repair. Temple University--Theses

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Yang, Meng. "Calcium influx, celluar signaling and the biology of candida albicans." Thesis, University of Aberdeen, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499748.

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FIG1 is a gene that encodes a transmembrane protein involved in calcium influx a process that is important for stress responses in pathogens fungi such as Candida albicans. A Cafig1 null mutant took up less calcium ions in mating than control strains confirming its role in Ca2+ uptake. Furthermore, C. albicans strains with deletions of FIG1 in other calcium channel mutant backgrounds displayed distinctive phenotypes under vegetative growth conditions, which suggested that Fig1 may be a regulator of other calcium influx systems. Using GFP and LacZ reporter constructs it was shown that in C. albicans FIG1 was induced by mating pheromone and during the interactions of strains of compatible mating type. Localization of Fig1-GFP studied by con-focal imaging showed that the protein had a peri-nuclear distribution and was also found in the plasma membrane at the tips of shmoos. The protein appeared to be located within microdomains and the protein sequence was found to contain a putative site for cysteine palmitoylation that may promote such localization. Because the expression of FIG1 was strongly induced during mating, the induction of FIG1 was used to try to detect where mating took place during experimental infection in mice. Surprisingly FIG1 expression could be observed in the murine gut in control inoculations using C. albicans strains that could not undergo mating. Therefore FIG1 expression is not always strictly mating-dependent. MAP kinases and calcium-calcineurin signalling pathways, in which Fig1 is involved, were studied using bioinformatics approaches. It was shown that these signalling pathways contain conserved signalling components taking part in signal transduction via phosphorelay but they had diverged receptors, sensors, effectors, and phosphorelay regulators across different fungal species.

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Pejović, Vojislav. "Glutamate induced potentiation of calcium influx in primary hippocampal culture neurons." [S.l.] : [s.n.], 2001. http://ArchiMeD.uni-mainz.de/pub/2001/0027/diss.pdf.

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McVicker, Clare Geldard. "Calcium influx mechanisms during mediator-induced responses in human airway smooth muscle." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404814.

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Makarewich, Catherine Anne. "MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/266828.

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Molecular and Cellular Physiology Ph.D. Pathological cardiac stressors, including persistent hypertension or damage from ischemic heart disease, induce a chronic demand for enhanced contractile performance of the heart. The cytosolic calcium (Ca2+) transient that regulates myocyte contraction must be persistently increased in disease states in order to maintain cardiac output to sustain the metabolic requirements of the body. Associated with this enhanced intracellular Ca2+ ([Ca2+]i) state is pathological cardiac myocyte hypertrophy, which results in large part from the activation of Ca2+-dependent activation of calcineurin (Cn)-nuclear factor of activated T cells (NFAT) signaling. The puzzling feature of this hypertrophic signaling is that the cytosolic [Ca2+] that controls contractility appears to be separate from the [Ca2+] which activates Cn-NFAT signaling. The overarching theme of this dissertation is to explore the source and spatial constraints of pathological hypertrophic signaling Ca2+ and to investigate how it is possible that sensitive and finely tuned Ca2+-dependent signaling pathways are regulated in the background of massive Ca2+ fluctuations that oscillate between 100nM and upwards of 1-2μM during each cardiac contractile cycle. L-type Ca2+ channels (LTCCs) are a major source of Ca2+ entry in cardiac myocytes and are known to play an integral role in the initiation of myocyte excitation contraction-coupling (EC-coupling). We performed a number of experiments to show that a small population of LTCCs reside outside of EC-coupling domains within caveolin (Cav-3) signaling microdomains where they provide a local source of Ca2+ to activate Cn-NFAT signaling. We designed a Cav-targeted LTCC blocker that could eliminate Cn-NFAT activation but did not reduce myocyte contractility. The activity of Cav-targeted LTCCs could also be upregulated to enhance hypertrophic signaling without affecting contractility. Therefore, we believe that caveolae-localized LTCCs do not participate in EC-coupling, but instead act locally to control the coordinated activation of Cn-NFAT signaling that drives pathological remodeling. Transient Receptor Potential (TRP) channels are also thought to provide a source of Ca2+ for activation of hypertrophic signaling. The canonical family of TRP channels (TRPC) is expressed at low levels in normal adult cardiac tissue, but these channels are upregulated in disease conditions which implicates them as stress response molecules that could potentially provide a platform for hypertrophic Ca2+ signaling. We show evidence that TRPC channel abundance and function increases in cardiac stress conditions, such as myocardial infarction (MI), and that these channels are associated with hypertrophic responses, likely through a Ca2+ microdomain effect. While we found that TRPC channels housed in caveolae membrane microdomains provides a source of [Ca2+] for induction of cardiac hypertrophy, this effect also requires interplay with LTCCs. We also found that TRPC channels have negative effects on cardiac contractility, which we believe are due to local activation of Ca2+/calmodulin-dependent protein kinase (CaMKII) and subsequent modulation of ryanodine receptors (RyRs). Further, we found that inhibiting TRPC channels in a mouse model of MI led to increased basal myocyte contractility and reduced hypertrophy and cardiac structural and functional remodeling, as well as increased survival. Collectively, the data presented in this dissertation provides comprehensive evidence that Ca2+ regulation of Cn-NFAT signaling and resultant pathological hypertrophy can be coordinated by spatially localized and regulated Ca2+ channels. The compartmentalization of LTCCs and TRPC channels in caveolae membrane microdomains along with pathological hypertrophy signaling effectors makes for an attractive explanation for how Ca2+-dependent signaling pathways are regulated under conditions of continual Ca2+ transients that mediate cardiac contraction during each heart beat. Elucidation of additional Ca2+ signaling microdomains in adult cardiac myocytes will be important in more comprehensively resolving how myocytes differentiate between signaling versus contractile Ca2+. Temple University--Theses

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Kortekaas, Phaedra. "Development and function of calcium influx in pyramidal neurons of the hippocampal CA1 region." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/55584.

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DeJong, Danica. "Calcium Alleviates Symptoms in Hyperkalemic Periodic Paralysis by Reducing the Abnormal Sodium Influx." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23487.

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Hyperkalemic periodic paralysis, HyperKPP, is an inherited progressive disorder of the muscles caused by mutations in the voltage gated sodium channel (NaV1.4). The objectives of this thesis were to develop a technique for measurement symptoms in vivo using electromyography (EMG) and to determine the mechanism by which Ca2+ alleviates HyperKPP symptoms, since this is unknown. Increasing extracellular [Ca2+] ([Ca2+]e) from 1.3 to 4 mM did not result in any increases in45Ca2+ influx suggesting no increase in intracellular [Ca2+] ([Ca2+]i) acting on an intracellular signaling pathway or on an ion channel such as the Ca2+sensitive K+ channels. HyperKPP muscles have larger TTX-sensitive22Na+ influx than wild type muscles because of the defective NaV1.4 channels. When [Ca2+] was increased from 1.3 to 4 mM, the abnormal 22Na+ influx was completely abolished. Thus, one mechanism by which Ca2+alleviates HyperKPP symptoms is by reducing the abnormal Na+ influx caused by the mutation in the NaV1.4 channel.

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Hoffman, Nicholas. "Mitochondrial Calcium Influx is Determined by Multiple Protein Components Including SLC25A23 and MICU1." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/287159.

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Biochemistry Ph.D. Ca2+ control mechanisms employed by the cell at the plasma membrane include receptor operated, voltage-sensitive, and store operated channels for Ca2+ import. Upon entry into the cytosol, Ca2+ is sequestered by Ca2+ binding proteins, the endoplasmic reticulum (ER), or by mitochondria. The largest Ca2+ store in the cell is the ER where Ca2+ levels approach millimolar levels. The ER regulates cytosolic Ca2+ homeostasis by using Ca2+ binding proteins, the SERCA pump, second messenger Ca2+ release upon IP3 receptor activation, and Ca2+-induced Ca2+ release by ryanodine receptors. Basal cytosolic Ca2+ levels are maintained at around 100nM. The mitochondria begins clearing GPRC-depended cytosolic Ca2+elevation after a short time delay during which the cytosolic Ca2+ concentration exceeds 3M. Then, the mitochondria sacrifices a portion of its membrane potential to drive Ca2+ influx across the mitochondrial inner membrane into the matrix. The membrane potential of the mitochondria is created in part by the electron transport, which while transferring electrons, ejects protons from the matrix to the inner membrane space. The rapid mitochondrial Ca2+ uptake decreases mitochondrial membrane potential thus reducing or fully collapsing the mitochondria's ability to generate ATP. This uncoupling of the electron transport chain results in ROS production and decreased cell survival. Mitochondria provide the body with energy that allows a heart to beat, a brain to store memories, and fuels locomotive function. As a stand-alone energy generator, the mitochondria would be interesting, but not dynamic. The dynamic flow of information to the mitochondria through Ca2+ signaling with all the components of symbiotic precision is a true biological phenomenon. In the mitochondria, a complex Ca2+ buffering system of channels, pores, and exchangers directly affects the conversion of chemical potential to ATP. Recent, discoveries of the Ca2+ uniporter (MCU) and other system components have provided the tools to tackle levels of mitochondrion physiologic studies that were not possible only a couple of years ago. There remains a great need for advancement in the understanding of mitochondrial bioenergetics, and undoubtedly, the mitochondria will be viewed as a determinant factor for survival. The mitochondrial inner membrane through its curious construction of 3:1 protein to lipid ratio, carefully regulates the permeability of ions and metabolites. The transport of Ca2+ and other small ions across the inner membrane is an essential signaling pathway for mitochondrial maintenance of metabolic functions, but the mechanisms are still unclear due to a lack of mitochondrial systems biology. For example, the oligomeric MCU with two transmembrane domains is a core component of the major Ca2+ import pathway in mitochondria, and ablation of MCU lowers mitochondrial Ca2+ uptake, however portions such as the highly conserved linker between the two transmembrane was unstudied until recently. Other complex components such as MICU1 and MCUR1, which negatively and positively regulate MCU, are beginning to have their mechanism solved. MICU1 is associated with the mitochondrial inner membrane and has two EF hands, which indicated a possible role in Ca2+ sensing. This role as a Ca2+ sensor proved to be necessary for proper MICU1 inhibition of MCU, but not determinant of MICU1/MCU interaction. MICU1, MCUR1, and MCU are modified in numerous diseases in which a particular component is disproportionately expressed. This is in part due to the classical coupling of gene function to associated transcription factor meaning that because MICU1, MCUR1, and MCU have a Ca2+ flux function, their transcription is also probably controlled by Ca2+ and is altered in chronic inflammation or hypoxic systems such as Ca2+ overload during ischemia/reperfusion. In spite of the low affinity of uniporter, mitochondrial Ca2+ overload occurs due to the close proximity of mitochondria to the ER, however physical tethering of the mitochondria and ER is still not widely accepted. When Ca2+ is physiologically cleared from the cytosol to the mitochondria, it acts as a synchronizing signal to the numerous EF hands present on inner membrane transmembrane proteins and matrix-targeted proteins. . Synchronization of mitochondrial activities is critical for efficiency which has direct implication for both cell growth or damage through the byproduct of inefficiency, mROS (superoxide). Therefore, the EF hands and other Ca2+ response elements enhance the ratio of ATP to superoxide, thus supporting mitogenic function and healthy growth. The inefficient flow of energy leads to dysfunction such as the release of reactive oxygen species (ROS) from the mitochondria. ROS carries its own energy in the chemical form of a radical. This translates into thermodynamically favorable but harmful cellular damage. Sustained import of Ca2+ results in electron transport malfunction followed by loss of membrane potential as seen in ischemia. A common EF hand motif exists on many calcium sensitive proteins. This helix-loop-helix topology recognizes a specific range of calcium concentrations based on the primary and tertiary structure of the domain. Thus, not all EF hands are active at a given physiological Ca2+ concentrations. The Ca2+ is situated in the loop portion by 12 key interactions in a pentagonal bipyramidal geometry. The position of 12th residue supplies two of the interacting oxygen atoms for Ca2+ binding and are conserved as either Glutamate or Aspartate. EF-hand containing proteins do not necessarily transport Ca2+ alone, as many other solutes have also been reported. The EF hand motif can be found on many mitochondrial sensors including LETM-1, MICU1, and non- Ca2+ transporters (Nakayama, Moncrief et al. 1992), suggesting Ca2+ is often the synchronizing signaling molecule but not necessarily transported by the mitochondrial channel of interest. The discovery of the uniporter (MCU) is an exciting event in the field, as many relationships between different transport mechanisms affecting Ca2+ and membrane potential will be elucidated. One such relationship that should be explored is between the uniporter and inorganic phosphate exchange. This relationship may modulate cell death through a critical uptake dynamic between adenine, phosphate and Ca2+ through alternative pathways such as solute carriers. Mitochondrial carriers are crucial for transport across the inner membrane. There are two groups of Ca2+ binding solute carriers in the mitochondria, the aspartate/glutamate carriers (Palmieri, Pardo et al. 2001) and the ATP-magnesium carriers (SCaMC) (Satrustegui, Pardo et al. 2007). Carrier proteins transport molecules by changing shape and therefore can be saturated. Solute carrier activators have been previously reported to include Ca2+, adenosine 3'5'-cyclic monophosphate, protein kinases, and inositol polyphosphates (Dransfield and Aprille 1993). Other previous work has also reported transport of multiple different solutes (Fiermonte, De Leonardis et al. 2004). The higher eukaryote, vertebrate calcium systems, should functionally if not physically interact with conserved lower eukaryote systems such as solute carriers. All known mitochondrial carriers are members of the same family based on three tandem repeats and are predicted to function as oligomers. The human family of these inner mitochondrial membrane proteins is SLC25, and members of the SLC25 family have been identified as the cause of Stanley Syndrome and Amish Microcephaly suggesting the importance of SLC25. SLC25A23 has been proposed to be an ATP-Mg/Pi exchange carrier that allows for both uptake and release of ATP-Mg from mitochondria. As a putative ADP/Pi translocase, it is an interesting component as both ADP and Pi have been shown to play a role in cell survival and cell death. This SLC25A family member is likely to be the critical regulator of these two dynamic molecules. These carriers are stimulated by submicromolar Ca2+ to regulate adenine nucleotide levels in the cytosol and mitochondria. Previous literature has shown SLC25A25 knockout to have little effect on mouse metabolism. SLC25A24 has been shown to be involved in ADP/ATP ratios in the mitochondrial matrix resulting in cytosolic Ca2+ buffering enhancement (21). The functions of SLC25A23 largely remain unknown. It should be pointed out that SLC25A23, SLC25A24, and SLC25A25, Ca2+ induced changes, are not necessarily based on Ca2+ as a channel solute. The ATP/ADP maintained by SLC25 family members may contribute to Ca2+ uptake in the mitochondria and therefore may play a role in cell death through PTP opening. PTP opening is a point of convergence for many cell death pathways. The PTP, which behaves as a voltage-operated channel, can be triggered to open by high mitochondrial Ca2+, ROS, or low membrane potential. In previous studies, SLC25A24 knockdown resulted in increased PTP opening and decreased Ca2+ buffering. Solute carrier family 25 (mitochondrial carrier; phosphate carrier), which includes SLC25A23, SLC25A24, and SLC25A25, transport solutes across the inner membrane, are predicted to form six transmembrane domains sensitive to Ca2+ due to four Ca2+ binding EF hand motifs, and localize to the mitochondria (del Arco and Satrustegui 1998; Iijima, Yamamoto et al. 2001). Based on membrane topology predictions, SLC25 isoforms contain six transmembrane domains with several EF hand motifs. Although the solute carriers in the SCaMC family have been hypothesized to transport adenine, (Aprille 1988) they have never been fully characterized. Mitochondrial solute carriers are found only in eukaryotes (Carafoli and Lehninger 1971; Uribe, Rangel et al. 1992; Palmieri 2004), however Sal1 in yeast has high sequence homology (Kucejova, Li et al. 2008). SLC25A25 knockout was reported to have little effects on mouse metabolism. SLC25A24 has been shown to be involved in ADP/ATP ratios in the mitochondrial matrix resulting in cytosolic Ca2+ buffering enhancement (Traba, Del Arco et al. 2011). The functions of these solute carriers in mitochondrial Ca2+ uptake and mitochondrial ROS are largely unknown. Temple University--Theses

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Torihashi, Shigeko, Toyoshi Fujimoto, Claudia Trost, Shinsuke Nakayama, and 茂子鳥橋. "Calcium oscillation linked to pacemaking of interstitial cells of Cajal;Requirement of calcium influx and localisation of TRP4 in caveolae." The American Society for Biochemistry and Molecular Biology, 2002. http://hdl.handle.net/2237/7447.

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Obolensky, Anna. "Pharmacological modulation of calcium influx in freshly isolated rat lymphocytes and lymphoma cell lines." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249555.

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Книги з теми "Influx de calcium"

Perrella, Joel. Effect of estrogen on glutamate-induced neuronal cell death and calcium influx. 2005.

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Heine, Christopher L. Malignant Hyperthermia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0025.

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In this chapter we discuss the pathophysiology of malignant hyperthermia, identify those who are known to be susceptible to MH, delineate how best to prepare the operating for those patients, and provide step by step treatment recommendations for patients that develop MH. Malignant hyperthermia (MH) is a pharmacogenetic disease. When susceptible individuals are exposed to a triggering agent, a hypermetabolic response develops. Succinylcholine and halogenated, inhaled anesthetics are triggers of MH. The MH reaction is initiated by a rapid influx of calcium ions into the myoplasm that triggers uncontrolled muscle contraction. Prompt recognition and treatment of the reaction is critical to a successful outcome.

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Fomberstein, Kenneth, Marissa Rubin, Dipan Patel, John-Paul Sara, and Abhishek Gupta. Perioperative Opioid Analgesics of Use in Pain Management for Spine Surgery. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0004.

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This chapter compares the basic properties of several opioid analgesics and explores their applications in perioperative pain control in spine surgery. Parenteral opioids have long been the cornerstone of treatment for postoperative pain; they work by inhibiting voltage-gated calcium channels and increasing potassium influx, which results in reduced neuronal excitability, thereby inhibiting the ascending transmission of painful stimuli and activating the descending inhibitory pathways. This chapter reviews concepts including opioid conversion and rotation, opioid tolerance, and opioid cross-tolerance. It discusses common opioid side effects, and it explores the perioperative use of several specific opioids including remifentanil, sufentanil, methadone, oxycodone, morphine, and tapentadol and discusses their use in spine surgery. Additionally, this chapter discusses patient-controlled analgesia (PCA) and its importance in postoperative pain control.

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Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.

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Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes the nerve membrane resting potential. When activated by a voltage change to threshold, sodium influx generates an action potential, or a sudden alteration in membrane potentials, that can be conducted along an axon. The myelin sheaths around an axon, increase the speed of conduction and conserve energy. The pathology of MS disrupts the myelin structures, disturbs conduction, and leads to neurodegeneration. Ion channels have been the target of investigation for both restoration of conduction and neuroprotection.

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Частини книг з теми "Influx de calcium"

Belrose, Jillian C., Fabiana A. Caetano, Kai Yang, Brian M. W. Lockhart, Michael F. Jackson, and John F. MacDonald. "Mechanisms of Calcium Influx Following Stroke." In Metal Ion in Stroke. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-9663-3_2.

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Petersen, O. H. "Control of Calcium Influx and Internal Calcium Release in Electrically Non-Excitable Cells." In Calcium Transport and Intracellular Calcium Homeostasis. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_2.

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Ghazal, Nasab, and Jennifer Q. Kwong. "Analyzing Mitochondrial Calcium Influx in Isolated Mitochondria." In Methods in Molecular Biology. Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-4164-4_12.

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Taschenberger, Holger, Kun-Han Lin, and Shuwen Chang. "Presynaptic Ca2+ Influx and Its Modulation at Auditory Calyceal Terminals." In Modulation of Presynaptic Calcium Channels. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6334-0_9.

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Borowiec, Anne-Sophie, Gabriel Bidaux, and Thierry Capiod. "Are Calcium Channels More Important Than Calcium Influx for Cell Proliferation?" In Trends in Stem Cell Proliferation and Cancer Research. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_4.

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Colucci, Wilson S., and Giovanni Sperti. "Phorbol Esters Stimulate Calcium Influx via Voltage-Dependent Channels in A7r5 Vascular Smooth-Muscle Cells." In Cell Calcium Metabolism. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_9.

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Yagodin, Sergey, Lynne A. Holtzclaw, and James T. Russell. "Subcellular calcium oscillators and calcium influx support agonist-induced calcium waves in cultured astrocytes." In Signal Transduction Mechanisms. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2015-3_15.

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Hanson, John B., Magaly Rincon, and Sharon A. Rogers. "Controls on Calcium Influx in Corn Root Cells." In Molecular and Cellular Aspects of Calcium in Plant Development. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2177-4_31.

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MacKenzie, E. T., and J. McCulloch. "Glutamate Antagonism as a Pharmacological Approach to Prevent Calcium Influx in Focal Cerebral Ischemia." In Cerebral Ischemia and Calcium. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_22.

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Bers, Donald M. "Calcium influx and sarcoplasmic reticulum calcium release in cardiac excitation-contraction coupling." In Developments in Cardiovascular Medicine. Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3311-8_5.

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Тези доповідей конференцій з теми "Influx de calcium"

Lange, Ingo, and Dana-Lynn T. Koomoa. "Abstract 3781: MYCN-induced TRPM7 mediates calcium influx and promotes neuroblastoma cell migration." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3781.

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Jetta, Deekshitha, Deepika Verma, Mohammad M. Maneshi, and Susan Z. Hua. "Shear Stress Induced Calcium Dependent Nuclear Deformation in Epithelial Cells." In ASME 2018 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/imece2018-87650.

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External mechanical forces can reach the cell nucleus causing changes in nuclear morphology, size and motility. A common explanation is that these forces are transmitted by surrounding cytoskeleton network through its linkage to nuclear envelope; shear stress causes reorganization of cytoskeleton, thus, the changes in nuclear shape. In this study, we measured nuclear shape and intracellular Ca2+ under fluid shear stress in MDCK cells using a parallel plate microfluidic chip. We show that fluid shear stress (1.1 dyn/cm2, 3 hrs) causes significant changes in nuclear shape in cells, from a flat disk shape having larger area to a thicker disk having smaller area. An increase in intracellular Ca2+ is required for shear induced nucleus deformation. Inhibiting Ca2+ influx with GsMTx4 and Gd3+ eliminated Ca2+ influx and abolished the nuclear deformation. The cytoskeleton reorganization occurred in parallel with Ca2+ rise in the cells. Increasing intracellular Ca2+ with thapsigargin that depletes the Ca2+ stores resumed the nuclear deformation. This suggests that shear induced nuclear deformation is a Ca2+ dependent process.

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Mecklenburg, Anne, Anton Albrecht, Franziska Gniech, Cynthia Olotu, Sven Hammerschmidt, and Rainer Kiefmann. "In Pulmonary Endothelial Cells Calcium Signaling By S. Pneumoniae Is Regulated By Calcium Influx From The Extracellular Space But Also By Calcium Release From Intracellular Stores." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3281.

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Sadras, Francisco, Teneale A. Stewart, Melanie Robitaille, et al. "Abstract P6-06-15: Remodelling of calcium influx pathways in breast cancer associated fibroblasts." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p6-06-15.

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Xu, Ningyong, Donna L. Cioffi, Xiaogang Wang, Eugene A. Cioffi, Mikhail Alexeyev, and Troy Steves. "Orai1 Is A Critical Determinant Of Sodium Influx Through Store Operated Calcium Entry Channels." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5510.

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Fuzimoto, T., K. Fuzimura, and A. Kuramoto. "MEASUREMENT OF PLATELET IONIZED CALCIUM IN PATIENTS WITH MYELOPROLIFERATIVE DISORDERS BY AEQUORIN METHOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644573.

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In myeloproliferative disorders(MPD), bleeding tendency and thrombosis are encountered occasionally in the presence of high platelet counts. It has been reported that there are some abnormalities of membrane glycoprotein or arachidonate metabolism in platelets of MPD. We measured the intracellular change of calcium levels[Cai2+] after stimulation in platelets of the patients with MPD by Aequorin method. Eleven cases of chronic myelogenous leukemia(CML), 7 cases of polycythemia vera(PV), 4 cases of essential thrombocythemiaCET^ and 12 normal adults were studied, and as stimulators 0.5 U/ml thrombin and 2.5 μg/ml collagen were used. In the patients with CML, PV and ET, maximum intracellular calcium level was significantly lower and the reaction period reaching to the peak calcium level(the arrival time) was significantly prolonged than the normals after thrombin stimulation. On collagen stimulation, maximum[Cai2+] level in patient with CML and PV was significantly lower and the arrival time in patient with CML and ET was significantly prolonged than the normals. No correlation was found between maximum [Cai2+] level and maximum aggregation rate or platelet counts in those patients. The increasing rate of intracellular calcium levels after stimulation with A23187 in the presence of various concentration of extracellular calcium was proved lower in CML than in the normal. [45Ca2+] uptake rate into the CML platelets after thrombin stimulation showed lower rate compaired with normals. These results suggest that platelets in patients with MPD have some abnormalities of calcium influx mechanism. We already reported that platelet membrane glycoprotein (GP)IIIa was increased significantly in MPD platelets. The study is going to examine the relationship between this membrane abnormality and impaired calcium influx in MPD.

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Erickson, Geoffrey R., and Farshid Guilak. "Osmotic Stress Initiates Intracellular Calcium Waves in Chondrocytes Through Extracellular Influx and the Inositol Phosphate Pathway." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0580.

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Abstract The biophysical environment of the chondrocytes plays an important role in the health, turnover, and homeostasis of articular cartilage. Under normal physiologic loading, chondrocytes are exposed to a complex and diverse array of biophysical signals, including mechanical and osmotic stresses, fluid flow, and fluid pressures [4]. Due to the charged and hydrated nature of the extracellular matrix, mechanical compression causes exudation of interstitial fluid in cartilage, which alters the osmotic environment of the chondrocytes. Confocal microscopy studies have shown that chondrocytes lose or gain volume in response to tissue compression [4] or changes in extracellular osmolarity [3]. The active process of volume recovery subsequent to osmotic shock has been shown to initiate intracellular signaling cascades [2], which may in turn alter cellular metabolism [6]. Although the mechanisms of intracellular signaling in response to osmotic stress are not fully understood, it has been hypothesized that intracellular transients and oscillations of calcium ion (Ca2+) are involved. The objective of this study was to examine the hypothesis that osmotic stress initiates a transient increase in the concentration of intracellular calcium ion ([Ca2+]i), and to determine the mechanisms of Ca2+ mobilization in isolated chondrocytes exposed to hypo- and hyper-osmotic stress.

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Monteith, Greg, Francisco Sadras, Teneale Stewart, et al. "Abstract 99: Remodeling of calcium influx pathways in models of cancer associated fibroblasts in breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-99.

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Kingston, P. R., K. R. Bruckdorfer, and R. A. Hutton. "AGONIST INDUCED CALCIUM MOBILISATION IN PLATELETS OF PATIENTS WITH "ASPIRIN-LIKE" DEFECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644570.

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A group of patients have been described with a condition often referred to as an'Aspirin-like" defect, which is characterised by easy bruising and prolonged bleeding following dental extraction or surgery. Initial studies eliminated a deficiency in coagulation factors, plasma factors, platelet glycoproteins or platelet storage granules as being the cause of this condition and demonstrated a diminished aggregatory and/or secretory response in platelet-rich-plasma to ADP and collagen. Aggregation responses in isolated platelets to thrombin, arachidonic acid and ionomycin are within the normal range, however the response to AD? is dimished. Recent studies have concentrated on the various mechanisms involved in platelet aggregation amongst which is the change in intracellular calcium concentration with accompanied secretion.Using the fluorescent indicator quin2 we have monitored the intracellular calcium changes induced by various agonists in the presence and absence of extracellular calcium in five patients with an "Aspirin-like" defect. In the presence of ImM extracellular calcium, thrombin and ionomycin caused a rapid elevation in intracellular calcium to greater than 1μM within 30 seconds of stimulation. In the absence of extracellular calcium, thrombin and ionomycin caused rises in intracellular calcium of 200nM and 300nM respectively. All the responses observed were within the normal range and indicate that both influx of extracellular calcium and mobilisation of calcium from internal stores has occurred. Therefore the defect that causes this "Aspirin-like" condition is not commonly associated with a defect in calcium mobilisation.

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Звіти організацій з теми "Influx de calcium"

Yalovsky, Shaul, and Julian Schroeder. The function of protein farnesylation in early events of ABA signal transduction in stomatal guard cells of Arabidopsis. United States Department of Agriculture, 2002. http://dx.doi.org/10.32747/2002.7695873.bard.

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Loss of function mutations in the farnesyltransferase β subunit gene ERA1 (enhanced response to abscisic acid), cause abscisic acid hypersensitivity in seedlings and in guard cells. This results in slowed water loss of plants in response to drought. Farnesyltransferase (PFT) catalyses the attachment of the 15-carbon isoprenoid farnesyl to conserved cysteine residues located in a conserved C-terminal domain designated CaaX box. PFT is a heterodimeric protein comprised of an a and b sununits. The a subunit is shared between PFT and geranylgeranyltransferase-I (PGGTI) which catalyses the attachemt of the 20-carbon isoprenoid geranylgeranyl to CaaX box proteins in which the last amino acid is almost always leucine and in addition have a polybasic domain proximal to the CaaL box. Preliminary data presented in the proposal showed that increased cytoplasmic Ca2+ concentration in stomal guard cells in response to non-inductive ABA treatements. The goals set in the proposal were to characterize better how PFT (ERA1) affects ABA induced Ca2+ concentrations in guard cells and to identify putative CaaX box proteins which function as negative regulators of ABA signaling and which function is compromised in era1 mutant plants. To achieve these goals we proposed to use camelion Ca2+ sensor protein, high throughput genomic to identify the guard cell transcriptome and test prenylation of candidate proteins. We also proposed to focus our efforts of RAC small GTPases which are prenylated proteins which function in signaling. Our results show that farnesyltransferaseprenylates protein/s that act between the points of ABA perception and the activation of plasma membrane calcium influx channels. A RAC protein designated AtRAC8/AtRop10 also acts in negative regulation of ABA signaling. However, we discovered that this protein is palmitoylated and not prenylated although it contains a C-terminal CXXX motif. We further discovered a unique C-terminal sequence motif required for membrane targeting of palmitoylatedRACs and showed that their function is prenylation independent. A GC/MS based method for expression in plants, purification and analysis of prenyl group was developed. This method would allow highly reliable identification of prenylated protein. Mutants in the shared α subunit of PFT and PGGT-I was identified and characterized and was shown to be ABA hypersensitive but less than era1. This suggested that PFT and PGGT-I have opposing functions in ABA signaling. Our results enhanced the understanding of the role of protein prenylation in ABA signaling and drought resistance in plants with the implications of developing drought resistant plants. The results of our studies were published 4 papers which acknowledge support from BARD.

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