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Academic literature on the topic 'InsP3R'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "InsP3R"

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MACKRILL, John J., Robert A. WILCOX, Atsushi MIYAWAKI, Katsuhiko MIKOSHIBA, Stefan R. NAHORSKI, and R. A. John CHALLISS. "Stable overexpression of the type-1 inositol 1,4,5-trisphosphate receptor in L fibroblasts: subcellular distribution and functional consequences." Biochemical Journal 318, no. 3 (September 15, 1996): 871–78. http://dx.doi.org/10.1042/bj3180871.

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InsP3 receptor (InsP3R)/Ca2+-release channels differ markedly in abundance in different tissues/cell types and InsP3R expression levels may be modulated in response to a variety of external cues. Cell lines overexpressing InsP3Rs will provide useful models for the study of the influence of receptor density and subtype on InsP3-mediated Ca2+ signalling. We have investigated the properties of InsP3Rs in mouse L fibroblast cell lines transfected with either type-1 InsP3R cDNA (L15) or vector control (Lvec). L15 cells express approximately eightfold higher levels of the type-1 InsP3R protein than Lvec cells, as assessed by radioligand binding and immunoblotting. Increased expression was stable since it did not alter over ten cell passages. Both L15 and Lvec cells express predominantly the type-1 InsP3R isoform, indicating that functional differences in the InsP3-mediated Ca2+ signalling in these cell lines are due to alteration in the levels of receptor rather than changes in the isoform expressed. Type-1 InsP3R in L15 cells is largely associated with subcellular membrane fractions bearing the sarco/endoplasmic reticulum Ca2+ ATPase pump, appropriate for rapidly exchanging Ca2+ pools. Functionally, there is an approximately fourfold increase in the sensitivity of permeabilized L15-cell Ca2+ mobilization in response to increasing concentrations of Ins(1,4,5)P3. This study indicates that L15/Lvec cells provide a suitable model for studying the effects of InsP3R expression level on InsP3-induced Ca2+ mobilization.

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Mak, Don-On Daniel, Sean McBride, and J. Kevin Foskett. "Regulation by Ca2+ and Inositol 1,4,5-Trisphosphate (Insp3) of Single Recombinant Type 3 Insp3 Receptor Channels." Journal of General Physiology 117, no. 5 (April 30, 2001): 435–46. http://dx.doi.org/10.1085/jgp.117.5.435.

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The inositol 1,4,5-trisphosphate (InsP3) receptor (InsP3R) is an endoplasmic reticulum–localized Ca2+-release channel that controls complex cytoplasmic Ca2+ signaling in many cell types. At least three InsP3Rs encoded by different genes have been identified in mammalian cells, with different primary sequences, subcellular locations, variable ratios of expression, and heteromultimer formation. To examine regulation of channel gating of the type 3 isoform, recombinant rat type 3 InsP3R (r-InsP3R-3) was expressed in Xenopus oocytes, and single-channel recordings were obtained by patch-clamp electrophysiology of the outer nuclear membrane. Gating of the r-InsP3R-3 exhibited a biphasic dependence on cytoplasmic free Ca2+ concentration ([Ca2+]i). In the presence of 0.5 mM cytoplasmic free ATP, r-InsP3R-3 gating was inhibited by high [Ca2+]i with features similar to those of the endogenous Xenopus type 1 InsP3R (X-InsP3R-1). Ca2+ inhibition of channel gating had an inhibitory Hill coefficient of ∼3 and half-maximal inhibiting [Ca2+]i (Kinh) = 39 μM under saturating (10 μM) cytoplasmic InsP3 concentrations ([InsP3]). At [InsP3] < 100 nM, the r-InsP3R-3 became more sensitive to Ca2+ inhibition, with the InsP3 concentration dependence of Kinh described by a half-maximal [InsP3] of 55 nM and a Hill coefficient of ∼4. InsP3 activated the type 3 channel by tuning the efficacy of Ca2+ to inhibit it, by a mechanism similar to that observed for the type 1 isoform. In contrast, the r-InsP3R-3 channel was uniquely distinguished from the X-InsP3R-1 channel by its enhanced Ca2+ sensitivity of activation (half-maximal activating [Ca2+]i of 77 nM instead of 190 nM) and lack of cooperativity between Ca2+ activation sites (activating Hill coefficient of 1 instead of 2). These differences endow the InsP3R-3 with high gain InsP3–induced Ca2+ release and low gain Ca2+–induced Ca2+ release properties complementary to those of InsP3R-1. Thus, distinct Ca2+ signals may be conferred by complementary Ca2+ activation properties of different InsP3R isoforms.

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Yule, D. I., S. V. Straub, and J. I. E. Bruce. "Modulation of Ca2+ oscillations by phosphorylation of Ins(1,4,5)P3 receptors." Biochemical Society Transactions 31, no. 5 (October 1, 2003): 954–57. http://dx.doi.org/10.1042/bst0310954.

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Activation of InsP3Rs (InsP3 receptors) represents the major mechanism underlying intracellular calcium release in non-excitable cells such as hepatocytes and exocrine cells from the pancreas and salivary glands. Modulation of calcium release through InsP3Rs is therefore a major route whereby the temporal and spatial characteristics of calcium waves and oscillations can potentially be ‘shaped’. In this study, the functional consequences of phosphoregulation of InsP3Rs were investigated. Pancreatic and parotid acinar cells express all three types of InsP3R in differing abundance, and all are potential substrates for phosphoregulation. PKA (protein kinase A)-mediated phosphorylation of InsP3Rs in pancreatic acinar cells resulted in slowed kinetics of calcium release following photo-release of InsP3. In contrast, activation of PKA in parotid cells resulted in a marked potentiation of calcium release. In pancreatic acinar cells the predominant InsP3R isoform phosphorylated was the type 3 receptor, while the type 2 receptor was markedly phosphorylated in parotid acinar cells. In order to further decipher the effects of phosphorylation on individual InsP3R subtypes, DT-40 cell lines expressing homotetramers of a single isoform of InsP3R were utilized. These data demonstrate that phosphoregulation of InsP3Rs results in subtype-specific effects and may play a role in the specificity of calcium signals by ‘shaping’ the spatio-temporal profile of the response.

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Kaznacheyeva, Elena, Vitalie D. Lupu, and Ilya Bezprozvanny. "Single-Channel Properties of Inositol (1,4,5)-Trisphosphate Receptor Heterologously Expressed in HEK-293 Cells." Journal of General Physiology 111, no. 6 (June 1, 1998): 847–56. http://dx.doi.org/10.1085/jgp.111.6.847.

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The inositol (1,4,5)-trisphosphate receptor (InsP3R) mediates Ca2+ release from intracellular stores in response to generation of second messenger InsP3. InsP3R was biochemically purified and cloned, and functional properties of native InsP3-gated Ca2+ channels were extensively studied. However, further studies of InsP3R are obstructed by the lack of a convenient functional assay of expressed InsP3R activity. To establish a functional assay of recombinant InsP3R activity, transient heterologous expression of neuronal rat InsP3R cDNA (InsP3R-I, SI− SII+ splice variant) in HEK-293 cells was combined with the planar lipid bilayer reconstitution experiments. Recombinant InsP3R retained specific InsP3 binding properties (Kd = 60 nM InsP3) and were specifically recognized by anti–InsP3R-I rabbit polyclonal antibody. Density of expressed InsP3R-I was at least 20-fold above endogenous InsP3R background and only 2–3-fold lower than InsP3R density in rat cerebellar microsomes. When incorporated into planar lipid bilayers, the recombinant InsP3R formed a functional InsP3-gated Ca2+ channel with 80 pS conductance using 50 mM Ba2+ as a current carrier. Mean open time of recombinant InsP3-gated channels was 3.0 ms; closed dwell time distribution was double exponential and characterized by short (18 ms) and long (130 ms) time constants. Overall, gating and conductance properties of recombinant neuronal rat InsP3R-I were very similar to properties of native rat cerebellar InsP3R recorded in identical experimental conditions. Recombinant InsP3R also retained bell-shaped dependence on cytosolic Ca2+ concentration and allosteric modulation by ATP, similar to native cerebellar InsP3R. The following conclusions are drawn from these results. (a) Rat neuronal InsP3R-I cDNA encodes a protein that is either sufficient to produce InsP3-gated channel with functional properties identical to the properties of native rat cerebellar InsP3R, or it is able to form a functional InsP3-gated channel by forming a complex with proteins endogenously expressed in HEK-293 cells. (b) Successful functional expression of InsP3R in a heterologous expression system provides an opportunity for future detailed structure–function characterization of this vital protein.

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DAVIS, Richard J., R. A. John CHALLISS, and Stefan R. NAHORSKI. "Enhanced purinoceptor-mediated Ca2+ signalling in L-fibroblasts overexpressing type 1 inositol 1,4,5-trisphosphate receptors." Biochemical Journal 341, no. 3 (July 26, 1999): 813–20. http://dx.doi.org/10.1042/bj3410813.

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Mouse L-fibroblast cells stably transfected with either type 1 Ins(1,4,5)P3 receptor (InsP3R) cDNA (L15) or the vector control (Lvec) have been used to investigate the functional consequences of increased InsP3R density on receptor-mediated Ca2+ signalling. L15 cells express approx. 8-fold higher levels of the type 1 InsP3R compared with Lvec cells, which endogenously express essentially only the type 1 InsP3R protein. Stimulation of Lvec and L15 cells with UTP or ATP increased cytosolic Ca2+ concentration to a greater extent in L15 cells at all agonist concentrations. UTP and ATP were equipotent, suggestive of the presence of endogenous cell-surface metabotropic P2Y2-purinoceptors. In both cell clones the purinoceptors were coupled via pertussis-toxin-insensitive G-protein(s) to phospholipase C activation, resulting in similar concentration-dependent accumulations of InsP3. Single-cell microfluorimetry revealed that overexpression of InsP3Rs reduced the threshold for purinoceptor-mediated Ca2+ signalling. L-fibroblasts also exhibited temporally complex sinusoidal cytosolic Ca2+ oscillations in response to submaximal agonist concentrations, with significant increases in oscillatory frequencies exhibited by cells overexpressing InsP3Rs. Sustainable oscillatory responses were dependent on Ca2+ entry and, at higher agonist concentrations, cytosolic Ca2+ oscillations were superseded by biphasic peak-and-plateau Ca2+ responses. Overexpression of InsP3Rs in L15 cells resulted in a 4-fold reduction in the threshold for this change in the temporal pattern of Ca2+ mobilization. These data provide the first direct evidence demonstrating that altering the expression of the type 1 InsP3R significantly affects receptor-mediated InsP3-induced Ca2+ mobilization.

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Ashhad, Sufyan, Daniel Johnston, and Rishikesh Narayanan. "Activation of InsP3 receptors is sufficient for inducing graded intrinsic plasticity in rat hippocampal pyramidal neurons." Journal of Neurophysiology 113, no. 7 (April 2015): 2002–13. http://dx.doi.org/10.1152/jn.00833.2014.

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The synaptic plasticity literature has focused on establishing necessity and sufficiency as two essential and distinct features in causally relating a signaling molecule to plasticity induction, an approach that has been surprisingly lacking in the intrinsic plasticity literature. In this study, we complemented the recently established necessity of inositol trisphosphate (InsP3) receptors (InsP3R) in a form of intrinsic plasticity by asking if InsP3R activation was sufficient to induce intrinsic plasticity in hippocampal neurons. Specifically, incorporation of d-myo-InsP3 in the recording pipette reduced input resistance, maximal impedance amplitude, and temporal summation but increased resonance frequency, resonance strength, sag ratio, and impedance phase lead. Strikingly, the magnitude of plasticity in all these measurements was dependent on InsP3 concentration, emphasizing the graded dependence of such plasticity on InsP3R activation. Mechanistically, we found that this InsP3-induced plasticity depended on hyperpolarization-activated cyclic nucleotide-gated channels. Moreover, this calcium-dependent form of plasticity was critically reliant on the release of calcium through InsP3Rs, the influx of calcium through N-methyl-d-aspartate receptors and voltage-gated calcium channels, and on the protein kinase A pathway. Our results delineate a causal role for InsP3Rs in graded adaptation of neuronal response dynamics, revealing novel regulatory roles for the endoplasmic reticulum in neural coding and homeostasis.

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NOSYREVA, Elena, Tomoya MIYAKAWA, Zhengnan WANG, Lyuba GLOUCHANKOVA, Akiko MIZUSHIMA, Masamitsu IINO, and Ilya BEZPROZVANNY. "The high-affinity calcium–calmodulin-binding site does not play a role in the modulation of type 1 inositol 1,4,5-trisphosphate receptor function by calcium and calmodulin." Biochemical Journal 365, no. 3 (August 1, 2002): 659–67. http://dx.doi.org/10.1042/bj20011789.

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Modulation of the inositol 1,4,5-trisphosphate (InsP3) receptors (InsP3R) by cytosolic calcium (Ca2+) plays an essential role in Ca2+ signalling, but structural determinants and mechanisms responsible for the InsP3R regulation by Ca2+ are poorly understood. In the present study, we expressed rat InsP3R type 1 (InsP3R1) in Spodoptera frugiperda cells using a baculovirus-expression system and reconstituted the recombinant InsP3R1 into planar lipid bilayers for functional analysis. We observed only minor effects of 0.5mM of calmodulin (CaM) antagonist W-7 on the Ca2+ dependence of InsP3R1. Based on a previous analysis of mouse InsP3R1 [Yamada, Miyawaki, Saito, Nakajima, Yamamoto-Hino, Ryo, Furuichi and Mikoshiba (1995) Biochem J. 308, 83–88], we generated the Trp1577→Ala (W1577A) mutant of rat InsP3R1 which lacks the high-affinity Ca2+—CaM-binding site. We found that the W1577A mutant displayed a bell-shaped Ca2+ dependence similar to the wild-type InsP3R1 in planar lipid bilayers. Activation of B cell receptors resulted in identical Ca2+ signals in intact DT40 cells lacking the endogenous InsP3R and transfected with the wild-type InsP3R1 or the W1577A mutant cDNA subcloned into a mammalian expression vector. In the planar lipid bilayer experiments, we showed that both wild-type InsP3R1 and W1577A mutant were equally sensitive to inhibition by exogenous CaM. From these results, we concluded that the interaction of CaM with the high-affinity Ca2+—CaM-binding site in the coupling domain of the InsP3R1 does not play a direct role in biphasic modulation of InsP3R1 by cytosolic Ca2+ or in InsP3R1 inhibition by CaM.

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Foskett, J. Kevin, Carl White, King-Ho Cheung, and Don-On Daniel Mak. "Inositol Trisphosphate Receptor Ca2+ Release Channels." Physiological Reviews 87, no. 2 (April 2007): 593–658. http://dx.doi.org/10.1152/physrev.00035.2006.

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The inositol 1,4,5-trisphosphate (InsP3) receptors (InsP3Rs) are a family of Ca2+ release channels localized predominately in the endoplasmic reticulum of all cell types. They function to release Ca2+ into the cytoplasm in response to InsP3 produced by diverse stimuli, generating complex local and global Ca2+ signals that regulate numerous cell physiological processes ranging from gene transcription to secretion to learning and memory. The InsP3R is a calcium-selective cation channel whose gating is regulated not only by InsP3, but by other ligands as well, in particular cytoplasmic Ca2+. Over the last decade, detailed quantitative studies of InsP3R channel function and its regulation by ligands and interacting proteins have provided new insights into a remarkable richness of channel regulation and of the structural aspects that underlie signal transduction and permeation. Here, we focus on these developments and review and synthesize the literature regarding the structure and single-channel properties of the InsP3R.

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Ramos-Franco, Josefina, Daniel Galvan, Gregory A. Mignery, and Michael Fill. "Location of the Permeation Pathway in the Recombinant Type 1 Inositol 1,4,5-Trisphosphate Receptor." Journal of General Physiology 114, no. 2 (August 1, 1999): 243–50. http://dx.doi.org/10.1085/jgp.114.2.243.

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The inositol 1,4,5-trisphosphate receptor (InsP3R) forms ligand-regulated intracellular Ca2+ release channels in the endoplasmic reticulum of all mammalian cells. The InsP3R has been suggested to have six transmembrane regions (TMRs) near its carboxyl terminus. A TMR-deletion mutation strategy was applied to define the location of the InsP3R pore. Mutant InsP3Rs were expressed in COS-1 cells and single channel function was defined in planar lipid bilayers. Mutants having the fifth and sixth TMR (and the interceding lumenal loop), but missing all other TMRs, formed channels with permeation properties similar to wild-type channels (gCs = 284; gCa = 60 pS; PCa/PCs = 6.3). These mutant channels bound InsP3, but ligand occupancy did not regulate the constitutively open pore (Po > 0.80). We propose that a region of 191 amino acids (including the fifth and sixth TMR, residues 2398–2589) near the COOH terminus of the protein forms the InsP3R pore. Further, we have produced a constitutively open InsP3R pore mutant that is ideal for future site-directed mutagenesis studies of the structure–function relationships that define Ca2+ permeation through the InsP3R channel.

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Mak, Don-On Daniel, Sean McBride, and J. Kevin Foskett. "Atp-Dependent Adenophostin Activation of Inositol 1,4,5-Trisphosphate Receptor Channel Gating." Journal of General Physiology 117, no. 4 (March 12, 2001): 299–314. http://dx.doi.org/10.1085/jgp.117.4.299.

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The inositol 1,4,5-trisphosphate (InsP3) receptor (InsP3R) is a ligand-gated intracellular Ca2+ release channel that plays a central role in modulating cytoplasmic free Ca2+ concentration ([Ca2+]i). The fungal metabolite adenophostin A (AdA) is a potent agonist of the InsP3R that is structurally different from InsP3 and elicits distinct calcium signals in cells. We have investigated the effects of AdA and its analogues on single-channel activities of the InsP3R in the outer membrane of isolated Xenopus laevis oocyte nuclei. InsP3R activated by either AdA or InsP3 have identical channel conductance properties. Furthermore, AdA, like InsP3, activates the channel by tuning Ca2+ inhibition of gating. However, gating of the AdA-liganded InsP3R has a critical dependence on cytoplasmic ATP free acid concentration not observed for InsP3-liganded channels. Channel gating activated by AdA is indistinguishable from that elicited by InsP3 in the presence of 0.5 mM ATP, although the functional affinity of the channel is 60-fold higher for AdA. However, in the absence of ATP, gating kinetics of AdA-liganded InsP3R were very different. Channel open time was reduced by 50%, resulting in substantially lower maximum open probability than channels activated by AdA in the presence of ATP, or by InsP3 in the presence or absence of ATP. Also, the higher functional affinity of InsP3R for AdA than for InsP3 is nearly abolished in the absence of ATP. Low affinity AdA analogues furanophostin and ribophostin activated InsP3R channels with gating properties similar to those of AdA. These results provide novel insights for interpretations of observed effects of AdA on calcium signaling, including the mechanisms that determine the durations of elementary Ca2+ release events in cells. Comparisons of single-channel gating kinetics of the InsP3R activated by InsP3, AdA, and its analogues also identify molecular elements in InsP3R ligands that contribute to binding and activation of channel gating.

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Dissertations / Theses on the topic "InsP3R"

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Salb, Katharina [Verfasser], Jens [Akademischer Betreuer] Schlossmann, and Achim [Akademischer Betreuer] Göpferich. "Funktion von IRAG für cGMP-Kinase-I-Komplexe sowie für die InsP3R-I-Phosphorylierung / Katharina Salb. Betreuer: Jens Schlossmann ; Achim Göpferich." Regensburg : Universitätsbibliothek Regensburg, 2011. http://d-nb.info/1025386124/34.

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Gouin, Olivier. "Etude du rôle de PAR-2 dans l'inflammation neurogène cutanée." Thesis, Brest, 2017. http://www.theses.fr/2017BRES0030/document.

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L’inflammation neurogène cutanée (INC) est une inflammation de la peau induite par l’activation des fibres nerveuses intra-épidermiques qui secrètent des neuropeptides tels que la substance P (SP). L’INC est impliquée dans des dermatoses inflammatoires prurigineuses comme le psoriasis, la dermatite atopique (DA) et le syndrome de Netherton (SN). Un nouveau concept émerge, suggérant que les kératinocytes sont également des acteurs majeurs de l’INC. Le récepteur activé par des protéases de type 2 (PAR-2) est fortement incriminé dans l’INC associée à ces dermatoses, ce qui permet de comprendre les voies du prurit non-histaminergique. Les enjeux thérapeutiques sont de taille puisqu’il n’existe actuellement aucun traitement efficace permettant la prise en charge spécifique du prurit histamino-indépendant au cours des dermatoses prurigineuses associées à l’INC.Bien que le rôle de PAR-2 dans la sécrétion de neuropeptides à partir des neurones sensoriels soit clairement établi, son implication dans la modulation de gènes pouvant contribuer à l’entretien ou l’amplification de l’INC reste méconnue. Le rôle inflammatoire de PAR-2 a également été démontré sur des kératinocytes cultivés en monocouche via la sécrétion de cytokines par des mécanismes dépendants du Ca2+. La surexpression de PAR-2 et la perte d’expression de certains canaux calciques impliqués dans sa réponse calcique dans les kératinocytes différenciés suggèrent des mécanismes d’action de PAR-2 différents pour ceux-ci. Dans le but d’étudier le rôle pro-inflammatoire de PAR-2 au cours des dermatoses prurigineuses, nous avons analysé l’effet de son activation sur des monocultures de neurones sensoriels issus de ganglions rachidiens dorsaux (GRD) de rat et de kératinocytes humains différenciés (DhPK), en criblant l’expression de médiateurs de l’inflammation. Pour approfondir, les voies calciques de PAR-2 sous-jacente à la modulation d’expression dans les kératinocytes différenciés, des expériences d’imagerie calcique ont été réalisées et différents antagonistes ont été utilisés pour analyser les acteurs impliqués.Dans le cadre d’un partenariat avec les laboratoires dermatologiques d’Uriage, nous avons testé les effets de l’eau thermale d’Uriage sur la modulation de gènes induite par PAR-2 dans les DhPK. Nous avons également utilisé une lignée de PC12 différenciables en neurones par le NGF afin de les utiliser comme alternatives des neurones sensoriels issus des GRD de rat pour l’étude de l’INC.L’ensemble des résultats obtenus au cours du criblage des gènes modules par PAR-2 confirme le rôle pro-inflammatoire de PAR-2 dans les neurones sensoriels de rat et dans les DhPK. La découverte d’une nouvelle voie calcique de PAR-2 dans les DhPK offre de nouvelles pistes thérapeutiques pour les dermatoses prurigineuses telles que le psoriasis, la DA et le NS. Les résultats obtenus avec l’eau thermale d’Uriage peuvent présenter une perspective thérapeutique pour les patients souffrants de dermatoses prurigineuses réfractaires aux traitements conventionnels. L’utilisation d’une lignée neuronale comme lesPC12 pour l’étude de l’INC serait une alternative utile dans le développement des tests cosmétiques avec les industriels pour notre laboratoire
Cutaneous neurogenic inflammation (CNI) is an inflammation of the skin induced by the activation of intraepidermal nerve fibers that release neuropeptides such as substance P (SP). CNI is involved in pruritic inflammatory skin disorders such as psoriasis, atopic dermatitis (AD) and Netherton syndrome (NS). A new concept is growing, suggesting that keratinocytes could also trigger INC. The proteases activated receptor 2 (PAR-2) is strongly incriminated in CNI associated with these dermatoses, which allow to understand the histamine-independent itching pathways. The therapeutic stakes are high since there is currently no effective treatment allowing the specific management of histamine-independent pruritus during skin disorders associated with CNI.Although the role of PAR-2 in the secretion of neuropeptides from sensory neurons is clearly established, its involvement in the modulation of genes involved in the maintenance or amplification of CNI remains unknown. The inflammatory role of PAR-2 on keratinocytes has also been demonstrated through the production of cytokines in a Ca2+-dependent mechanisms. The overexpression of PAR-2 and the loss of ORAI1 expression, a calcium channel following keratinocytes differentiation suggest different signaling pathways downstream to PAR-2 activation between undifferentiated and differentiated keratinocytes.In order to study the pro-inflammatory role of PAR-2 during pruritic dermatoses, we analyzed the effect of its activation on rat primary sensory neurons from dorsal spinal ganglia (DRG) and on differentiated human primary keratinocytes (DhPK) by screening the expression of inflammatory mediators. To deepen the Ca2+ pathways underlying PAR-2-mediated inflammatory mediator modulation in DhPK, we performed Ca2+ imaging experiments and different antagonists were used to analyze the involvement of intracellular actors. In a partnership with the dermatological laboratories of Uriage, we tested the effects of Uriage thermal water on PAR-2-induced gene modulation in DhPK. We also used a PC12 cell line differentiable in neurons by the NGF in order to use them as alternatives of rat primary sensory neurons from DRG for the study of INC. We also used a PC12 cell line differentiable in neurons by the NGF use them as alternatives of rat primary sensory neurons from DRG for the study of INC.The results obtained during the screening of the PAR-2-modulated genes confirmed the proinflammatory role of PAR-2 in rat primary sensory neurons and in DhPK. The discovery of a new PAR-2-mediated Ca2+ pathway in DhPK offers new therapeutic pathways for pruritic dermatoses such as psoriasis, AD and NS. The results obtained with the thermal water of Uriage can present a therapeutic perspective for patients suffering from pruritic dermatoses refractory to conventional treatments. The use of a neuronal cell line as the PC12 for the study of INC would be an useful alternative in the development of cosmetic tests

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Kilari, Rajagopal Sharada. "Roles of inositol diphosphates in DNA repair and effects of aspirin analogues on oesophageal cancer." Thesis, University of Wolverhampton, 2014. http://hdl.handle.net/2436/346328.

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Inositol phosphates (IPs) are important signalling molecules with various biological roles in a cell. One such role it is often associated with is DNA repair. The DNA repair process following DNA insult is considered crucial for the genomic integrity and stability. Failure to perform this task will result in mutations and possibly disease. Thus, it is important that we expand our knowledge on how these repair processes occur and identify the key factors involved in its regulation. The aim of this project was to investigate whether DNA repair was mediated by inositol diphosphates (IDPs). Using a family of yeast knockout mutants with modulated levels of IPs, it was found that IDPs are crucial in repair of DNA following insult with bleomycin and 5-fluorouracil. The observed sensitivity of the mutants was thought to be due to lack of functional repair protein, UDG-like or APE-like, in the absence of essential cofactor such as IDPs. Experiments conducted revealed that the hypersensitive kcs1Δ contain both the repair proteins required to process the DNA lesions. However, extreme extraction methods were required to access these proteins, suggesting that the proteins are mislocalised and unavailable to access the damage site and perform DNA repair. GFP-tagging the proteins Ung1, Apn1 and Rad52 in kcs1Δ proved to be of little use as it failed to show exact localisation, movement and functionality status of these proteins following bleomycin insult. The enzymes accountable for the dephosphorylation of the IDPs in vivo are the diphosphoinositol polyphosphate phosphohydrolases (DIPPs). Little is known regarding the Michaelis-Menten kinetics parameters for Ddp1p/DIPPs. In this study, using improved methods for the enzymatic synthesis and electrophoretic purification of 1-InsP7, 5-InsP7 and InsP8, the DIPP family has been kinetically characterised. Each DIPP was found to ii display similar Km values for every substrate tested (range: 35-148 nM). The rank order of Kcat values (1-InsP7 > 5-InsP7 = InsP8) was identical for each enzyme, although DIPP-1 activity was observed to be 10- to 60-fold more than DIPP-2α/β and DIPP-3α/β, irrespective of the substrate. This study reveals that Ddp1, the yeast DIPP, is capable of hydrolysing not only 5-InsP7 but also 1-InsP7 and InsP8 to a single product, InsP6. The HPLC data found InsP7 accumulation to be relatively little during InsP8 breakdown by DIPPs. Such low build-up was found to be due to rapid conversion of InsP7 to InsP6. Through this study it is also clear that InsP8 prefers to dephosphorylate through 1-InsP7. In contrary, metabolically and functionally significant steady-state route of InsP8 synthesis was observed to be via 5-InsP7. Oesophageal cancer is considered as one of the deadliest cancers worldwide because of its aggressive nature and low survival rate. Epidemiologic studies have shown that low-dose daily intake of aspirin can decrease the incidence of oesophageal cancer. The data presented in this study show the effects of a number of in-house synthesized novel aspirin analogues on oesophageal cancer cell lines, squamous cell carcinoma (SSC) and adenocarcinoma (ADC). The aspirin analogues, fumaryldiaspirin (PN517) and benzoylsalicylates (PN524, PN528 and PN529), were observed to be more potent against the oesophageal cell lines than aspirin itself. Both, quantitative and qualitative apoptosis experiments conducted revealed that these compounds largely induced apoptosis, although some necrosis was evident with PN528 and PN529. Failure to recover following the treatment with these analogues emphasized that these drugs are largely cytotoxic in nature. The SSC cells (oe21) displayed increased sensitivity to the aspirin analogues compared to the ADC cell lines (flo-1 and oe33). The anticancer properties of these novel aspirin compounds appear to not involve the COX-enzymes at the tested concentrations. These initial findings support further studies into the potential of these aspirin analogues as chemotherapeutic agents against oesophageal cancer.

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Keddie, Neil S. "The synthesis and biological evaluation of d-myo-inositol 1,4,5-trisphosphate receptor ligands." Thesis, University of St Andrews, 2010. http://hdl.handle.net/10023/963.

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The intracellular second messenger InsP₃ is a vital molecule in the regulation of Ca²⁺ signalling. Ca²⁺ mediates a wide range of cellular activities from fertilisation and cell differentiation through to apoptoisis. Using X-ray crystal structure data and molecular modelling, a series of novel InsP₃ analogues were designed as selective InsP₃R-antagonists. Two novel synthetic routes have been developed for the synthesis of these analogues. The first route uses a Ferrier-II rearrangement to provide enantiopure inositol intermediates, whereas, the second route employs a diastereomeric resolution to obtain the enantiopure inositols. The successful synthesis of InsP₃ and a series of 5-position modified analogues are reported herein.

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Wegiriya, Hemantha Chandani. "Dietary effects on instar number, instar duration and adult performance in Helicoverpa armigera." Thesis, University of Reading, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385175.

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Rückl, Martin. "Interaction of Ca2+ with fully stochastic InsP3 receptor dynamics." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19236.

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Intrazelluläre Calcium Signale bilden einen der wichtigsten Bestandteile vieler Signalwege in der Zellbiologie. Der Fokus dieser Arbeit liegt auf der hierachischen Struktur der Calcium Muster, welche durch die Rückkopplung von Ip3 Rezeptor (Ip3R) mit Calcium verursacht wird. Auf der obersten Stufe stehen zellweite Wellen aus Calcium. Das zweite Level der Hierarchie bilden sogenante Puffs oder Sparks und entspricht der Freisetzung von Calcium von einzelnen Clustern. Das untere Ende wird durch Blibs gebildet: kleine Calcium Signale einzelner Kanäle. Die Entstehung der Calcium Wellen und der Zusammenhang mit den Ip3 Bindungszuständen individueller Ip3 Kanäle stehen dabei im Vordergund. Ein erstes Modell verwendet ein System von Reaktions-Diffusions-Gleichungen zur Beschreibung der Calciumentwicklung in der Umgebung einzelner Cluster. Es wird festgestellt, dass ein Cluster nicht-stereotype Puffs erzeugen kann, wobei Dauer und Amplitude durch die Ip3-Konzentration moduliert werden. Stärkere Ip3-Stimulation erhöht die Wahrscheinlichkeit, lang anhaltende Freisetzungsereignisse zu beobachten, welche als die Quelle der Wellenbildung identifiziert werden. Die simulierten Daten werden mit experimentellen Ergebnissen aus Xenopus-Oozyten verglichen, wo eine ähnliche Durchsetzung der Wellen- und Puff-Muster beobachtet werden kann. Ein zweites grobkörniges und phänomenologisches Modell auf Basis von ODEs ermöglicht das Sampling langer Trajektorien für ein größeres System aus gekoppelten Clustern mit vertretbarem Rechenaufwand. Auf einem Gitter von Clustern wird gezeigt, dass die wellenartigen Freisetzungsereignisse sich synchronisieren. Während die Wellenfrequenz mit Ip3 zunimmt, gibt es eine optimale Synchronisation für die mittlere Ip3-Anregung. Dieses Modell zeigt, dass die Terminierung der Wellen durch Dissosation von Ip3 erreicht werden kann, was dazu führt, dass sich Kanäle nicht mehr öffnen, und somit eine anhaltende Freisetzung von Ca2+ verhindert wird.
The dynamics of intracellular calcium represent one of the most important signal pathways in cell biology. Within this work, the focus lies on the hierarchical structure of calcium release events emerging from the feedback of Ip3 receptor Ca2+ ion channel with Ca2+ itself. The head of this hierarchy consists of calcium waves or global oscillations. Release events from individual clusters of channels, constitute the intermediate level. Single channel release events are called blibs. This work investigates the emergence and termination of waves by using a stochastic Ip3R model with non-equilibrium Ip3 binding and discrete individual channel states. First, a system of reaction diffusion equations of calcium and buffers around a single cluster is used as a description of the calcium evolution. It is found, that a cluster can produce non stereotype puffs, where duration and amplitude are modulated by the Ip3 concentration. For increasing Ip3 stimulation, the likelihood to observe long lasting release events increases, and these events are identified as the source of wave formation. The simulated data is compared to experimental results from Xenopus oocytes, where a similar interspersion of puffs between waves can be observed. Specifically, experiments and simulations support the hypothesis of wave-like events already on a single cluster scale. The insights of the first model are then used to develop a second coarse grained and phenomenological model based on ODEs. It allows sampling of long trajectories of a system of coupled clusters with reasonable computational effort. Within a grid of coupled clusters, it is showed that the wave-like release events synchronize. While the wave frequency increases with Ip3, there is an optimal synchronization for intermediate Ip3 excitation. This model indicates that wave termination is achieved by unbinding of Ip3 from the receptor, which renders the channel unable to open, and hence prohibits any further sustained release.

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Fajnorová, Markéta. "Návrh marketingové strategie firmy Inspur Group Co. ltd. pro český trh." Master's thesis, Vysoká škola ekonomická v Praze, 2011. http://www.nusl.cz/ntk/nusl-82017.

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The diploma thesis is structured into three chapters, while the first chapter informs about theoretical concept of B-2-B marketing, defines basic specifics of B-2-B market and concerns about actual trends and frequent mistakes, which are made while preparing B-2-B marketing strategy. Next chapter informs about actual situation on the server market in the Czech Republic and mainly focuses on the external and internal environment of the firm. The last chapter is based on the personal discussion with potential distribution and service partners that provided useful information about the concurrence, actual situation on the market and defined trade requirements towards Inspur.

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Olsson, Oskar. "Samhällsnyttan av geografisk information och INSPIRE." Thesis, Uppsala universitet, Kulturgeografiska institutionen, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-167773.

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Rusch, Thomas, and Achim Zeileis. "Discussion on Fifty Years of Classification and Regression Trees." Wiley, 2014. http://dx.doi.org/10.1111/insr.12062.

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In this discussion paper, we argue that the literature on tree algorithms is very fragmented. We identify possible causes and discuss good and bad sides of this situation. Among the latter is the lack of free open-source implementations for many algorithms. We argue that if the community adopts a standard of creating and sharing free open-source implementations for their developed algorithms and creates easy access to these programs the bad sides of the fragmentation will be actively combated and will benefit the whole scientific community. (authors' abstract)

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Funk, Annika. "Mitbestimmung in EU-Auslandsgesellschaften nach "Inspire Art" /." Baden-Baden : Nomos, 2007. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=015734153&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Books on the topic "InsP3R"

1

Rensburg, Gerhard Van. Leadership thoughts: Inspire yourself, inspire others. Pretoria: Van Schaik, 2009.

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Howard, Vernon Linwood. Inspire yourself. Boulder City, NV: New Life Foundation, 1990.

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INSPEC. INSPEC thesaurus. [London]: Institution of Electrical Engineers, 1993.

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Women who inspire. Kuching, Sarawak, Malaysia: Bumi Serasi, 2006.

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Kirsten, Keith. Gardens to inspire. Cape Town, South Africa: Struik Lifestyle, 2013.

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Splatt, Sophie. Dream, create, inspire. Scoresby, Victoria: Five Mile Press, 2015.

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De Meyer, Arnoud, and Sam Garg. Inspire to Innovate. London: Palgrave Macmillan UK, 2005. http://dx.doi.org/10.1057/9780230512061.

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Lee, Roddy, ed. Writing to inspire. Crowborough: Highland, 1989.

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Inspire a dream. Tulsa, Okla: Honor Books, 2000.

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Anderson, Niki. Inspur-r-rational stories for cat lovers. Tulsa, Okla: Honor Books, 1999.

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Book chapters on the topic "InsP3R"

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Markin, Vladislav S., and Ilya Bezprozvanny. "Regulation of InsP3R by Ca2+ and Cytosolic Ca2+ Dynamics." In Integrative Aspects of Calcium Signalling, 109–30. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-1901-4_7.

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Butchart, Alexander, Susan Hillis, and Stephanie Burrows. "Inspire." In Violence Against Children, 39–63. 1 Edition. | New York : Routledge, 2018.: Routledge, 2017. http://dx.doi.org/10.4324/9781351248433-3.

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Heppner, John B., D. G. Boucias, J. C. Pendland, Andrei Sourakov, Timothy Ebert, Roger Downer, Kun Yan Zhu, et al. "Instar." In Encyclopedia of Entomology, 2012. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_1553.

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Hui, Xin, and Peter Lipp. "Investigating the InsP3 Receptor in Living Cells by Caged InsP3." In Methods in Molecular Biology, 121–29. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0167-9_10.

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Im, Yang Ju, Brian Q. Phillippy, and Imara Y. Perera. "InsP3 in Plant Cells." In Lipid Signaling in Plants, 145–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_10.

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Bettendorf, Gerhard. "Insler, Vaclav." In Zur Geschichte der Endokrinologie und Reproduktionsmedizin, 257–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79152-9_104.

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Komac, Marko. "InSAR." In Encyclopedia of Earth Sciences Series, 517–18. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73568-9_171.

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Komac, Marko. "InSAR." In Selective Neck Dissection for Oral Cancer, 1–2. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-12127-7_171-1.

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Long, Teng, Cheng Hu, Zegang Ding, Xichao Dong, Weiming Tian, and Tao Zeng. "Geosynchronous InSAR and D-InSAR." In Geosynchronous SAR: System and Signal Processing, 231–72. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7254-3_6.

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Hooper, Andrew. "InSAR and A-InSAR: Theory." In Encyclopedia of Earthquake Engineering, 1–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-36197-5_220-1.

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Conference papers on the topic "InsP3R"

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Dobaj, Jürgen. "INSpIRA." In ICSE '18: 40th International Conference on Software Engineering. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3194133.3194159.

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Ortiz, Jordi, Ramon Sanchez-Iborra, Jorge Bernal Bernabe, Antonio Skarmeta, Chafika Benzaid, Tarik Taleb, Pol Alemany, et al. "INSPIRE-5Gplus." In ARES 2020: The 15th International Conference on Availability, Reliability and Security. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3407023.3409219.

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Teodor, Vlad. "IMPLEMENTING INSPIRE COORDINATE TRANSFORMATION SERVICES - ROMANIAN INSPIRE GEOPORTAL." In 14th SGEM GeoConference on INFORMATICS, GEOINFORMATICS AND REMOTE SENSING. Stef92 Technology, 2014. http://dx.doi.org/10.5593/sgem2014/b23/s11.086.

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Vasile, Cristian. "IMPLEMENTING INSPIRE NETWORK SERVICES FOR THE ROMANIAN INSPIRE GEOPORTAL." In 13th SGEM GeoConference on INFORMATICS, GEOINFORMATICS AND REMOTE SENSING. Stef92 Technology, 2013. http://dx.doi.org/10.5593/sgem2013/bb2.v1/s08.018.

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Alnabhan, Ahmed, and Brian Tomaszewski. "INSAR." In the Sixth ACM SIGSPATIAL International Workshop. New York, New York, USA: ACM Press, 2014. http://dx.doi.org/10.1145/2676528.2676535.

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Chapman, Gail. "Inspire, Innovate, Improve!" In SIGCSE '17: The 48th ACM Technical Symposium on Computer Science Education. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3017680.3025047.

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Kurdyukova, Ekaterina. "Inspire, guide, and entertain." In the 11th International Conference. New York, New York, USA: ACM Press, 2009. http://dx.doi.org/10.1145/1613858.1613947.

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Guthrie, Richard, Emma Reid, John Richmond, Parwant Ghuman, and Yves Cormier. "InSAR and the Pipeline Geohazards Toolbox: Instructions for Use As of 2018." In 2018 12th International Pipeline Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/ipc2018-78571.

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Interferometric Synthetic Aperture Radar (InSAR) is a type of active remote sensing whereby a satellite transmits electromagnetic radiation (microwaves) at the ground and measures the differential phase of the reflected signal over multiple images (or multiple antennas on a single satellite). InSAR has the potential to provide centimeter and even millimeter-scale measurements of displacement over time, but is sensitive to vegetation, topography, and atmospheric effects. We consider herein, the application of InSAR at two known landslides on the Enbridge pipeline system, and discuss the strengths, weaknesses, values, and limitations of its application in the Geohazard Management of landslides impacting pipeline ROW’s. We compare information provided at each site by InSAR (both L-band and X-band) to data derived by mapping using Light Detection and Ranging (LiDAR) or air photographs, to differential LiDAR techniques, and to data derived from subsurface measurements (slope inclinometers). In doing so we find that L-Band data can be an effective tool to establish the extent or footprint of movement (or lack of movement) at known landslide locations, extending the interpretive power of a specialist and the understanding of event magnitude, and potentially affecting the mitigation options. Further, L-Band InSAR can be used in a supporting role to pre-screen areas for active landslides along the right of way (ROW), however, data gaps, a lack of explanatory power, and considerable noise in the results mean that a user step that further considers the terrain, other sources of data, and the identified magnitude, is essential. X-Band InSAR appeared impractical for ROW monitoring where vegetation prevented coherence between images, however, X-Band InSAR was able to detect small displacements at above ground infrastructures.

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"ANAIS DO XX CONGRESSO DE MEDICINA UCPEL: "O QUE TE INSPIRA?"." In XX CONGRESSO DE MEDICINA UCPEL: "O QUE TE INSPIRA?". Revista Eletrônica Acervo Saúde, 2019. http://dx.doi.org/10.25248/anais.e4332.2019.

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"Anais DO 20° CONGRESSO DE MEDICINA UCPEL: "O QUE TE INSPIRA?"." In 20° Congresso de Medicina UCPL:´´O que Te Inspira?´´. Revista Eletrônica Acervo Saúde, 2019. http://dx.doi.org/10.25248/anais.e4332.2020.

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Reports on the topic "InsP3R"

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Kumar, Nagi. Project INSPIRE-HBCU Undergraduate Collaborative Summer Training Program to Inspire Students in Prostate Cancer Research. Fort Belvoir, VA: Defense Technical Information Center, February 2009. http://dx.doi.org/10.21236/ada525845.

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Kumar, Nagi. Project INSPIRE-HBCU Undergraduate Collaborative Summer Training Program to Inspire Students in Prostate Cancer Research. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada479299.

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Kumar, Nagi. Project INSPIRE-HBCU Undergraduate Collaborative Summer Training Program to Inspire Students in Prostate Cancer Research. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada470231.

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Adams, Cole. INSPIRE and SPIRES Log File Analysis. Office of Scientific and Technical Information (OSTI), August 2012. http://dx.doi.org/10.2172/1049732.

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Garton, Byron, Jonathan Broderick, and Michael Clement. Mindbreeze InSpire Search Appliance Implementation and Lessons Learned. Engineer Research and Development Center (U.S.), September 2020. http://dx.doi.org/10.21079/11681/38188.

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White, J., and R. Mellors. Measuring UCG cavity development with InSAR. Office of Scientific and Technical Information (OSTI), October 2012. http://dx.doi.org/10.2172/1089519.

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Mellors, R., W. Foxall, and X. Yang. Detecting and monitoring UCG subsidence with InSAR. Office of Scientific and Technical Information (OSTI), March 2012. http://dx.doi.org/10.2172/1047778.

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Samsonov, S. V., A. Trishchenko, K. F. Tiampo, P. J. González, J. Fernández, and Y. Zhang. Seasonal tropospheric oscillations observed in InSAR time series. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2015. http://dx.doi.org/10.4095/296137.

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Li, J., S. Wang, C. Michel, and H. A. J. Russell. InSAR measurement of surface deformations in south Ontario. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2019. http://dx.doi.org/10.4095/313591.

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Short, N., A. M. LeBlanc, W. E. Sladen, M. Allard, and V. Mathon-Dufour. Seasonal surface displacement derived from InSAR, Iqaluit, Nunavut. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2012. http://dx.doi.org/10.4095/289606.

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