Relevant bibliographies by topics / IP3Rs

Academic literature on the topic 'IP3Rs'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "IP3Rs"

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Foulon, Arthur, Pierre Rybarczyk, Nicolas Jonckheere, Eva Brabencova, Henri Sevestre, Halima Ouadid-Ahidouch, and Lise Rodat-Despoix. "Inositol (1,4,5)-Trisphosphate Receptors in Invasive Breast Cancer: A New Prognostic Tool?" International Journal of Molecular Sciences 23, no. 6 (March 9, 2022): 2962. http://dx.doi.org/10.3390/ijms23062962.

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Breast cancer is the leading cause of cancer death among women in worldwide and France. The disease prognosis and treatment differ from one breast cancer subtype to another, and the disease outcome depends on many prognostic factors. Deregulation of ion flux (especially Ca2+ flux) is involved in many pathophysiology processes, including carcinogenesis. Inside the cell, the inositol-trisphosphate receptor (IP3R) is a major player in the regulation of the Ca2+ flux from the endoplasmic reticulum to the cytoplasm. The IP3Rs (and particularly the IP3R3 subtype) are known to be involved in proliferation, migration, and invasion processes in breast cancer cell lines. The objective of the present study was to evaluate the potential value of IP3Rs as prognostic biomarkers in breast cancer. We found that expression levels of IP3R3 and IP3R1 (but not IP3R2) were significantly higher in invasive breast cancer of no special type than in non-tumor tissue from the same patient. However, the IP3R3 subtype was expressed more strongly than the IP3R1 and IP3R2 subtypes. Furthermore, the expression of IP3R3 (but not of IP3R1 or IP3R2) was positively correlated with prognostic factors such as tumor size, regional node invasion, histologic grade, proliferation index, and hormone receptor status. In an analysis of public databases, we found that all IP3Rs types are significantly associated with overall survival and progression-free survival in patients with breast cancer. We conclude that relative to the other two IP3R subtypes, IP3R3 expression is upregulated in breast cancer and is correlated with prognostic factors.
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Lee, Su Youn, Hee-Seop Yoo, Hye-Seung Choi, Ka Young Chung, and Min-Duk Seo. "Structural and dynamic insights into the subtype-specific IP3-binding mechanism of the IP3 receptor." Biochemical Journal 473, no. 20 (October 11, 2016): 3533–43. http://dx.doi.org/10.1042/bcj20160539.

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There are three subtypes of vertebrate inositol 1,4,5-trisphosphate (IP3) receptor (IP3R), a Ca2+-release channel on the ER membrane — IP3R1, IP3R2, and IP3R3 — each of which has a distinctive role in disease development. To determine the subtype-specific IP3-binding mechanism, we compared the thermodynamics, thermal stability, and conformational dynamics between the N-terminal regions of IP3R1 (IP3R1-NT) and IP3R3 (IP3R3-NT) by performing circular dichroism (CD), isothermal titration calorimetry (ITC), and hydrogen–deuterium exchange mass spectrometry (HDX-MS). Previously determined crystal structures of IP3R1-NT and HDX-MS results from this study revealed that both IP3R1 and IP3R3 adopt a similar IP3-binding mechanism. However, several regions, including the α- and β-interfaces, of IP3R1-NT and IP3R3-NT show significantly different conformational dynamics upon IP3 binding, which may explain the different IP3-binding affinities between the subtypes. The importance of the interfaces for subtype-specific IP3 binding is also supported by the different dynamic conformations of the two subtypes in the apo-states. Furthermore, IP3R1-NT and IP3R3-NT show different IP3-binding affinities and thermal stabilities, but share similar thermodynamic properties for IP3 binding. These results collectively provide new insights into the mechanism underlying IP3 binding to IP3Rs and the subtype-specific regulatory mechanism.
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3

Rahman, Taufiq. "Dynamic clustering of IP3 receptors by IP3." Biochemical Society Transactions 40, no. 2 (March 21, 2012): 325–30. http://dx.doi.org/10.1042/bst20110772.

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The versatility of Ca2+ as an intracellular messenger stems largely from the impressive, but complex, spatiotemporal organization of the Ca2+ signals. For example, the latter when initiated by IP3 (inositol 1,4,5-trisphosphate) in many cells manifest hierarchical recruitment of elementary Ca2+ release events (‘blips’ and then ‘puffs’) en route to global regenerative Ca2+ waves as the cellular IP3 concentration rises. The spacing of IP3Rs (IP3 receptors) and their regulation by Ca2+ are key determinants of these spatially organized Ca2+ signals, but neither is adequately understood. IP3Rs have been proposed to be pre-assembled into clusters, but their composition, geometry and whether clustering affects IP3R behaviour are unknown. Using patch-clamp recording from the outer nuclear envelope of DT40 cells expressing rat IP3R1 or IP3R3, we have recently shown that low concentrations of IP3 cause IP3Rs to aggregate rapidly and reversibly into small clusters of approximately four IP3Rs. At resting cytosolic Ca2+ concentrations, clustered IP3Rs open independently, but with lower open probability, shorter open duration and lesser IP3-sensitivity than lone IP3Rs. This inhibitory influence of clustering on IP3R is reversed when the [Ca2+]i (cytosolic free Ca2+ concentration) increases. The gating of clustered IP3Rs exposed to increased [Ca2+]i is coupled: they are more likely to open and close together, and their simultaneous openings are prolonged. Dynamic clustering of IP3Rs by IP3 thus exposes them to local Ca2+ rises and increases their propensity for a CICR (Ca2+-induced Ca2+ rise), thereby facilitating hierarchical recruitment of the elementary events that underlie all IP3-evoked Ca2+ signals.
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NAGALEEKAR, VISWAS K., SEAN DIEHL, Ignacio Juncadella, Colette Charland, Lee Ann Garrett-Sinha, Natarajan Muthusamy, Juan Anguita, and Mercedes Rincón. "Ets1-dependent IP3R3 expression in naïve CD4+ T cells is required for cytokine gene expression (87.22)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S132. http://dx.doi.org/10.4049/jimmunol.178.supp.87.22.

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Abstract IP3 receptors (IP3Rs) are critical for the release of Ca++ from intracellular stores in response to IP3 generated upon T cell receptor (TCR) ligation. However, little is known about the expression of the different IP3Rs in CD4+ T cells and their contribution to cytokine gene expression during antigen stimulation. Here, we show for the first time that prior to activation, naïve CD4+ T cells only express IP3R3, but not IP3R1 and IP3R2. IP3R3-mediated Ca++ flux for cytokine gene expression is required for an extended period of time on the order of hours that varies for specific cytokine. IP3R3 gene expression in CD4+ T cells is dependent on the transcription factor Ets1 and is downregulated during the activation due to the loss of this transcription factor. The downregulation of IP3R3 in activated cells correlates with the failure of TCR ligation to trigger intracellular Ca++ mobilization in these cells. Thus, IP3R3 plays an important role in cytokine gene expression during early activation of naïve CD4+ T cells.
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Yue, Lili, Liuqing Wang, Yangchun Du, Wei Zhang, Kozo Hamada, Yoshifumi Matsumoto, Xi Jin, et al. "Type 3 Inositol 1,4,5-Trisphosphate Receptor is a Crucial Regulator of Calcium Dynamics Mediated by Endoplasmic Reticulum in HEK Cells." Cells 9, no. 2 (January 22, 2020): 275. http://dx.doi.org/10.3390/cells9020275.

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Being the largest the Ca2+ store in mammalian cells, endoplasmic reticulum (ER)-mediated Ca2+ signalling often involves both Ca2+ release via inositol 1, 4, 5-trisphosphate receptors (IP3R) and store operated Ca2+ entries (SOCE) through Ca2+ release activated Ca2+ (CRAC) channels on plasma membrane (PM). IP3Rs are functionally coupled with CRAC channels and other Ca2+ handling proteins. However, it still remains less well defined as to whether IP3Rs could regulate ER-mediated Ca2+ signals independent of their Ca2+ releasing ability. To address this, we generated IP3Rs triple and double knockout human embryonic kidney (HEK) cell lines (IP3Rs-TKO, IP3Rs-DKO), and systemically examined ER Ca2+ dynamics and CRAC channel activity in these cells. The results showed that the rate of ER Ca2+ leakage and refilling, as well as SOCE were all significantly reduced in IP3Rs-TKO cells. And these TKO effects could be rescued by over-expression of IP3R3. Further, results showed that the diminished SOCE was caused by NEDD4L-mediated ubiquitination of Orai1 protein. Together, our findings indicate that IP3R3 is one crucial player in coordinating ER-mediated Ca2+ signalling.
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Mikoshiba, Katsuhiko. "The IP3 receptor/Ca2+ channel and its cellular function." Biochemical Society Symposia 74 (January 12, 2007): 9–22. http://dx.doi.org/10.1042/bss2007c02.

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The IP3R [IP3 (inositol 1,4,5-trisphosphate) receptor] is responsible for Ca2+ release from the ER (endoplasmic reticulum). We have been working extensively on the P400 protein, which is deficient in Purkinje-neuron-degenerating mutant mice. We have discovered that P400 is an IP3R and we have determined the primary sequence. Purified IP3R, when incorporated into a lipid bilayer, works as a Ca2+ release channel and overexpression of IP3R shows enhanced IP3 binding and channel activity. Addition of an antibody blocks Ca2+ oscillations indicating that IP3R1 works as a Ca2+ oscillator. Studies on the role of IP3R during development show that IP3R is involved in fertilization and is essential for determination of dorso-ventral axis formation. We found that IP3R is involved in neuronal plasticity. A double homozygous mutant of IP3R2 (IP3R type 2) and IP3R3 (IP3R type 3) shows a deficit of saliva secretion and gastric juice secretion suggesting that IP3Rs are essential for exocrine secretion. IP3R has various unique properties: cryo-EM (electron microscopy) studies show that IP3R contains multiple cavities; IP3R allosterically and dynamically changes its form reversibly (square form–windmill form); IP3R is functional even though it is fragmented by proteases into several pieces; the ER forms a meshwork but also forms vesicular ER and moves along microtubules using a kinesin motor; X ray analysis of the crystal structure of the IP3 binding core consists of an N-terminal β-trefoil domain and a C-terminal α-helical domain. We have discovered ERp44 as a redox sensor in the ER which binds to the luminal part of IP3R1 and regulates its activity. We have also found the role of IP3 is not only to release Ca2+ but also to release IRBIT which binds to the IP3 binding core of IP3R.
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Bultynck, Geert, Daniela Rossi, Geert Callewaert, Ludwig Missiaen, Vincenzo Sorrentino, Jan B. Parys, and Humbert De Smedt. "The Conserved Sites for the FK506-binding Proteins in Ryanodine Receptors and Inositol 1,4,5-Trisphosphate Receptors Are Structurally and Functionally Different." Journal of Biological Chemistry 276, no. 50 (October 11, 2001): 47715–24. http://dx.doi.org/10.1074/jbc.m106573200.

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We compared the interaction of the FK506-binding protein (FKBP) with the type 3 ryanodine receptor (RyR3) and with the type 1 and type 3 inositol 1,4,5-trisphosphate receptor (IP3R1 and IP3R3), using a quantitative GST-FKBP12 and GST-FKBP12.6 affinity assay. We first characterized and mapped the interaction of the FKBPs with the RyR3. GST-FKBP12 as well as GST-FKBP12.6 were able to bind ∼30% of the solubilized RyR3. The interaction was completely abolished by FK506, strengthened by the addition of Mg2+, and weakened in the absence of Ca2+but was not affected by the addition of cyclic ADP-ribose. By using proteolytic mapping and site-directed mutagenesis, we pinpointed Val2322, located in the central modulatory domain of the RyR3, as a critical residue for the interaction of RyR3 with FKBPs. Substitution of Val2322for leucine (as in IP3R1) or isoleucine (as in RyR2) decreased the binding efficiency and shifted the selectivity to FKBP12.6; substitution of Val2322for aspartate completely abolished the FKBP interaction. Importantly, the occurrence of the valylprolyl residue as α-helix breaker was an important determinant of FKBP binding. This secondary structure is conserved among the different RyR isoforms but not in the IP3R isoforms. A chimeric RyR3/IP3R1, containing the core of the FKBP12-binding site of IP3R1 in the RyR3 context, retained this secondary structure and was able to interact with FKBPs. In contrast, IP3Rs did not interact with the FKBP isoforms. This indicates that the primary sequence in combination with the local structural environment plays an important role in targeting the FKBPs to the intracellular Ca2+-release channels. Structural differences in the FKBP-binding site of RyRs and IP3Rs may contribute to the occurrence of a stable interaction between RyR isoforms and FKBPs and to the absence of such interaction with IP3Rs.
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Song, Tengyao, Qiongyu Hao, Yun-Min Zheng, Qing-Hua Liu, and Yong-Xiao Wang. "Inositol 1,4,5-trisphosphate activates TRPC3 channels to cause extracellular Ca2+ influx in airway smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 12 (December 15, 2015): L1455—L1466. http://dx.doi.org/10.1152/ajplung.00148.2015.

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Transient receptor potential-3 (TRPC3) channels play a predominant role in forming nonselective cation channels (NSCCs) in airway smooth muscle cells (ASMCs) and are significantly increased in their activity and expression in asthmatic ASMCs. To extend these novel findings, we have explored the regulatory mechanisms that control the activity of TRPC3 channels. Our data for the first time reveal that inositol 1,4,5-trisphosphate (IP3), an important endogenous signaling molecule, can significantly enhance the activity of single NSCCs in ASMCs. The analog of diacylglycerol (DAG; another endogenous signaling molecule), 1-oleyl-2-acetyl- sn-glycerol (OAG), 1-stearoyl-2-arachidonoyl- sn-glycerol (SAG), and 1-stearoyl-2-linoleoyl- sn-glycerol (SLG) all augment NSCC activity. The effects of IP3 and OAG are fully abolished by lentiviral short-hairpin (sh)RNA-mediated TRPC3 channel knockdown (KD). The stimulatory effect of IP3 is eliminated by heparin, an IP3 receptor (IP3R) antagonist that blocks the IP3-binding site, but not by xestospongin C, the IP3R antagonist that has no effect on the IP3-binding site. Lentiviral shRNA-mediated KD of IP3R1, IP3R2, or IP3R3 does not alter the excitatory effect of IP3. TRPC3 channel KD greatly inhibits IP3-induced increase in intracellular Ca2+ concentration. IP3R1 KD produces a similar inhibitory effect. TRPC3 channel and IP3R1 KD both diminish the muscarinic receptor agonist methacholine-evoked Ca2+ responses. Taking these findings together, we conclude that IP3, the important intracellular second messenger, may activate TRPC3 channels to cause extracellular Ca2+ influx, in addition to opening IP3Rs to induce intracellular Ca2+ release. This novel extracellular Ca2+ entry route may play a significant role in mediating IP3-mediated numerous cellular responses in ASMCs and other cells.
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Zhao, Guiling, Zachary P. Neeb, M. Dennis Leo, Judith Pachuau, Adebowale Adebiyi, Kunfu Ouyang, Ju Chen, and Jonathan H. Jaggar. "Type 1 IP3 receptors activate BKCa channels via local molecular coupling in arterial smooth muscle cells." Journal of General Physiology 136, no. 3 (August 16, 2010): 283–91. http://dx.doi.org/10.1085/jgp.201010453.

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Plasma membrane large-conductance Ca2+-activated K+ (BKCa) channels and sarcoplasmic reticulum inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) are expressed in a wide variety of cell types, including arterial smooth muscle cells. Here, we studied BKCa channel regulation by IP3 and IP3Rs in rat and mouse cerebral artery smooth muscle cells. IP3 activated BKCa channels both in intact cells and in excised inside-out membrane patches. IP3 caused concentration-dependent BKCa channel activation with an apparent dissociation constant (Kd) of ∼4 µM at physiological voltage (−40 mV) and intracellular Ca2+ concentration ([Ca2+]i; 10 µM). IP3 also caused a leftward-shift in BKCa channel apparent Ca2+ sensitivity and reduced the Kd for free [Ca2+]i from ∼20 to 12 µM, but did not alter the slope or maximal Po. BAPTA, a fast Ca2+ buffer, or an elevation in extracellular Ca2+ concentration did not alter IP3-induced BKCa channel activation. Heparin, an IP3R inhibitor, and a monoclonal type 1 IP3R (IP3R1) antibody blocked IP3-induced BKCa channel activation. Adenophostin A, an IP3R agonist, also activated BKCa channels. IP3 activated BKCa channels in inside-out patches from wild-type (IP3R1+/+) mouse arterial smooth muscle cells, but had no effect on BKCa channels of IP3R1-deficient (IP3R1−/−) mice. Immunofluorescence resonance energy transfer microscopy indicated that IP3R1 is located in close spatial proximity to BKCa α subunits. The IP3R1 monoclonal antibody coimmunoprecipitated IP3R1 and BKCa channel α and β1 subunits from cerebral arteries. In summary, data indicate that IP3R1 activation elevates BKCa channel apparent Ca2+ sensitivity through local molecular coupling in arterial smooth muscle cells.
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Alzayady, Kamil J., and Richard J. H. Wojcikiewicz. "The role of Ca2+ in triggering inositol 1,4,5-trisphosphate receptor ubiquitination." Biochemical Journal 392, no. 3 (December 6, 2005): 601–6. http://dx.doi.org/10.1042/bj20050949.

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The IP3R (inositol 1,4,5-trisphosphate receptor) forms tetrameric Ca2+ channels in ER (endoplasmic reticulum) membranes, where channel activity is largely under the control of the co-agonists IP3 and Ca2+. In cells stimulated using extracellular ligands that persistently elevate phosphoinositidase C activity, IP3Rs are rapidly ubiquitinated and then degraded by the proteasome through as yet undefined mechanisms. Whereas binding of IP3 has been suggested to be a key event in the triggering of IP3R ubiquitination the role of Ca2+ in this process remains unknown. In the present study we use αT3-1 mouse pituitary cells expressing exogenous wild-type or mutant-type-I IP3Rs (IP3R1) to provide several lines of evidence that Ca2+ is also a trigger. Firstly, depletion of ER Ca2+ stores with thapsigargin blocked wild-type IP3R1 ubiquitination. Secondly, ubiquitination was blocked by mutating Glu2100 to Asp, which is known to markedly suppress Ca2+-binding to IP3R1 and the potency of Ca2+ as a stimulus for channel opening. Thirdly, mutating Asp2550 to Ala, which inhibits Ca2+ flux through the channel pore, partially inhibited ubiquitination indicating that Ca2+ released via wild-type IP3R1 contributes to triggering ubiquitination. Fourthly, and consistent with this conclusion, although suppression of increases in cytoplasmic Ca2+ concentration did not inhibit the ubiquitination of wild-type IP3R1, it strongly inhibited the ubiquitination of the Asp2550 to Ala mutant. Overall, these results show that Ca2+ plays an important role in triggering IP3R ubiquitination. Additional experiments with IP3R1 containing an Arg265 to Gln mutation, which decreases IP3-binding affinity, confirmed that IP3-binding also plays a role. Finally, the mutations at Glu2100, Asp2550 and Arg265 inhibited IP3R1 degradation to an extent that paralleled their inhibitory effects on ubiquitination. We conclude that IP3R ubiquitination and degradation are triggered by the concerted action of IP3- and Ca2+-binding.
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Dissertations / Theses on the topic "IP3Rs"

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Nougarede, Adrien. "Molecular basis of BCL2L10/Nrh oncogenic activity in breast cancer." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1192/document.

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L'apoptose, ou « mort cellulaire programmée », joue un rôle clé dans de nombreux processus biologiques. Les protéines de la famille Bcl-2, dont l'expression est souvent altérée dans les cellules tumorales, sont les principaux régulateurs de l'apoptose. Parmi cette famille, la fonction exacte du répresseur apoptotique Nrh, aussi appelé BCL2L10 ou Bcl-B, reste à ce jour mal comprise. Bien que son expression ne soit pas détectable dans la plupart des tissus sains, on retrouve des niveaux élevés de Nrh corrélés à un mauvais pronostique dans les cancers du sein et de la prostate. Nous avons mis au jour un nouveau mécanisme selon lequel Nrz, l'orthologue de Nrh chez le poisson zèbre, interagit avec le domaine de liaison du ligand IP3 du canal calcique IP3R1. Il s'est avéré que la régulation négative des flux calciques par Nrz est critique lors du développement embryonnaire du poisson zèbre. Grâce à ces nouvelles données, nous avons cherché à comprendre la fonction de Nrh chez l'Homme, dans un contexte pathologique. Nous avons montré que Nrh interagit via son domaine BH4 avec le domaine de liaison du ligand du récepteur IP3R1 humain pour réguler l'homéostasie calcique et la mort cellulaire. Cette interaction définit Nrh comme la seule protéine de la famille Bcl-2 à réguler négativement la mort cellulaire exclusivement au niveau du réticulum endoplasmique. Pour aller plus loin, nous avons montré que la dissociation du complexe Nrh/IP3Rs sensibilise des cellules tumorales mammaires à l'action d'agents chimiothérapeutiques. Pour finir, nos résultats apportent une explication moléculaire sur la contribution de Nrh dans la résistance aux thérapies anti-tumorales
Apoptosis, also called “Programmed Cell Death”, plays a key role in many biological processes and pathologies. The B-cell lymphoma 2 (Bcl-2) proteins, whose expression is often altered in tumor cells, are the main regulators of apoptosis.Among this family, the actual physiological function of the human apoptosis inhibitor Nrh, also referred to as BCL2L10 or Bcl-B, remains elusive. Although in most healthy tissues the Nrh protein is nearly undetectable, clinical studies have shown that Nrh expression is correlated with poor prognosis in breast and prostate carcinomas. We have shed light on a novel mechanism by which Nrz, the zebrafish ortholog of Nrh, was found to interact with the Ligand Binding Domain (LBD) of the Inositol-1,4,5-triphosphate receptor (IP3R) type-I Ca2+ channel. Indeed, the regulation of IP3Rs-mediated Ca2+ signaling by Nrz was shown to be critical during zebrafish embryogenesis. We used the knowledge gained with the zebrafish model to investigate Nrh function in cancer. We showed that Nrh interacts with the LBD of IP3Rs via its BH4 (Bcl-2 Homology 4) domain, which is critical to regulate intracellular Ca2+ trafficking and cell death. Actually, this interaction seems to be unique among the Bcl-2 family, and sets Nrh as the only Bcl-2 homolog to negatively regulate apoptosis by acting exclusively at the Endoplasmic Reticulum. Furthermore, we showed that disruption of the Nrh/IP3Rs complex primes Nrh-dependent cells to apoptotic cell death and enhances chemotherapy efficiency in breast cancer cell lines.Lastly our results bring a new insight to the role of Nrh regarding chemotherapy resistance
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Criollo-Cespedes, Alfredo. "Regulation of autophagy by IP3R and IKK complex." Paris 11, 2009. http://www.theses.fr/2009PA11T099.

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Yang, Xiaofei. "Domestic innovation and joint ventures: IPRs, tariff, and spillovers." Connect to online resource, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3256420.

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Torti, Valerio. "IPRs and competition in standard setting : objectives and tensions." Thesis, University of Southampton, 2012. https://eprints.soton.ac.uk/348326/.

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Competition and intellectual property rights (IPRs) are both necessary for a market to work efficiently and to promote consumer welfare. The tension between them is only apparent. Properly applied, intellectual property rules define a legal framework which allows undertakings to profit from their inventions. This in turn encourages competition among firms and enhances dynamic efficiency, to the benefit of consumer welfare. From this perspective, IPRs and competition generate a fruitful symbiosis. Standard setting represents one of the fields where the interaction between competition law and IPRs clearly comes to light. The collaborative goal of standard setting organizations (SSOs) is to adopt and promote standards that either do not conflict with anyone’s right or, if they do, are developed under condition that patents are licensed under defined terms. On the one hand, patents are important to promote innovation, as they confer exclusive rights to the inventors. On the other, standards are paramount for enhancing the interoperability of products, expanding network externalities, and facilitating the dissemination of knowledge. Conflicts between IP and competition laws may arise in case IPRs owners in standardization contexts overexploit the rights they have been granted. This may lead to the hold-up problem, which represents both a private and public concern. How to strike, then, the optimal balance between IPRs and industry standards? By answering the question, this work aims at filling a gap in the academic literature, which does not appear so far to have attempted an in-depth assessment of the right equilibrium between investment incentives and competition goals in standard setting. Any abuse of market power may harm significantly consumer well-being. At the same time, any form of control of market power should preserve the incentives of firms to invest in the market. The crucial aim, hence, is to define the optimal balance in order to avoid risks of significant losses in consumer and societal welfare.
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Criollo, Céspedes Alfredo. "Regulación de la autofagia por el receptor del inositol trisfosfato (IP3R)." Tesis, Universidad de Chile, 2009. http://repositorio.uchile.cl/handle/2250/105178.

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Doctor en Bioquímica
La macroautofagia, comúnmente referida como “autofagia” es la principal vía de degradación de proteínas, organelos y material citoplasmático, permitiendo de este modo el reciclaje del material intracelular. Este proceso consiste en el englobamiento de fracciones citosólicas por una estructura multimembranar llamada “autofagosoma”, el cual posteriormente se fusiona con el lisosoma para formar el “autofagolisosoma”. Luego el material comprendido en el autofagolisosoma es degradado por enzimas hidrolíticas. Un estudio mostró que la inhibición de la enzima inositolmonofosfatasa (IMPasa) usando litio y L690.330, inducía una disminución de los niveles basales del IP3 y en consecuencia la generación de autofagia. Nuestros resultados confirmaron estos datos previos, demostrando que el pre tratamiento con mio-inositol revierte la autofagia inducida por litio y L-690.330. Además se demuestra que el pre tratamiento con mio-inositol también revertía la autofagia inducida por privación de nutrientes. IP3 es ligando de su receptor de IP3 (IP3R), el cual es el principal canal de Ca2+ a nivel del retículo endoplásmico. El principal objetivo de esta tesis es evaluar el rol del IP3R en la regulación de la autofagia. Los resultados mostraron que la disminución de los niveles proteicos del IP3R usando siRNA específicos, así como el tratamiento con antagonistas químicos del IP3R, tales como xestosponginas B y C, estimulaban significativamente el aumento en los niveles de autofagia. Además, xestospongina B, así como también la privación de nutrientes, indujo una pérdida en la interacción entre Bcl-2 y Beclin-1, los cuales interactúan en condiciones basales. El tratamiento con xestospongina B no perturbó los niveles de Ca2+, tanto en retículo endoplásmico como en el citosol, concluyendo que la autofagia inducida por xestospongina B es independiente de una fluctuación del Ca2+. Los experimentos de inmunoprecipitación mostraron que Beclin-1 (regulador clave en la inducción de la autofagia) interactúa tanto con IP3R así como con Bcl-2 en condiciones basales, y la interacción de este complejo es atenuado bajo condiciones de privación de nutrientes o por tratamiento con ABT737, el cual es un mimetizador de dominios BH3. Este resultado sugiere la presencia de un complejo proteico en la regulación de la autofagia. El papel del retículo endoplásmico en el desarrollo de la autofagia toma gran significancia debido al reclutamiento de proteínas clave (IP3R, Beclin-1 and Bcl-2). La relación entre autofagia y estrés de retículo no es clara y por lo tanto se evaluó el efecto de agentes inductores de estrés de retículo en la inducción de la autofagia. Los resultados mostraron que tunicamicina, tapsigargina y brefeldina-A (agentes inductores de estrés de retículo) activaron el UPR (respuesta a proteínas mal plegadas) e indujeron autofagia. La disminución de los niveles de proteínas claves en el desarrollo de la autofagia (Atg5, Atg10, Atg12, Vps34 y Beclin-1) usando específicos RNAs interferentes atenuaron la autofagia inducida por agentes inductores de estrés de retículo y xestospongina B. Además, la sobreexpresión de Bcl-2 y Bcl-XL con destinación a retículo endoplásmico atenuó la autofagia inducida por xestospongina B e inhibidores de la IMPasa. Esta tesis muestra novedosos resultados, los cuales dan cuenta de un complejo proteico IP3R/Beclin-1/Bcl-2 en la regulación de la autofagia.
Macroautophagy (herein referred to as “autophagy”) is the major catabolic pathway for entire organelles, long-lived/ aberrant proteins and superfluous portions of the cytosol. It consists of the stepwise engulfment of substrate elements into distinctive multimembraned “autophagosomes”, which after fusion with lysosomes form singlemembraned autophagolysosomes. Into the autophagolysosome, the engulfed material is degradated by lisosomal hidrolytic enzymes, leading the recyclage of intracellular material. A study has suggested that myo-inositol-1,4,5-trisphosphate (IP3) could regulate autophagy because inhibition of inositol monophosphatase (IMPasa) by lithium or L-690.330 stimulates autophagy through the depletion of IP3. Our results have confirmed that the reduction of intracellular IP3 levels by IMPasa inhibitors (lithium and L.690.330) stimulates autophagy, whereas the enhancement of IP3 levels by pre treatment whit mio-inositol inhibits the lithium and L.690.330 effect. Moreover we have demostred that autophagy induced by nutrient privation was also inhibited by treatment with mio-inositol, but the effect of nutrient privation in the intracellular IP3 basal levels was not evaluated. IP3 acts on the IP3 receptor (IP3R), an IP3‑activated Ca2+ channel of the endoplasmic reticulum membrane and consequently we wanted to evaluate de roll of IP3R in the regulation of autophagy. The results obtained in this thesis show that knockdown of the IP3 receptor (IP3R) with specifics small interfering RNAs and pharmacological IP3R antagonist (xestospongin B and C) are a strong stimulus for the induction of autophagy, in addition, xestospongin B (like nutrient starvation) induced loss in the interaction between Beclin-1 and Bcl-2. Moreover, the autophagy promoted by xestospongin B not produced alterations in the steady-state Ca2+ levels in the ER or in the cytosol, therefore the autophagy induced by xestospongin B was Ca2+-independent. Immunoprecipitation assays shown that Beclin- 1 (key protein in the regulation of autophagy) interacts with IP3R and Bcl-2 in basal conditions, and this interaction may be attenuated both by nutrient starvation or ABT737 treatment, which is a mimetic compound of BH3. These results suggest the presence of a protein complex in the regulation of autophagy. The treatment whit ER stressors such as tunicamycin, thapsigargin and brepheldine A induced Unfolded Protein Responses (UPR) and autophagy. The autophagy induced by these agents showed to be IRE1α dependent, but the inhibition of autophagy showed an increase in the cell death, indicating a pro survival function of the autophagy upon endoplasmic reticumum stress conditions. The autophagy induced by treatment with xestospongin B and ER stressors was inhibited by knockdown of Atg5, Atg10, Atg12, Vps34 and Beclin-1, which are keys proteins in the autophagic process. We have also evaluated the roll of Bcl-2 and Bcl-XL in the inhibition of autophgy, and the results showed that Autophagy triggered by IMPasa inhibitors and xestospongin B was inhibited by Bcl-2 and Bcl-XL over expression specifically targeted to ER but not Bcl-2 or Bcl-XL proteins targeted to mitocondria. Altogether, these results suggest that IP3R form a regulator complex with Bcl-2 and Beclin-1, which exerts a major role in the physiological control of autophagy
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Ikebara, Juliane Midori. "Role of intracellular calcium receptor inositol 1,4,5-trisphosphate type 1 (IP3R1) in rat hippocampus after neonatal anoxia." reponame:Repositório Institucional da UFABC, 2016.

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Orientador: Prof. Dr. Alexandre Hiroaki Kihara
Dissertação (mestrado) - Universidade Federal do ABC, Programa de Pós-Graduação em Neurociência e Cognição, 2016.
Anóxia é uma das maiores causas de morbidade e mortalidade neonatal, especialmente em neonatos pré-maturos, constituindo um importante problema de saúde pública devido às sequelas neurológicas permanentes em pacientes. A privação de oxigênio dispara uma série de cascatas, culminando em morte celular em regiões cerebrais mais vulneráveis, como o hipocampo. Neste processo de morte celular causada pela privação de oxigênio, o cálcio citosólico possui um papel crucial. Receptores intracelulares de inositol 1,4,5-trifosfato (IP3Rs) são importantes reguladores de níveis de deste cálcio, no entanto, não se sabe sobre sua função na anóxia. O objetivo deste estudo é analisar se os IP3Rs do tipo 1 (IP3R1) participam no processo de morte no hipocampo de ratos após a anóxia neonatal. A análise quantitativa de real-time PCR revelou uma diminuição da expressão gênica de IP3R1 24 horas após a anóxia neonatal. Na análise da distribuição de células IP3R1-positivas foi observada uma densidade de IP3R1 na região de CA1 em ambos os grupos, porém, não se observou diferença entre os grupos controle e anóxia. Interessantemente os animais anóxia apresentaram uma alta colocalização de IP3R1 e marcador de núcleo (DAPI), sugerindo que a anóxia causa uma translocação de IP3R1 para o núcleo nas células hipocampais. Além disso, o padrão de marcação mostrou diferentes tamanhos de clusters dos receptores, indicando uma organização diferente entre os grupos. Foi injetado 2-APB, um bloqueador de IP3R1, ou veículo, no hipocampo de forma bilateral após a anóxia. Foi utilizado metodologias de marcação de células degeneradas e foi visto que no grupo 2APB houve uma diminuição do número de células FJC-positivas e TUNEL-positivas em comparação ao grupo veículo anóxia. Porém, não foi observado nenhuma diferença de marcação entre os grupos na imunofluorescência de caspase-3 ativada. Não foi detectada nenhuma diferença entre os grupos no teste de labirinto de Barnes. No teste de campo aberto, observou-se que o grupo 2APB apresentam maiores níveis de ansiedade. Desta forma, este estudo pode contribuir com novas perspectivas na investigação de mecanismos de neurodegeneração ativadas pela privação de oxigênio.
Anoxia is one of the most prevalent causes of neonatal morbidity and mortality, especially in preterm neonates, constituting an important public health problem due to permanent neurological sequelae observed in patients. Oxygen deprivation triggers a series of simultaneous cascades, culminating in cell death mainly located in more vulnerable metabolic brain regions, such as the hippocampus. In the process of cell death by oxygen deprivation, cytosolic calcium plays crucial roles. Intracellular inositol 1,4,5-trisphosphate receptors (IP3Rs) are important regulators of cytosolic calcium levels, although the role of these receptors in neonatal anoxia is completely unknown. This study focused on the functional role of inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) in rat hippocampus after neonatal anoxia. Quantitative real-time PCR analysis revealed a decrease of IP3R1 gene expression 24 hours after neonatal anoxia. Distribution analysis of IP3R-positive cells was performed and we observed higher IP3R1 pixels quantity in CA1 of both groups; however, we were not able to observe alterations between control and anoxia animals. Interestingly, we observed that anoxia animals present a higher colocalization of IP3R1 and nucleus marker (DAPI), suggesting that neonatal anoxia may cause IP3R1 translocation to the nucleus in hippocampal cells. Furthermore, puncta-labelling pattern showed different cluster sizes, larger in control group, indicating different organization between groups. We injected 2-APB, an IP3R1 blocker, or vehicle in hippocampus bilaterally after anoxia. Labelling techniques of degenerate cells was performed and we observed that 2APB group decrease the number of FJC-positive cells compared to vehicle anoxia group. In contrast, TUNEL labelling and active caspase-3 immunofluorescence showed no difference between groups. Barnes maze test showed no differences between 2APB group and anoxia vehicle group. On the other hand, the open field test showed that 2APB group presents higher anxiety levels than vehicle group. In this way, this study may contribute to new perspectives in the investigation of neurodegenerative mechanisms triggered by oxygen deprivation.
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Ritaine, Abigaël. "On the mechanisms of regulation of the IP3R activity by its interaction with Bcl-2." Thesis, Lille, 2018. http://www.theses.fr/2018LIL1S101.

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L’homéostasie calcique est régulée par de nombreux canaux ioniques, parmi lesquels des canaux intracellulaires perméables au Ca2+, comme l’IP3R. Récemment, la protéine Bcl-2 a été montré comme régulant l’activité de ce canal ionique. Cependant, les acteurs moléculaires précis de cette interaction ne sont pas très bien établis. Ici nous montrons grâce à une nouvelle technique que l’IP3R est inhibé par le domaine BH4 de Bcl-2 et que ce domaine est nécessaire et suffisant pour inhiber son activité. De plus, la liaison de l’ABT-199 dans la poche hydrophobe de Bcl-2 conduit à un changement de structure du domaine BH4. Le niveau d’expression des différentes isoformes d’IP3R ainsi que des protéines Bcl-2 et Bcl-xL ont été étudié dans différentes lignées cancéreuses prostatiques. De manière intéressante, l’expression du récepteur à l’IP3 de type 3 (IP3R3) est augmentée en fonction de l’agressivité des lignées cancéreuses prostatiques. De plus, nous pouvons observer un effet important de l’IP3R3 sur la migration et l’invasion des lignées humaines de cancer de la prostate. Globalement, ces données montrent que l’IP3R3 participe à l’augmentation du potentiel métastatique des cellules cancéreuses prostatiques. Par conséquent, l’IP3R3 peut être un marqueur diagnostic intéressant ainsi qu’une cible thérapeutique, notamment pour les stades avancés de cancer de la prostate
Calcium homeostasis is regulated by various ion channels, among which intracellular Ca2+-permeable channels, such as IP3R. Lately, Bcl-2 protein have been shown to regulate this ion channel activity. However, the study of the functional properties of IP3R in interaction with Bcl-2 is not a straightforward procedure and the molecular players implicated in that interaction are still not well established. Here, we show with the use of a new electrophysiological method, that the IP3R is inhibited by Bcl-2 via its BH4 domain and that the BH4 domain of Bcl-2 can inhibit by itself the single channel activity of the IP3R. Moreover, the binding of the ABT-199 in the hydrophobic groove of Bcl-2 leads to a tail-flip structural change in BH4 domain. We also studied the expression level of different IP3R isoforms as well as Bcl-2 and Bcl-xL protein in different prostate cancer cell lines. Interestingly, IP3R type 3 (IP3R3) expression is increased according the aggressiveness of prostate cancer cell lines. Indeed, IP3R3 was expressed preferentially in highly aggressive prostate cancer cell lines. Moreover, we can observe an significantly important effect of the IP3R3 on migration and invasion properties of human prostate cancer cell lines. Our study also revealed that IP3R3 was not involved in viability, proliferation. Overall, these data provide evidence on IP3R3 contribution to the increased metastatic potential of human prostate cancer cells. Therefore, IP3R3 could provide new perspective molecular target for the disease suppression, in particular at its advances stages
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Georgeon, Chartier Carole. "Evaluation des effets du vieillissement sur la signalisation calcique des cellules musculaires lisses des artères cérébrales dans les modèles murins C57BL6/J, SAMR1 et SAMP8 dans des conditions normales et sous restriction calorique." Thesis, Bordeaux 1, 2012. http://www.theses.fr/2012BOR14692/document.

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Au cours du vieillissement, les artères cérébrales subissent des modifications structurelles et fonctionnelles, notamment au niveau des cellules musculaires lisses (CML). La CML a pour rôle de maintenir la réactivité vasculaire via une signalisation calcique qui fait intervenir différents acteurs pouvant ainsi réguler deux phénomènes : la contraction et la relaxation. Ces acteurs rassemblent, au sein d’une même cellule, des canaux (CCVD, RYR, IP3R), des pompes calciques (SERCA, PMCA, NCX, STIM/ORAI) et leurs régulateurs (PLB, FKBP12.6, TRPP2, SARAF, TRIC). La restriction calorique (RC), apparaît comme étant un facteur retardant le vieillissement et ses pathologies. Notre travail s’est donc fortement impliqué dans l’étude de la signalisation calcique de la CML, en se focalisant sur les altérations génomiques et fonctionnelles au cours du vieillissement des artères cérébrales chez la souris C57Bl6/j. Nous avons ainsi pu mettre en évidence une altération de la signalisation calcique qui passe en partie par une modulation des niveaux d’expressions génique et protéique des canaux et pompes calciques impliqués dans ce phénomène, et par une modification fonctionnelle en termes de signaux calciques et de contraction. Après 5 mois de régime RC, il a été mis en évidence un ralentissement des altérations de la signalisation calcique liées au vieillissement et une diminution de l’oxydation des CML
During aging, cerebral arteries undergo structural and functional changes, particularly in smooth muscle cells (SMC). SMC is responsible for maintaining vascular reactivity via calcium signaling involving different actors and can regulate two phenomena: contraction and relaxation. These actors regroup channels (CCVD, RYR, IP3R) calcium pumps (SERCA, PMCA, NCX, STIM / ORAI) and their regulators (PLB, FKBP12.6, TRPP2, SARAF, TRIC). Caloric restriction (CR) appears as a factor in delaying aging and its pathologies. Our work is strongly involved in the study of calcium signaling in SMC, focusing on genomic and functional alterations during aging of cerebral arteries in mice C57BL6/J. We were able to demonstrate an altered calcium signaling, which is partly through modulation of gene and protein expression levels of calcium channels and pumps involved in this phenomenon, and a functional change in terms of calcium signals and contraction. After 5 months under RC, it was highlighted a slow calcium signaling alterations associated with aging and a decrease of SMC oxidation by SAMP8
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Mataragka, Stefania. "High-resolution optical analyses of IP3-evoked Ca2+ signals." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/289124.

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Ca2+ is a universal intracellular messenger that regulates many cellular responses. Most cells express inositol 1,4,5-trisphosphate receptors (IP3R) that mediate Ca2+ release from the endoplasmic reticulum (ER) when they bind IP3 produced after activation of cell-surface receptors. Vertebrate genomes encode three closely related subtypes of IP3R (IP3R1-3). High-resolution optical analyses have revealed a hierarchy of IP3-evoked Ca2+ signals that are thought to arise from the co-regulation of IP3Rs by IP3 and Ca2+. The smallest events ('blips') report the opening of single IP3Rs, Ca2+ 'puffs' report the almost simultaneous opening of a few clustered IP3Rs, and as stimulus intensities increase further Ca2+ signals propagate regeneratively as Ca2+ waves. The aim of this study was to establish whether all three IP3R subtypes can generate Ca2+ puffs. I first used a haploid cell line (HAP1 cells) to generate, using CRISPR/Cas9, a line lacking all endogenous IP3Rs. However, for analyses of Ca2+ puffs, I used HEK cells that had been engineered, using CRISPR/Cas9 to disrupt endogenous genes, to express single IP3R subtypes. Local Ca2+ signals evoked by flash-photolysis of caged- IP3 were recorded using Cal520 and total internal reflection fluorescence (TIRF) microscopy in human embryonic kidney (HEK) cells. The Flika algorithm was used, and validated, for automated detection of Ca2+ puffs and to measure their properties. IP3 evoked Ca2+ puffs in wild-type HEK cells and in cells expressing single IP3R subtypes. In wild-type cells, the Ca2+ signals invariably propagated regeneratively to give global increases in cytosolic [Ca2+]. This occurred less frequently in cells expressing single IP3R subtypes, commensurate with their lower overall levels of IP3R expression. The properties of the Ca2+ puffs, including their rise and decay times, durations, the size of the unitary fluorescence steps as channels closed channel during the falling phase, and the estimated number of active IP3Rs in each Ca2+ puff, were broadly similar in each of the four cell lines. The latter observation suggests that despite lower overall levels of IP3R expression (~30%) in cells with single subtypes relative to WT cells, there is a mechanism that ensures formation of similarly sized IP3R clusters. The only significant differences between cell lines were the slower kinetics of the Ca2+ puffs evoked by IP3R2, which may suggest dissociation of IP3 from its receptor contributes to the termination of Ca2+ puffs. My results demonstrate, for the first time, that all three IP3R subtypes can generate Ca2+ puffs. I conclude that Ca2+ puffs are fundamental building blocks of all IP3-evoked Ca2+ signals.
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陶, 晟辰. "循環器における小胞体タンパク質TRICに関する研究." 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/188726.

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Books on the topic "IP3Rs"

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Manjula, Guru, ed. Biotechnology, IPRs, and biodiversity. New Delhi: Pearson, 2007.

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Khor, Martin. Rethinking IPRs and the TRIPS Agreement. Penang, Malaysia: Third World Network, 2001.

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Liu, Kung-Chung, and Uday S. Racherla, eds. Innovation and IPRs in China and India. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0406-3.

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Federation of Indian Micro and Small & Medium Enterprises, ed. Identification and valuation of IPRs in MSMEs: Selected research papers. New Delhi: Federation of Indian Micro and Small & Medium Enterprises, 2012.

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Globalization, technology, and competition: IPRs, Indian pharmaceutical industry, and W.T.O. New Delhi: Serials Publications, 2007.

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Pakistan. Chaudhry's the intellectual property, intellectual property laws in Pakistan and international treaties on IPRs. Rawalpindi: Federal Law House, 2005.

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Intellectual property rights, external effects, and antitrust law: Leveraging IPRs in the communications industry. Oxford: Oxford University Press, 2003.

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Intellectual property rights (IPRs): TRIPS agreement and Indian laws : copyright, trade marks, geographical indications, industrial designs, patents, layout-designs, trade secrets. New Delhi, India: New Century Publications, 2012.

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Law and Economics of IPRs. Nova Science Publishers, Incorporated, 2016.

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Nomani, Zafar Mahfooz. Intellectual Property Rights (IPRs) and Economic Development. New Century Publications, 2020.

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Book chapters on the topic "IP3Rs"

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Zekos, Georgios I. "AI and IPRs." In Economics and Law of Artificial Intelligence, 461–89. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-64254-9_11.

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Racherla, Uday S. "Do IPRs Promote Innovation?" In Innovation and IPRs in China and India, 25–52. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0406-3_2.

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Racherla, Uday S. "Other Forms of IPRs." In Intellectual Assets for Engineers and Scientists, 175–206. First edition. | Boca Raton, FL: CRC Press/Taylor & Francis Group, 2019.: CRC Press, 2018. http://dx.doi.org/10.1201/9780429436918-6.

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Serysheva, Irina I., Mariah R. Baker, and Guizhen Fan. "Structural Insights into IP3R Function." In Advances in Experimental Medicine and Biology, 121–47. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55858-5_6.

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Racherla, Uday S. "Fundamentals of Intellectual Property Rights (IPRs)." In Intellectual Assets for Engineers and Scientists, 23–45. First edition. | Boca Raton, FL: CRC Press/Taylor & Francis Group, 2019.: CRC Press, 2018. http://dx.doi.org/10.1201/9780429436918-2.

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Racherla, Uday S., Kenneth Guang-Lih Huang, and Kung-Chung Liu. "Introduction: China and India as Contrast Pair in Innovation and IP." In Innovation and IPRs in China and India, 3–24. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0406-3_1.

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Rao, Venkata. "Technology and Business Innovation: Role and Value Measurement of IPRs." In Innovation and IPRs in China and India, 53–74. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0406-3_3.

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Huang, Kenneth Guang-Lih, and Fiona E. Murray. "Does Patent Strategy Shape the Long-Run Supply of Public Knowledge?" In Innovation and IPRs in China and India, 75–117. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0406-3_4.

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Ashok, Arathi. "Innovation, IP and India: The Dichotomy Between Facts and Fiction." In Innovation and IPRs in China and India, 121–42. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0406-3_5.

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Banerjee, Arpan. "The Law and Politics of Pharmaceutical Patents in India." In Innovation and IPRs in China and India, 143–58. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0406-3_6.

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Conference papers on the topic "IP3Rs"

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Madni, I. K., and M. Khatib-Rahbar. "Modeling and Phenomenological Aspects of Severe Accidents in Integral Pressurized Water Reactors." In ASME 2011 Small Modular Reactors Symposium. ASMEDC, 2011. http://dx.doi.org/10.1115/smr2011-6618.

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This paper focuses on modeling and phenomenological issues relevant to analysis of severe accidents in integral Pressurized Water Reactors (iPWRs). It identifies relevant thermal-hydraulics, melt progression and fission product release and transport phenomena, and discusses the applicability of the MELCOR computer code to modeling of severe accidents in iPWRs. Areas where the current MELCOR severe accident modeling framework has limitations in the representation of phenomenological processes are identified and examples of possible modeling remedies are discussed. The paper identifies modeling and phenomenological issues that contribute to differences in the calculated reactor coolant system and containment response for iPWRs as compared to traditional PWRs under severe accident conditions.
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Laliberty, Thomas J., David W. Hildum, Norman M. Sadeh, John McA’Nulty, Dag Kjenstad, Robert V. E. Bryant, and Stephen F. Smith. "A Blackboard Architecture for Integrated Process Planning/Production Scheduling." In ASME 1996 Design Engineering Technical Conferences and Computers in Engineering Conference. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/96-detc/dfm-1291.

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Abstract As companies increase the level of customization in their products, move towards smaller lot production and experiment with more flexible customer/supplier arrangements such as those made possible by Electronic Data Interchange (EDI), they increasingly require the ability to quickly, accurately and competitively respond to customer requests for bids on new products and efficiently work out supplier/subcontractor arrangements for these new products. This in turn requires the ability to rapidly convert standard-based product specifications into process plans and quickly integrate process plans for new orders into the existing production schedule to best accommodate the current state of the manufacturing enterprise. This paper describes IP3S, an Integrated Process Planning/Production Scheduling (IP3S) Shell for Agile Manufacturing. The IP3S Shell is designed around a blackboard architecture that emphasizes (1) concurrent development and dynamic revision of integrated process planning/production scheduling solutions, (2) the use of a common representation for exchanging process planning and production scheduling information, (3) coordination with outside information sources such as customer and supplier sites, (4) mixed initiative decision support, enabling the user to interactively explore a number of tradeoffs, and (5) portability and ease of integration with legacy systems. The system is scheduled for initial evaluation in a large and highly dynamic machine shop at Raytheon’s Andover manufacturing facility.
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SKUPIN, ALEXANDER, and MARTIN FALCKE. "THE ROLE OF IP3R CLUSTERING IN Ca2+ SIGNALING." In Proceedings of the 8th Annual International Workshop on Bioinformatics and Systems Biology (IBSB 2008). IMPERIAL COLLEGE PRESS, 2008. http://dx.doi.org/10.1142/9781848163003_0002.

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Sadeh, Norman M., David W. Hildum, Stephen F. Smith, Dag Kjenstad, Thomas J. Laliberty, and John McA’Nulty. "Integration of Process Planning and Production Scheduling for Agile Manufacturing: A Case Study." In ASME 1997 Design Engineering Technical Conferences. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/detc97/dfm-4330.

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Abstract As companies increasingly customize their products, move towards smaller lot production and experiment with more flexible customer/supplier arrangements, such as those made possible by Electronic Data Interchange (EDI), they increasingly require the ability to (1) respond quickly, accurately and competitively to customer requests for bids on new products and (2) efficiently work out supplier/subcontractor arrangements for these new products. This in turn requires the ability to (1) rapidly convert standard-based product specifications into process plans and (2) quickly integrate process plans for new orders into the existing production schedule to best accommodate the current state of the manufacturing enterprise. This paper describes IP3S, an Integrated Process Planning/Production Scheduling shell for agile manufacturing. IP3S utilizes a blackboard architecture that supports (1) concurrent development and dynamic revision of integrated process planning/production scheduling solutions, (2) maintenance of multiple problem instances and solutions, (3) flexible user-oriented decision making, (4) declarative representation of control information, (5) the use of a common representation for exchanging information, (6) coordination with outside information sources and (7) portability and ease of integration with legacy systems. IP3S has been validated in the context of a large and highly dynamic machine shop at Raytheon’s Andover manufacturing facility. Empirical results show an average performance improvement of 23% in solution quality over a decoupled approach to building process planning/production scheduling solutions.
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Lu, Xueying, Kirk E. Jordan, Mary F. Wheeler, Edward O. Pyzer-Knapp, and Matthew Benatan. "Bayesian Optimization for Field Scale Geological Carbon Sequestration." In SPE Reservoir Simulation Conference. SPE, 2021. http://dx.doi.org/10.2118/203950-ms.

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Abstract We present a framework of the application of Bayesian Optimization (BO) to well management in geological carbon sequestration. The coupled compositional flow and poroelasticity simulator, IPARS, is utilized to accurately capture the underlying physical processes during CO2 sequestration. IPARS is coupled to IBM Bayesian Optimization (IBO) for parallel optimizations of CO2 injection strategies during field-scale CO2 sequestration. Bayesian optimization builds a probabilistic surrogate for the objective function using a Bayesian machine learning algorithm, Gaussian process regression, and then uses an acquisition function that leverages the uncertainty in the surrogate to decide where to sample. IBO addresses the three weak points of the standard BO in that it supports parallel (batch) executions, scales better for high-dimensional problems, and is more robust to initializations. We demonstrate these algorithmic merits by an application to the optimization of the CO2 injection schedule in the Cranfield site using field data. The performance is benchmarked with genetic algorithm (GA) and covariance matrix adaptation evolution strategy (CMA-ES). Results show that IBO achieves competitive objective function value with over 60% less number of forward model evaluations. Furthermore, the Bayesian framework that BO builds upon allows uncertainty quantification and naturally extends to optimization under uncertainty.
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Wei, Zhang, and Fang Hai-yan. "IPRs protection's influences on FDI — Based on bertrand competition." In 2013 International Conference on Management Science and Engineering (ICMSE). IEEE, 2013. http://dx.doi.org/10.1109/icmse.2013.6586438.

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Mitsumori, Yaeko, Hiroshi Kato, Akiko Kato, and Koichi Kamijo. "An Analysis of COVID-19 Related IPRs : Should they be Promoted, Waived or Pooled?" In 2022 Portland International Conference on Management of Engineering and Technology (PICMET). IEEE, 2022. http://dx.doi.org/10.23919/picmet53225.2022.9882853.

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Chen, Iris Yi-juen, and Ta-Jung Lu. "Strategy of intellectual property right for the Internet of Things: How IPRs strategy adds value?" In 2016 Portland International Conference on Management of Engineering and Technology (PICMET). IEEE, 2016. http://dx.doi.org/10.1109/picmet.2016.7806684.

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Mitsumori, Yaeko, Hiroshi Kato, and Koichi Kamijo. "[Invited] An Analysis of Life Tech Related IPRs : A comparison study on Pharmaceutical vs. Non-Pharmaceutical Patents." In 2022 IEEE 4th Global Conference on Life Sciences and Technologies (LifeTech). IEEE, 2022. http://dx.doi.org/10.1109/lifetech53646.2022.9754812.

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Pannier, Christopher P., and Radek Škoda. "Small Modular Reactor and Large Nuclear Reactor Fuel Cost Comparison." In 2014 22nd International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/icone22-30903.

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Small modular reactors (SMRs) offer simple, standardized, and safe modular designs for new nuclear reactor construction. Factory built SMRs promise competitive economy when compared with the current reactor fleet. Construction cost of a majority of the projects, which are mostly in their design stages, is not publicly available, but variable costs can be determined from fuel enrichment, average burn-up, and plant thermal efficiency, which are published design parameters for many near-term SMR projects. This paper gives a simulation of the fuel cost of electricity generation for selected SMRs and large reactors, including calculation of optimal tails assay in the uranium enrichment process. The fuel costs of several SMR designs are compared between one another and with current generation large reactor designs providing a rough comparison of the long-term economics of a new nuclear reactor project. SMRs are predicted to have higher fuel costs than large reactors. Particularly, integral pressurized water reactors (iPWRs) are shown to have from 15% to 60% higher fuel costs than large reactors. Fuel cost sensitivities to reactor design parameters are presented.
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Reports on the topic "IP3Rs"

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Lall, Sanjaya. Indicators of the Relative Importance of IPRs in Developing Countries. Geneva, Switzerland: International Centre for Trade and Sustainable Development, 2003. http://dx.doi.org/10.7215/ip_ip_20030601b.

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Storrick, Gary D., Bojan Petrovic, Luca Oriani, Lawrence E. Conway, and Diego Conti. Instrumentation Needs for Integral Primary System Reactors (IPSRs) - Task 1 Final Report. Office of Scientific and Technical Information (OSTI), September 2005. http://dx.doi.org/10.2172/933156.

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