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Статті в журналах з теми "IP3Rs"
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.
Повний текст джерелаLee, 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.
Повний текст джерелаRahman, 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.
Повний текст джерелаNAGALEEKAR, 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.
Повний текст джерелаYue, 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.
Повний текст джерелаMikoshiba, 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.
Повний текст джерелаBultynck, 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.
Повний текст джерелаSong, 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.
Повний текст джерелаZhao, 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.
Повний текст джерелаAlzayady, 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.
Повний текст джерелаДисертації з теми "IP3Rs"
Nougarede, Adrien. "Molecular basis of BCL2L10/Nrh oncogenic activity in breast cancer." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1192/document.
Повний текст джерелаApoptosis, 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
Criollo-Cespedes, Alfredo. "Regulation of autophagy by IP3R and IKK complex." Paris 11, 2009. http://www.theses.fr/2009PA11T099.
Повний текст джерелаYang, 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.
Повний текст джерелаTorti, Valerio. "IPRs and competition in standard setting : objectives and tensions." Thesis, University of Southampton, 2012. https://eprints.soton.ac.uk/348326/.
Повний текст джерелаCriollo, 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.
Повний текст джерелаLa 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
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.
Знайти повний текст джерелаDissertação (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.
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.
Повний текст джерелаCalcium 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
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.
Повний текст джерелаDuring 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
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.
Повний текст джерела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.
Повний текст джерелаКниги з теми "IP3Rs"
Manjula, Guru, ed. Biotechnology, IPRs, and biodiversity. New Delhi: Pearson, 2007.
Знайти повний текст джерелаKhor, Martin. Rethinking IPRs and the TRIPS Agreement. Penang, Malaysia: Third World Network, 2001.
Знайти повний текст джерелаLiu, 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.
Повний текст джерелаFederation 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.
Знайти повний текст джерелаGlobalization, technology, and competition: IPRs, Indian pharmaceutical industry, and W.T.O. New Delhi: Serials Publications, 2007.
Знайти повний текст джерелаPakistan. Chaudhry's the intellectual property, intellectual property laws in Pakistan and international treaties on IPRs. Rawalpindi: Federal Law House, 2005.
Знайти повний текст джерелаIntellectual property rights, external effects, and antitrust law: Leveraging IPRs in the communications industry. Oxford: Oxford University Press, 2003.
Знайти повний текст джерелаIntellectual 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.
Знайти повний текст джерелаLaw and Economics of IPRs. Nova Science Publishers, Incorporated, 2016.
Знайти повний текст джерелаNomani, Zafar Mahfooz. Intellectual Property Rights (IPRs) and Economic Development. New Century Publications, 2020.
Знайти повний текст джерелаЧастини книг з теми "IP3Rs"
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.
Повний текст джерелаRacherla, 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.
Повний текст джерелаRacherla, 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.
Повний текст джерелаSerysheva, 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.
Повний текст джерелаRacherla, 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.
Повний текст джерелаRacherla, 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.
Повний текст джерелаRao, 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.
Повний текст джерелаHuang, 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.
Повний текст джерелаAshok, 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.
Повний текст джерелаBanerjee, 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.
Повний текст джерелаТези доповідей конференцій з теми "IP3Rs"
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.
Повний текст джерелаLaliberty, 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.
Повний текст джерелаSKUPIN, 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.
Повний текст джерелаSadeh, 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.
Повний текст джерелаLu, 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.
Повний текст джерелаWei, 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.
Повний текст джерелаMitsumori, 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.
Повний текст джерелаChen, 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.
Повний текст джерелаMitsumori, 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.
Повний текст джерелаPannier, 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.
Повний текст джерелаЗвіти організацій з теми "IP3Rs"
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.
Повний текст джерелаStorrick, 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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