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Littérature scientifique sur le sujet « IP3R3 »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "IP3R3"

Kochkina, Ekaterina N., Elizaveta Е. Kopylova, Olga A. Rogachevskaja, et al. "Agonist-Induced Ca2+ Signaling in HEK-293-Derived Cells Expressing a Single IP3 Receptor Isoform." Cells 13, no. 7 (2024): 562. http://dx.doi.org/10.3390/cells13070562.

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In mammals, three genes encode IP3 receptors (IP3Rs), which are involved in agonist-induced Ca2+ signaling in cells of apparently all types. Using the CRISPR/Cas9 approach for disruption of two out of three IP3R genes in HEK-293 cells, we generated three monoclonal cell lines, IP3R1-HEK, IP3R2-HEK, and IP3R3-HEK, with the single functional isoform, IP3R1, IP3R2, and IP3R3, respectively. All engineered cells responded to ACh with Ca2+ transients in an “all-or-nothing” manner, suggesting that each IP3R isotype was capable of mediating CICR. The sensitivity of cells to ACh strongly correlated wit

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Foulon, Arthur, Pierre Rybarczyk, Nicolas Jonckheere, et al. "Inositol (1,4,5)-Trisphosphate Receptors in Invasive Breast Cancer: A New Prognostic Tool?" International Journal of Molecular Sciences 23, no. 6 (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 prolifer

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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 (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 s

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NAGALEEKAR, VISWAS K., SEAN DIEHL, Ignacio Juncadella, et al. "Ets1-dependent IP3R3 expression in naïve CD4+ T cells is required for cytokine gene expression (87.22)." Journal of Immunology 178, no. 1_Supplement (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

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Hytönen, Marjo K., Julius Rönkkö, Sruthi Hundi, et al. "IP3 receptor depletion in a spontaneous canine model of Charcot-Marie-Tooth disease 1J with amelogenesis imperfecta." PLOS Genetics 21, no. 1 (2025): e1011328. https://doi.org/10.1371/journal.pgen.1011328.

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Inositol 1,4,5-trisphosphate receptors (IP3R) mediate Ca2+ release from intracellular stores, contributing to complex regulation of numerous physiological responses. The involvement of the three IP3R genes (ITPR1, ITPR2 and ITPR3) in inherited human diseases has started to shed light on the essential roles of each receptor in different human tissues and cell types. Variants in the ITPR3 gene, which encodes IP3R3, have recently been found to cause demyelinating sensorimotor Charcot-Marie-Tooth neuropathy type 1J (CMT1J). In addition to peripheral neuropathy, immunodeficiency and tooth abnormali

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Khan, Samir A., Ana M. Rossi, Andrew M. Riley, Barry V. L. Potter, and Colin W. Taylor. "Subtype-selective regulation of IP3 receptors by thimerosal via cysteine residues within the IP3-binding core and suppressor domain." Biochemical Journal 451, no. 2 (2013): 177–84. http://dx.doi.org/10.1042/bj20121600.

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IP3R (IP3 [inositol 1,4,5-trisphosphate] receptors) and ryanodine receptors are the most widely expressed intracellular Ca2+ channels and both are regulated by thiol reagents. In DT40 cells stably expressing single subtypes of mammalian IP3R, low concentrations of thimerosal (also known as thiomersal), which oxidizes thiols to form a thiomercurylethyl complex, increased the sensitivity of IP3-evoked Ca2+ release via IP3R1 and IP3R2, but inhibited IP3R3. Activation of IP3R is initiated by IP3 binding to the IBC (IP3-binding core; residues 224–604) and proceeds via re-arrangement of an interface

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Kopylova, E. Е., I. S. Masulis, O. A. Rogachevskaja, et al. "Cellular Model for the Analysis of IRBIT-Dependent Regulation of the Type 1 IP3 Receptor." Биологические мембраны Журнал мембранной и клеточной биологии 41, no. 1 (2024): 24–35. http://dx.doi.org/10.31857/s0233475524010023.

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In vertebrate genomes, three genes encode subunits of IP3 receptors, including IP3R1, IP3R2, and IP3R3. Despite high homology between different subunits, homotetrameric IP3 receptors formed by IP3R1, IP3R2, and IP₃R3 in the endoplasmic reticulum membrane are markedly distinct by their functional features and regulatory mechanisms. It was particularly reported that IP3R1 is specifically regulated by the IP3R binding protein released with IP₃ (IRBIT), which competes with IP3 for binding to IP3R1. In turn, affinity of IRBIT/IP₃R1 binding is regulated by phosphorylation of IRBIT. By using the CRIS

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HIROTA, Junji, Masashi BABA, Mineo MATSUMOTO, Teiichi FURUICHI, Kiyoshi TAKATSU, and Katsuhiko MIKOSHIBA. "T-cell-receptor signalling in inositol 1,4,5-trisphosphate receptor (IP3R) type-1-deficient mice: is IP3R type 1 essential for T-cell-receptor signalling?" Biochemical Journal 333, no. 3 (1998): 615–19. http://dx.doi.org/10.1042/bj3330615.

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Stimulation of T-cells via the T-cell receptor (TCR) complex is accompanied by an increase in intracellular Ca2+ concentration ([Ca2+]i). Recently, it was reported that a stable transformant of the human T-cell line, Jurkat, expressing an antisense cDNA construct of inositol 1,4,5-trisphosphate receptor (IP3R) type 1 (IP3R1), failed to demonstrate increased [Ca2+]i or interleukin-2 production after TCR stimulation and was also resistant to apoptotic stimuli. This cell line lacked IP3R1 expression, but expressed the type-2 and -3 receptors, IP3R2 and IP3R3 respectively [Jayaraman, Ondriasova, O

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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

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MORITA, Takao, Akihiko TANIMURA, Akihiro NEZU, Tomohiro KUROSAKI, and Yosuke TOJYO. "Functional analysis of the green fluorescent protein-tagged inositol 1,4,5-trisphosphate receptor type 3 in Ca2+ release and entry in DT40 B lymphocytes." Biochemical Journal 382, no. 3 (2004): 793–801. http://dx.doi.org/10.1042/bj20031970.

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We examined the function of GFP-IP3R3 (green fluorescent protein-tagged inositol 1,4,5-trisphosphate receptor type 3) in Ca2+ release and entry using a mutant DT40 cell line (IP3R-KO) in which all three IP3R genes had been disrupted. GFP-IP3R3 fluorescence largely overlapped with the distribution of endoplasmic reticulum, whereas a portion of GFP-IP3R3 apparently co-localized with the plasma membrane. The application of IP3 to permeabilized WT (wild-type) DT40 cells induced Ca2+ release from internal stores. Although this did not occur in IP3R-KO cells it was restored by expression of GFP-IP3R

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Thèses sur le sujet "IP3R3"

CORLIANÒ, VALERIA. "LPS-dependent NFAT activation in dendritic cells is regulated by IP4-mediated calcium entry through plasma membrane IP3R3." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/199025.

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Le cellule mieloidi del sistema immunitario innato sono in grado di riconoscere microbi o prodotti microbici attraverso recettori per i profili molecolari (PRRs, pattern recognition receptors). Tra questi, i recettori Toll-like (TLRs, Toll-like receptors) sono quelli più estensivamente caratterizzati. Il TLR4, insieme alle proteine CD14 e MD-2, forma il complesso multi-recettoriale che riconosce il Lipopolisaccaride (LPS), principale componente della membrana esterna dei batteri Gram-negativi. Il CD14 concentra il segnale dell’LPS e media la rilocalizzazione di TLR4 e MD-2 all’interno dell’end

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Vautrin-Glabik, Alexia. "Implication du récepteur de l'inositol 1,4,5-trisphosphate de type 3 (IP3R3) dans les processus migratoires des cellules cancéreuses mammaires humaines." Thesis, Amiens, 2017. http://www.theses.fr/2017AMIE0039/document.

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Le cancer du sein est le cancer féminin le plus fréquent et le plus létal chez la femme dans le monde. Malgré l'amélioration du dépistage dans les phases précoces du développement tumoral, il demeure diﬃcile de traiter les phases tardives lorsque les processus métastatiques sont engagés. Le développement métastatique dépend notamment de l'acquisition de capacités migratoires par les cellules épithéliales impliquant un remodelage du cytosquelette, hautement dépendant de la concentration calcique intracellulaire. Alors que les travaux se sont intéressés à l'implication des canaux ioniques membra

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Vautrin-Glabik, Alexia. "Implication du récepteur de l'inositol 1,4,5-trisphosphate de type 3 (IP3R3) dans les processus migratoires des cellules cancéreuses mammaires humaines." Electronic Thesis or Diss., Amiens, 2017. http://www.theses.fr/2017AMIE0039.

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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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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

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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 inositolmonofosfa

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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

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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 struc

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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), appara

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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' r

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Chapitres de livres sur le sujet "IP3R3"

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

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Ritaine, Abigaël, George Shapovalov, and Natalia Prevarskaya. "Metabolic Disorders and Cancer: Store-Operated Ca2+ Entry in Cancer: Focus on IP3R-Mediated Ca2+ Release from Intracellular Stores and Its Role in Migration and Invasion." In Store-Operated Ca²⁺ Entry (SOCE) Pathways. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57732-6_31.

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Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "IP3R1." In The Gene Knockout FactsBook. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50353-7.

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"Inositol Triphosphate Receptors (IP3Rs)." In Encyclopedia of Metalloproteins. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_100620.

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Zhang, Xiaoning, Rongzu Huang, Yang Zhou, Wenwen Zhou, and Xuhui Zeng. "IP3R Channels in Male Reproduction." In Prime Archives in Molecular Sciences. Vide Leaf, Hyderabad, 2021. http://dx.doi.org/10.37247/pacr.1.2020.17.

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FOMINA, A. F. "ROLE OF INTRACELLULAR CALCIUM RELEASE CHANNELS IN CALCIUM SIGNALING IN T LYMPHOCYTES." In ESSAYS ON NEUROPHYSIOLOGY BY PLATON KOSTYUK AND HIS STUDENTS. AKADEMPERIODYKA, 2020. https://doi.org/10.15407/biph.books.essneur.141.

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CD4+ helper T (Th) lymphocytes play a crucial role in immune responses, with calcium (Ca²⁺) signaling being essential for their activation and effector functions. Following T cell receptor (TCR) engagement, Ca²⁺ release from intracellular stores via inositol 1,4,5-trisphosphate receptors (IP3R) and ryanodine receptors (RyR) initiates a sustained Ca²⁺ influx through Ca²⁺ release-activated Ca²⁺ (CRAC) channels. This prolonged Ca²⁺ elevation regulates cytokine production, cytoskeletal remodeling, and proliferation. Disruptions in Ca²⁺ homeostasis can lead to immunodeficiency or autoimmunity. Phar

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Velázquez-Marrero, Cristina, and José R. Lemos. "Modulation of Oxytocin Release by Internal Calcium Stores." In Oxytocin and Social Function [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.112630.

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This chapter elucidates the role of depolarization-induced oxytocin (OT) vs. arginine vasopressin (AVP) secretion in the absence of external calcium, and calcium release from ryanodine-sensitive internal stores as a significant physiological contributor to neuropeptide secretion from hypothalamic neurohypophysial system (HNS) terminals. This has important therapeutic implications, given that exogenous administration of OT to children with autism spectrum disorders (ASD) has shown some success in improving social behavior and lowering anxiety. However, this nonspecific treatment has side effect

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Kevin Foskett, J., and Don-On Daniel Mak. "Regulation of IP3R Channel Gating by Ca2+ and Ca2+ Binding Proteins." In Current Topics in Membranes. Elsevier, 2010. http://dx.doi.org/10.1016/s1063-5823(10)66011-5.

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Fajmut, Aleš. "Molecular Mechanisms and Targets of Cyclic Guanosine Monophosphate (cGMP) in Vascular Smooth Muscles." In Muscle Cell and Tissue - Novel Molecular Targets and Current Advances [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97708.

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Molecular mechanisms and targets of cyclic guanosine monophosphate (cGMP) accounting for vascular smooth muscles (VSM) contractility are reviewed. Mathematical models of five published mechanisms are presented, and four novel mechanisms are proposed. cGMP, which is primarily produced by the nitric oxide (NO) dependent soluble guanylate cyclase (sGC), activates cGMP-dependent protein kinase (PKG). The NO/cGMP/PKG signaling pathway targets are the mechanisms that regulate cytosolic calcium ([Ca2+]i) signaling and those implicated in the Ca2+-desensitization of the contractile apparatus. In addit

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Actes de conférences sur le sujet "IP3R3"

Avalle, L., A. Camporeale, G. Morciano, et al. "PO-237 The pro-oncogenic transcription factor STAT3 regulates Ca2 +release and apoptosis from the endoplasmic reticulum via interaction with the Ca2 +CHANNEL IP3R3." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.270.

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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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Son, Jeongin, Saie Mogre, and Adam Glick. "Abstract 2029: The ER stress protein IRE1a regulates intracellular calcium, ROS, and the UV damage response through the IP3R inhibitor CIB1." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2029.

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Evasovic, J., C. Adajar, M. A. Hernandez, M. A. Ba та C. A. Singer. "IL-17A Reduces the Proliferative Capacity of Asthmatic Airway Smooth Muscle Independent of TGF-Β1 Concentration via Altered ERK1/2 Signaling and Modulated miR-106b∼25-dependent IP3R1 and TGFΒR2 Expression". У American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2850.

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