Relevant bibliographies by topics / RXRs

Academic literature on the topic 'RXRs'

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

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Journal articles on the topic "RXRs"

1

Yagishita, Naoko, Yoko Yamamoto, Tatsuya Yoshizawa, Keisuke Sekine, Yoshikatsu Uematsu, Hisashi Murayama, Yumiko Nagai, et al. "Aberrant Growth Plate Development in VDR/RXRγ Double Null Mutant Mice." Endocrinology 142, no. 12 (December 1, 2001): 5332–41. http://dx.doi.org/10.1210/endo.142.12.8544.

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Abstract VDR forms heterodimers with one of three RXRs, RXRα, RXRβ, and RXRγ, and it is thought that RXR ligands can also modulate the trans-activation function of VDR/RXR heterodimers. In the present study we generated VDR/RXRγ double null mutant mice to examine the convergent actions of vitamin D and vitamin A signaling and to explore the possibility of a functionally redundant VDR. Although RXRγ−/− mice exhibited no overt abnormalities, VDR−/−/RXRγ−/− mice appeared similar to VDR−/− mice, showing features typical of vitamin D-dependent rickets type II, including growth retardation, impaired bone formation, hypocalcemia, and alopecia. However, compared to VDR−/− mice, growth plate development in VDR−/−/RXRγ−/− mutant mice was more severely impaired. Normalizing mineral ion homeostasis through dietary supplementation with high calcium and phosphorous effectively prevented rachitic abnormalities, except for disarranged growth plates in VDR−/−/RXRγ−/− mutant mice, and alopecia in both VDR−/− and VDR−/−/RXRγ−/− mutant mice. Histological analysis of VDR−/−/RXRγ−/− growth plates revealed that development of the hypertrophic chondrocytes was selectively impaired. Thus, our findings indicated that the combined actions of VDR- and RXRγ-mediated signals are essential for the normal development of growth plate chondrocytes, and raised the possibility that a functionally redundant VDR is present on chondrocytes as a heterodimer with RXRγ.
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2

Dollé, Pascal. "Developmental expression of retinoic acid receptors (RARs)." Nuclear Receptor Signaling 7, no. 1 (January 2009): nrs.07006. http://dx.doi.org/10.1621/nrs.07006.

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Here, I review the developmental expression features of genes encoding the retinoic acid receptors (RARs) and the ‘retinoid X’ or rexinoid receptors (RXRs). The first detailed expression studies were performed in the mouse over two decades ago, following the cloning of the murine Rar genes. These studies revealed complex expression features at all stages of post-implantation development, one receptor gene (Rara) showing widespread expression, the two others (Rarb and Rarg) with highly regionalized and/or cell type-specific expression in both neural and non-neural tissues. Rxr genes also have either widespread (Rxra, Rxrb), or highly-restricted (Rxrg) expression patterns. Studies performed in zebrafish and Xenopus demonstrated expression of Rar and Rxr genes (both maternal and zygotic), at early pre-gastrulation stages. The eventual characterization of specific enzymes involved in the synthesis of retinoic acid (retinol/retinaldehyde dehydrogenases), or the triggering of its catabolism (CYP26 cytochrome P450s), all of them showing differential expression patterns, led to a clearer understanding of the phenomenons regulated by retinoic acid signaling during development. Functional studies involving targeted gene disruptions in the mouse, and additional approaches such as dominant negative receptor expression in other models, have pinpointed the specific, versus partly redundant, roles of the RARs and RXRs in many developing organ systems. These pleiotropic roles are summarized hereafter in relationship to the receptors’ expression patterns.
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Sugawara, Akira, Naoko Sanno, Nobuyuki Takahashi, R. Yoshiyuki Osamura, and Keishi Abe. "Retinoid X Receptors in the Kidney: Their Protein Expression and Functional Significance." Endocrinology 138, no. 8 (August 1, 1997): 3175–80. http://dx.doi.org/10.1210/endo.138.8.5351.

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Abstract Retinoid X receptors (RXRs) heterodimerize with 1,25-dihydroxyvitamin D3 (VD) receptor (VDR), and play important roles in VD-regulated transactivation. VD acts on many tissues including kidney for the regulation of calcium homeostasis. In the kidney, the expression of VDR in the tubular cells has been well studied. In contrast, little is known about the localization and the functional significance of RXRs there. In order to elucidate these questions, we first performed immunohistochemical analyses of rat kidney using isoform-specific antimouse RXR antibodies we have previously reported. Interestingly, all RXR isoforms, predominantly RXRα, mainly localized to the proximal and the distal tubules, but not to the glomeruli. The serial section staining using anti-VDR antibody showed the colocalization of RXRα and VDR in those tubular cells. In order to elucidate the functional significance of endogenous receptors in the tubular cells, we next performed transient transfection studies using the tubular-cell derived Madin-Darby bovine kidney cells, which express both endogenous VDR and RXR. We transfected a reporter plasmid containing direct repeat 3 (DR3) sequence, to which only RXR/VDR heterodimer can bind, and found that VD and 9-cis retinoic acid, as well as VD and RXR selective agonist LG100153, had an additive effect for the DR3 transactivation. Taken together, we speculate that endogenous RXRs co-localize with VDR, and coregulate VD-dependent genes in the tubular cells of the kidney as RXR/VDR heterodimer.
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Di Martino, Orsola, Margaret Y. Ferris, Hadwiger Gayla, Haixia Niu, and John S. Welch. "Endogenous Retinoid X Receptor Ligands Act As Tumor Suppressors in MLL-AF9 Mouse Leukemia." Blood 134, Supplement_1 (November 13, 2019): 2677. http://dx.doi.org/10.1182/blood-2019-128869.

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Retinoid therapy transformed response and survival outcomes in acute promyelocytic leukemia (APL), but has demonstrated only modest activity in non-APL forms of acute myeloid leukemia (AML). The retinoic acid receptors (RARs) and retinoid X receptors (RXRs) are ligand-activated transcription factors that influence hematopoietic stem cell self-renewal and differentiation. In normal hematopoiesis, RARA and RXRA are dynamically regulated during myeloid maturation, with highest expression in mature neutrophils. In acute myeloid leukemia (AML) RARA and RXRA have parallel expression among AML subtypes, with the highest expression in M4/M5 myelomonocytic and monocytic subtypes. Using a murine reporter assay, we found that natural RXRA ligands, but not RARA ligands, were present in vivo in primary mouse myelomonocytic leukemia cells (derived with an MLL-AF9 retrovirus) and acted as tumor suppressors. RXR ligands were absent in erythroleukemia (derived with TLS-ERG) or T-cell leukemia (derived with activated Notch1), suggesting the presence of natural RXRA ligands specifically in myelomonocytic leukemia. Moreover, we found that deletion of Rxra and Rxrb was naturally selected in MLL-AF9, but not in Notch1 or TLS-ERG leukemias, and that loss of Rxra and Rxrb accelerated leukemic growth. This suggests that Rxrs act as tumor suppressors, but only when exposed to natural ligands. In MLL-AF9 derived leukemia cells, pharmacologic treatment with single-agent retinoid led to modest growth inhibition due to non-permissive activity of the RARA:RXR heterodimer, whereas concurrent activation of both RARA, with all-trans retinoic acid (a pan-RAR ligand), and RXR, by bexarotene (a pan-RXR ligand), enabled efficient co-repressor release and synergistic leukemic apoptosis. We observed that co-repressors release (SMRT/NCoR) from the RARA:RXRA heterodimer was specifically associated with RARA activation, whereas growth inhibition required RXR binding, and this occurred through apoptosis rather than maturation. Generating a series of RXRA mutant proteins we demonstrated the active contribution of RXRA to the activity of the RARA:RXRA heterodimer, specifically requiring the activation domains (AF1 and AF2) and the ability to recruit co-activator to the RXRA element. Finally, we observed a significant dose-dependent effect of combination ATRA and bexarotene treatment in in vivo in MLL-AF9 leukemic mice with a striking reduction in the tumor burden of treated mice compared to the control cohort. These data provide a strategy for clinical retinoid therapies in leukemias beyond acute promyelocytic leukemia and provide a mechanism for integrating retinoid therapy into future clinical trials. Disclosures No relevant conflicts of interest to declare.
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Räuber, Saskia, Maximilian Fischer, Denise Messerer, Vanessa Wimmler, Kumaraswami Konda, Andrei Todica, Michael Lorenz, Anna Titova, Christian Schulz, and Tobias Weinberger. "Modulation of Rxrα Expression in Mononuclear Phagocytes Impacts on Cardiac Remodeling after Ischemia-Reperfusion Injury." Biomedicines 10, no. 6 (May 30, 2022): 1274. http://dx.doi.org/10.3390/biomedicines10061274.

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Retinoid X receptors (RXRs), as members of the steroid/thyroid hormone superfamily of nuclear receptors, are crucial regulators of immune response during health and disease. RXR subtype expression is dependent on tissue and cell type, RXRα being the relevant isoform in monocytes and macrophages. Previous studies have assessed different functions of RXRs and positive implications of RXR agonists on outcomes after ischemic injuries have been described. However, the impact of a reduced Rxrα expression in mononuclear phagocytes on cardiac remodeling after myocardial infarction (MI) has not been investigated to date. Here, we use a temporally controlled deletion of Rxrα in monocytes and macrophages to determine its role in ischemia-reperfusion injury. We show that reduced expression of Rxrα in mononuclear phagocytes leads to a decreased phagocytic activity and an accumulation of apoptotic cells in the myocardium, reduces angiogenesis and cardiac macrophage proliferation in the infarct border zone/infarct area, and has an impact on monocyte/macrophage subset composition. These changes are associated with a greater myocardial defect 30 days after ischemia/reperfusion injury. Overall, the reduction of Rxrα levels in monocytes and macrophages negatively impacts cardiac remodeling after myocardial infarction. Thus, RXRα might represent a therapeutic target to regulate the immune response after MI in order to improve cardiac remodeling.
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Negro-Vilar, A., U. Gatzemeier, R. Ramlau, S. L. Sun, R. Negro-Vilar, T. Hermann, J. K. Zhang, and Z. Dziewanowska. "Biomarker correlates of survival in NSCLC: Role of RXRβ and PPARγ in mediating bexarotene impact on patient survival." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 7227. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.7227.

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7227 Background: Bexarotene is a selective modulator of retinoid X nuclear receptors (RXRs), which form heterodimers with many other nuclear receptors playing a critical role in cell growth, differentiation, and apoptosis. Loss of RXRs is seen in many advanced tumors, including NSCLC and higher RXR levels in NSCLC lung biopsies (stages I-III) have been correlated with longer overall survival. Two large first line NSCLC Phase III trials reported at ASCO 2005 (SPIRIT I and II) showed that while no benefit in overall survival was seen adding bexarotene to two chemo regimens, a large (36%) subpopulation of patients in both trials that had high grade hypertriglyceridemia in response to bexarotene had significantly longer survival. A retrospective analysis was conducted to evaluate the baseline characteristics of these patients and to examine the level of expression of RXR and one of its partners (PPARγ) in lung tumor tissue biopsies obtained from a subgroup of patients in both studies. Methods: RXRs (α,β,γ) and PPARγ expression levels in lung tumor tissue from patients in SPIRIT I and II trials (stage IIIB/IV) taken prior to study entry were assessed by Q-PCR analysis of RNA isolated from microdissected lung tumor tissue biopsies. Cox regression and Kaplan-Meier survival estimation were used for statistical evaluations. Results: In an initial subset of 41 patients, RXRβ expression in lung tumor showed positive correlation with survival. High RXRβ = longer survival (median survival 438 days), low RXR shorter (MS = 317). Treatment with bexarotene increased the differences (RXRβ Hi, MS = 627 days; RXRβ low = 211 days). PPARγ showed a negative correlation with survival and those patients with RXRβ Hi/PPARγ low ratios had the longest MS (627 days vs. 226 days for the RXRβ low/PPARγ high group), a difference that was magnified by bexarotene treatment. Conclusions: RXRβ expression level correlates with a positive survival in late stage NSCLC while PPARγ shows negative correlation. Bexarotene treatment enhances the survival differences, supporting an involvement of triglyceride and lipid metabolism as regulated by these two key nuclear receptors in the longer survival seen in the 215 patients in the high triglyceride subgroup. [Table: see text]
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Vernet, Nadège, Christine Dennefeld, Cécile Rochette-Egly, Mustapha Oulad-Abdelghani, Pierre Chambon, Norbert B. Ghyselinck, and Manuel Mark. "Retinoic Acid Metabolism and Signaling Pathways in the Adult and Developing Mouse Testis." Endocrinology 147, no. 1 (January 1, 2006): 96–110. http://dx.doi.org/10.1210/en.2005-0953.

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As a first step in investigating the role of retinoic acid (RA) in mouse testis, we analyzed the distribution pattern of the enzymes involved in vitamin A storage (lecithin:retinol acyltransferase), RA synthesis (β-carotene 15,15′-monoxygenase and retinaldehyde dehydrogenases) and RA degradation (cytochrome P450 hydroxylases) as well as those of all isotypes of receptors transducing the RA signal [RA receptors (RARs) and rexinoid receptors (RXRs)]. Our data indicate that in adult testis 1) cytochrome P450 hydroxylase enzymes may generate in peritubular myoid cells a catabolic barrier that prevents circulating RA and RA synthesized by Leydig cells to enter the seminiferous epithelium; 2) the compartmentalization of RA synthesis within this epithelium may modulate, through paracrine mechanisms, the coupling between spermatogonia proliferation and spermatogenesis; 3) retinyl esters synthesized in round spermatids by lecithin:retinol acyltransferase may be transferred and stored in Sertoli cells, in the form of adipose differentiation-related protein-coated lipid droplets. We also show that RARα and RXRβ are confined to Sertoli cells, whereas RARγ is expressed in spermatogonia and RARβ, RXRα, and RXRγ are colocalized in step 7–8 spermatids. Correlating these expression patterns with the pathological phenotypes generated in response to RAR and RXR mutations and to postnatal vitamin A deficiency suggests that spermiation requires RXRβ/RARα heterodimers in Sertoli cells, whereas spermatogonia proliferation involves, independently of RXR, two distinct RAR-mediated signaling pathways in both Sertoli cells and spermatogonia. Our data also suggest that the involvement of RA in testis development starts when primary spermatogonia first appear.
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Davis, K. D., T. J. Berrodin, J. E. Stelmach, J. D. Winkler, and M. A. Lazar. "Endogenous retinoid X receptors can function as hormone receptors in pituitary cells." Molecular and Cellular Biology 14, no. 11 (November 1994): 7105–10. http://dx.doi.org/10.1128/mcb.14.11.7105-7110.1994.

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Retinoids regulate gene transcription by interacting with both retinoic acid (RA) receptors (RARs) and retinoid X receptors (RXRs). Since unliganded RXRs can act as heterodimerization partners for RARs and other nuclear hormone receptors, it is unclear whether ligand binding by RXRs actually regulates the expression of naturally occurring genes. To address this issue, we synthesized the RXR-selective retinoid SR11237 and confirmed its specificity in transient transfection and proteolytic susceptibility assays before using it to assess the contribution of ligand-activated RXRs to retinoid action. Unlike RAR ligands, SR11237 did not increase endogenous RAR beta mRNA levels in F9 embryonal carcinoma cells, even though it activated transcription of an RXR-responsive reporter gene in these cells. Thus, it is likely that RARs mediate the induction of RAR beta gene expression by RA. In contrast, the RXR-specific ligand induced rat growth hormone mRNA in GH3 pituitary cells, indicating that the effects of RA on growth hormone gene expression at least in part involve ligand binding to endogenous RXRs in vivo. Our results indicate that in addition to serving as cofactors for other nuclear hormone receptors, endogenous RXRs can function as ligand-dependent regulators of gene expression, i.e., classical nuclear hormone receptors.
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Davis, K. D., T. J. Berrodin, J. E. Stelmach, J. D. Winkler, and M. A. Lazar. "Endogenous retinoid X receptors can function as hormone receptors in pituitary cells." Molecular and Cellular Biology 14, no. 11 (November 1994): 7105–10. http://dx.doi.org/10.1128/mcb.14.11.7105.

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Retinoids regulate gene transcription by interacting with both retinoic acid (RA) receptors (RARs) and retinoid X receptors (RXRs). Since unliganded RXRs can act as heterodimerization partners for RARs and other nuclear hormone receptors, it is unclear whether ligand binding by RXRs actually regulates the expression of naturally occurring genes. To address this issue, we synthesized the RXR-selective retinoid SR11237 and confirmed its specificity in transient transfection and proteolytic susceptibility assays before using it to assess the contribution of ligand-activated RXRs to retinoid action. Unlike RAR ligands, SR11237 did not increase endogenous RAR beta mRNA levels in F9 embryonal carcinoma cells, even though it activated transcription of an RXR-responsive reporter gene in these cells. Thus, it is likely that RARs mediate the induction of RAR beta gene expression by RA. In contrast, the RXR-specific ligand induced rat growth hormone mRNA in GH3 pituitary cells, indicating that the effects of RA on growth hormone gene expression at least in part involve ligand binding to endogenous RXRs in vivo. Our results indicate that in addition to serving as cofactors for other nuclear hormone receptors, endogenous RXRs can function as ligand-dependent regulators of gene expression, i.e., classical nuclear hormone receptors.
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Mascrez, Bénédicte, Manuel Mark, Wojciech Krezel, Valérie Dupé, Marianne LeMeur, Norbert B. Ghyselinck, and Pierre Chambon. "Differential contributions of AF-1 and AF-2 activities to the developmental functions of RXRα." Development 128, no. 11 (June 1, 2001): 2049–62. http://dx.doi.org/10.1242/dev.128.11.2049.

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We have engineered a mouse mutation that specifically deletes most of the RXRα N-terminal A/B region, which includes the activation function AF-1 and several phosphorylation sites. The homozygous mutants (RXRαaf1o), as well as compound mutants that further lack RXRβ and RXRγ, are viable and display a subset of the abnormalities previously described in RXRα-null mutants. In contrast, RXRαaf1o/RAR−/−(α, β or γ) compound mutants die in utero and exhibit a large array of malformations that nearly recapitulate the full spectrum of the defects that characterize the fetal vitamin A-deficiency (VAD) syndrome. Altogether, these observations indicate that the RXRα AF-1 region A/B is functionally important, although less so than the ligand-dependent activation function AF-2, for efficiently transducing the retinoid signal through RAR/RXRα heterodimers during embryonic development. Moreover, it has a unique role in retinoic acid-dependent involution of the interdigital mesenchyme. During early placentogenesis, both the AF-1 and AF-2 activities of RXRα, β and γ appear to be dispensable, suggesting that RXRs act as silent heterodimeric partners in this process. However, AF-2 of RXRα, but not AF-1, is required for differentiation of labyrinthine trophoblast cells, a late step in the formation of the placental barrier.
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Dissertations / Theses on the topic "RXRs"

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Marceau, Geoffroy. "Facteurs de transcription nucléaires (RARs, RXRs, LXRs) et membranes amniotiques : métabolisme des rétinoïdes et stratégies d'identification de nouveaux gènes cibles des rétinoïdes." Clermont-Ferrand 1, 2007. http://www.theses.fr/2007CLF1MM01.

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Les membranes amniotiques humaines constituent une entité tissulaire et fonctionnelle singulière dont l'intégrité est indispensable au bon déroulement de la grossesse. Elles se composent essentiellement de deux feuillets, l'amnios et le chorion, dont toute altération peut conduire à leurs ruptures. Structure transitoire en apparence simple, les membranes amniotiques présentent un grand nombre d'évènements tissulaires et cellulaires, suggérant probablement une fine régulation moléculaire. Cependant les connaissances sur des processus comme l'angiogenèse, la prolifération, la différenciation, ou l'apoptose restent fragmentaires et leurs mécanismes moléculaires de régulation sont à ce jour peu connus. La vitamine A exerce une grande variété d'effets sur la différentiation, l'homéostasie tissulaire, la prolifération cellulaire et l'apoptose. Nous avons donc initié ce travail dans le but d'explorer le rôle de la vitamine A dans la physiologie des membranes et l'implication moléculaire des rétinoïdes via des facteurs de transcription nucléaires, les Retinoic Acid Receptors ou RARs et les Retinoid X Receptors ou RXRs. En 1er lieu, nous avons caractérisé le profil d'expression des différents acteurs moléculaires du métabolisme de la vitamine A au niveau des tissus et cellules des membranes. Deuxièmement, nous avons étudié, dans les tissus humains et murins, un partenaire hétérodimérisant avec RXR, impliqué dans la physiologie membranaire : LXR. Troisièmement, nous avons développé des techniques de bioinformatique, de culture d'explants et moléculaires permettant d'identifier des gènes cibles des rétinoïdes potentiellement impliqués dans la physiopathologie membranaire. Parmi ces gènes, nous avons choisi d'étudier plus particulièrement le +PA. Nous avons pu démontrer l'induction directe du +PA en transcrits et en protéines en culture d'explants d'amnios ainsi que le rôle du DR5 dans son activation transcriptionelle. En conclusion, l'étude du métabolisme du rétinol et l'étude de ses gènes cibles dans les membranes amniotiques, nous a permis d'aborder la régulation moléculaire de processus physiopathologiques dans cette structure. A terme, ces données pourront être utilisées pour une meilleure compréhension de la physiopathologie des membranes amniotiques afin de développer une meilleure prise en charge diagnostique (test biologique de rupture prématurée des membranes amniotiques) et thérapeutique ("amniopatch" à la vitamine A) en obstétrique.
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Quintas, Ameixa Maria Clara. "Regulation of RXRa gene expression in embryonic cells." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391704.

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Guzmán, Alerie. "RXR signalling in oligodendrocyte lineage cells." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708611.

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Di, Canio Ludovica. "Regulation of oligodendrocyte lineage cell function by the RXRγ nuclear receptor." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/289129.

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Remyelination is a spontaneous regenerative process whereby myelin sheaths are restored to demyelinated axons. Key players in this process are oligodendrocyte progenitor cells (OPCs), a widespread population of CNS progenitor cells which persist into adulthood. Remyelination is impaired in patients with chronic demyelinating conditions such as Multiple Sclerosis, and as with other regenerative processes, its efficiency declines with increasing age. Hence, there is a need for the development of therapeutic interventions that will aid in promoting endogenous remyelination when the endogenous regenerative potential is compromised. The nuclear receptor RXR$\gamma$ is an important positive regulator of OPC differentiation and an accelerator of endogenous remyelination in aged rats. RXR$\gamma$ functions as a ligand-induced transcription factor and is able to regulate gene transcription. It does so by heterodimerising with other nuclear receptors and recruiting co-regulators involved in chromatin remodelling. However, we lack understanding on the specific mechanism by which RXR$\gamma$ promotes OPC differentiation. With the work presented in this thesis I demonstrate that RXR$\gamma$ function is regulated at multiple signalling levels. Proximity ligation assays revealed that RXR$\gamma$ remains consistently bound to its partners throughout the oligodendrocyte lineage, and the biological relevance of each heterodimer is determined by the dynamic association of co-regulators. This is in turn influenced by ligand presence and subcellular receptor localisation. To identify the genes controlled by RXR$\gamma$ in OPCs I carried out ChIP sequencing, which revealed genes involved in proliferation and cell cycle control. Further functional assessments aided me in the development of a hypothesis whereby RXR$\gamma$ activation does not directly influence oligodendrocyte formation, but rather promotes cell cycle exit thereby accelerating and facilitating OPC differentiation. Altered nuclear receptor expression and ligand presence in ageing OPCs may consequently impair this process. My thesis provides an alternative hypothesis to how RXR$\gamma$ regulates lineage cell progression, highlighting a new avenue in the development of therapeutic interventions targeting generic stem cell functions for which drugs are already FDA approved, rather than oligodendrocyte-specific pathways.
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Krezel, Wojciech. "Fonction du recepteur nucleaire rxr chez la souris." Université Louis Pasteur (Strasbourg) (1971-2008), 1997. http://www.theses.fr/1997STR13090.

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L'acide retinoique (metabolite actif de la vitamine a) joue un role important au cours du developpement embryonnaire et dans la croissance et la differenciation cellulaires. Deux familles de recepteurs nucleaires des retinoides ont ete caracterisees : les recepteurs de l'acide retinoique, comprenant trois genes (rar, , ), et les recepteurs x de retinoides, comprenant egalement trois genes (rxr, , ). Nous avons etudie la fonction de rxr, en generant et analysant des souris portant une mutation nulle dans le gene correspondant. Il en ressort que rxr ne joue pas un role essentiel au cours de l'organogenese de la souris. D'autre part les souris rxr#+#/#-/rxr#-#/#-/rxr#-#/#- et rxr#-#/#-/rar (, ou ) sont viables et ne presentent pas de lesions majeures. Ceci suggere que rxr pourrait etre le mediateur principal de la fonction des rxrs au cours du developpement. Des etudes comportementales realisees chez les mutants rar/rxr et rxr/rxr ont revele que rxr joue un role dans le controle de l'activite locomotrice de la souris. Chez ces souris, nous avons observe une modification de l'expression des recepteurs dopaminergiques, ce qui pourrait etre a la base des problemes locomoteurs. Ce travail demontre pour la premiere fois un role des recepteurs des retinoides dans le fonctionnement du systeme nerveux central.
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Halftermeyer, Juliane. "Rôle de RXR sur la transformation par PML-RARα." Paris 7, 2011. http://www.theses.fr/2011PA077194.

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La leucémie aigüe promyélocytaire (LAP) est une maladie rare présentant une prolifération anormale de cellules bloquées au stade promyélocyte, majoritairement caractérisée par la translocation t(15,17) et la formation de la protéine de fusion PML-RARa. PML-RARa induirait notamment l'extinction de gènes essentiels à la différenciation des cellules myéloïdes. In vivo, les protéines RXR (Retinoid X Receptor) sont importantes dans ces mécanismes de transformation par PML-RARa. J'ai développé un modèle ex vivo de cellules primaires de moelle osseuse de souris transformées par PML-RARa dans lesquelles les RXRs peuvent être excisés de façon inductible. La perte des RXRs induit une baisse de la clonogénicité des cellules transformées et une diminution significative de leur survie en culture liquide. J'ai créé une lignée de souris RXRaf/f, RXRbf/f, RXRg-/- PML-RARa, et obtenu, suite à l'introduction de FLT3-ITD, une leucémie dans laquelle les RXRs peuvent être excisés de façon inductible. L'excision des RXRs in vivo provoque une différenciation des cellules leucémiques, comme observé en réponse à un traitement à l'acide rétinoïque (AR), mais sans dégradation de PML-RARa. La perte des RXRs permet aussi un allongement de la survie des souris leucémiques. La différenciation observée en réponse aux différents traitements de la LAP était considérée comme le résultat de la transcription active par PML-RARa. Cependant, mes résultats soutiennent un modèle de différenciation induite par la simple dérépression des gènes cibles de l'AR. La validation de ce nouveau modèle nécessite néanmoins l'étude de la liaison de PML-RARa à l'ADN en présence ou en absence de RXRa
Acute promyelocytic leukemia (APL) is induced in 99% of cases by a translocation t(15-17) leading to the PML-RARa fusion oncoprotein. PML-RARa acts as a transcriptional repressor, thus inducing a characteristic differentiation block of myeloid cells. In vivo, PML-RARa is always found in association with the nuclear receptor RXR (Retinoid X Receptor). Actually, RXR is an essential protein for PML-RARa driven transformation. During my thesis, I developed in vivo and ex vivo models to study the functional role of RXR in APL, both models using conditional excision of RXR in RXRaf/f, RXRbf/f, RXRg-/- mice and the Cre-ERT2/Lox System inducible by 4-OHT. In primary bone marrow cells transformed with PML-RARa, excision of RXRs induces a dramatic loss of clonogenicity and growth arrest ex vivo. I also constructed a transgenic model of PML-RARa mice, with RXRaf/f, RXRbf/f, RXRg-/-. After introduction of a constitutively active FLT3 and Cre-ERT2,1 obtained a murine APL in which I was able to excise RXRs. In vivo, loss of RXRs results in a prolongation of mice survival and elicits full differentiation of leukemic cells, similar to that induced by treatment with retinoic acid (RA), but does not degrade PML-RARa. RA treatment was previously thought to activate transcription of target genes and thus promote differentiation by converting PML-RARa from a repressor to an activator protein. However, my results support an other model in which treatment-induced differentiation is promoted by the mere derepression of PML-RARa target genes. Further studies are needed to evaluate the DNA binding of PML-RARa in presence or absence of RXR in order to verify this hypothesis
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Ma, Xingjie. "Identification d'un nouveau régulateur et d'une nouvelle fonction de la sénescence cellulaire." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1138.

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La sénescence cellulaire, arrêt stable de la prolifération cellulaire, est accompagnée de la sécrétion de nombreux facteurs pro-inflammatoires (programme sécrétoire associé à la sénescence appelé SASP). La sénescence est induite par divers stimuli, et joue un rôle clé dans de multiples contextes physiopathologiques. Cependant, la régulation de la sénescence est encore mal comprise. Notre laboratoire a récemment identifié le récepteur inositol 1,4,5-trisphosphate de type 2 (ITPR2, canal calcique du ER) comme nouveau régulateur de la sénescence. L'expression du gène ITPR2 est réprimée dans la plupart des cancers, mais sa régulation transcriptionnelle est peu connue. Dans ce contexte, le premier objectif de ma thèse était de caractériser de nouveaux régulateurs de l’expression d’ITPR2. Par un criblage (siRNA) et une analyse Nanostring, nous avons identifié le récepteur nucléaire RXRA comme répresseur transcriptionnel d’ITPR2. Nous avons montré que dans les fibroblastes primaires humains, le knockdown de RXRA induit l’expression d’ITPR2 et de ce fait la signalisation calcique, la production d’espèces réactives de l’oxygène (ROS), le dommage de l’ADN et finalement la sénescence via l’activation de la voie p53-p21. Inversement, la surexpression constitutive de RXRA retarde la sénescence réplicative. Les molécules du SASP, induisant ou renforçant la sénescence, peuvent réguler la signalisation calcique. Le deuxième objectif de ma thèse était d’étudier le rôle du SASP et la participation de la signalisation calcique dans celui-ci. Nous avons observé que le SASP induit la sénescence cellulaire accompagnée d’une différenciation neuroendocrine (NED) dans des cellules de cancer du sein. Le SASP induit une accumulation de calcium dans le cytoplasme qui paraît être impliquée dans la régulation de la NED. Une analyse de données d’échantillons de tumeurs du sein humaines et observé que les échantillons positifs pour la NED présentent des marques de sénescence
Cellular senescence is a stable proliferation arrest accompanied with senescence-associated secretory phenotype (SASP). Senescence is induced by diverse stimuli such as telomere shortening and oncogene activation and plays key roles in many physiopathological contexts like embryonic development, cancer and aging. However the molecular mechanisms regulating senescence remain partially understood. Our laboratory recently identified a new senescence regulator: the inositol 1,4,5-trisphosphate receptor type 2 (ITPR2), an ER calcium release channel. ITPR2 is repressed in many cancers, but its transcriptional regulation is barely known. Therefore, the first aim of my thesis was to characterize new ITPR2 regulators. Through siRNA screen and Nanostring analysis, we identified the nuclear receptor RXRA as a transcriptional repressor of ITPR2. We found that in primary human fibroblasts, RXRA knockdown induces ITPR2 expression and thereby calcium signaling, reactive oxygen species (ROS) production, DNA damage and ultimately senescence through p53-p21 axis. Conversely, RXRA overexpression delays replicative senescence. SASP has been described to induce/reinforce senescence, and most of the SASP factors are able to regulate calcium signaling through their receptors. The second aim of my thesis was to investigate the role of the SASP and the participation of calcium signaling in it. We observed that the SASP induces senescence accompanied with a neuroendocrine differentiation (NED) in some breast cancer cells. Interestingly, SASP triggers calcium accumulation in the cytoplasm which seems to be involved in the regulation of NED. We then analyzed human breast tumor datasets and observed that NED-positive samples display some senescence marks: functional p53, low proliferation level and Sprouty 2 expression. Altogether, my work identified RXRA as a new senescence regulator and showed calcium signaling is involved in SASP-induced NED in breast cancer cells
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Dias, Sandra Martha Gomes. "Estudos estruturais dos receptores nucleares humanos para os hormônios tireoidianos Isoforma ß1 (hTRß1) e para o ácido retinóico 9-cis Isoforma a (hRXRa)." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/76/76132/tde-21092007-141432/.

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Os receptores nucleares são de suma importância para os processos de sinalização intercelular nos eucariotos, uma vez que possuem a capacidade de convergir diferentes sinais internos e externos na regulação de programas genéticos. Estas proteínas funcionam, na sua maioria, como fatores de transcrição ativados por ligantes, sendo a via de comunicação direta entre as moléculas de sinalização e a resposta transcricional eliciada pelas mesmas. A programação genética, estabilizada ou modificada pelos receptores, afeta virtualmente todos os aspectos da vida dos organismos multicelulares, tais como a embriogênese, a homeostase, a reprodução, o crescimento e a morte celular. A regulação transcricional e a seletividade promovida por estas proteínas têm fomentado intensas pesquisas, as quais estão decifrando a complexa rede de eventos moleculares que relatam sua forma de ação. Será um desafio para o futuro o conhecimento completo das regras moleculares que definem sua maneira de promover o controle espacial e temporal da expressão gênica. Estas informações prometem trazer detalhes cruciais para o desenvolvimento de drogas mais eficientes e de grande valor terapêutico. Neste contexto, o principal objetivo dos estudos aqui apresentados foi o de aumentar o conhecimento sobre o comportamento e estrutura do receptor nuclear humano dos hormônios tireoidianos, isoforma β1 (hTRβ1), e do receptor nuclear humano do ácido retinóico 9-cis, isoforma ? (hRXRα). Para tal, aplicou-se a técnica de espalhamento de raios X a baixos ângulos para determinar-se, em solução, o envelope destes receptores contendo os domínios de ligação ao DNA e ao ligante. Paralelamente, investiu-se em diversas tentativas de cristalização dos mesmos. Os resultados obtidos permitiram a determinação da localização espacial dos diferentes domínios e as organizações quaternárias dos homodímeros e homotetrâmeros. Conseqüentemente, foram propostos os primeiros modelos estruturais de receptores nucleares contendo os domínios de ligação ao DNA e ao ligante. O comportamento oligomérico, em solução, do hTRβ1 também foi analisado qualitativamente. Verificou-se que a formação do homodímero e do homotetrâmero é influenciada pela presença do hormônio T3, pela concentração protéica, pelos domínios presentes e por mutações específicas. Estes estudos geraram a hipótese de que o receptor nuclear hTRβ1 é capaz de se autoreprimir. Até então, dentro da superfamília dos receptores nucleares, esta capacidade de autorepressão somente havia sido descrita para o receptor hRXRα. Por fim, cristalizou-se o domínio LBD do receptor hTRβ1 com os ligantes T3, Triac e GC-1. O objetivo foi o de determinar estruturas cristalográficas importantes para o futuro desenvolvimento de tiromiméticos de ação isoforma-seletiva.
In eukaryotes, nuclear receptors are of major importance for intercellular signaling because they join different intra and extracellular signals during regulation of genetic programs. The great majority of these proteins function as ligand activated transcription factors providing a direct link between signaling molecules and the transcriptional responses elicited by them. The genetic programs that these receptors establish or modify affect virtually all aspects of the multicellular organisms? life, such as embryogenesis, homeostasis, reproduction, cell growth, and death. Their gene-regulatory power and selectivity has prompted intense research which is now starting to decipher the complex network of molecular events involved in transcription regulation. The future challenge will be to uncover the molecular rules that define spatial and temporal control of gene expression. Such knowledge would be essential to the development of more efficient drugs with better therapeutic values. Therefore, the main purpose in this study was to extend the understanding on the behavior and the structure of human thyroid receptor, isoform ?1 (hTRβ1), and human retinoic acid X receptor, isoform ? (hRXRα). It was applied the small angle X-ray scattering technique to determine, in solution, the envelop of both receptors containing DNA and ligand binding domains. Beside this, several crystallization conditions were tried for both receptors. The results made possible to define the spatial localization of the domains and the quaternary structure of the homodimers and homotetramers. Consequently, we were able to propose the first structural models for nuclear receptors containing the DNA and ligand binding domains. The oligomeric behavior of the hTRβ1, in solution, was also analyzed qualitatively. We verified that it was influenced by the presence of T3 hormone, the protein concentration, the presence of both DNA and ligand binding domains, and by specific mutations. Based on these results, we were able to hypothesize that the hTRβ1 has the capacity of autorepression. Up to now, only the hRXRα, in the whole nuclear receptor superfamily, had been described to behave similarly. Finally, we crystallized the ligand binding domain of the hTRβ1 in the presence of the ligands T3, Triac, and GC-1. The objective was to solve crystallographic structures essential for the future development of tiromimetics with isoform-selective action.
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Alsudais, Hamood. "Activation of the Retinoid X Receptor Augments the Expression of Akt2 to Enhance Myogenic Differentiation." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33395.

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Cachexia or muscle atrophy is a condition that is associated with a variety of diseases such as chronic heart failure and cancer. In North America, Europe and Japan, more than 8 million patients suffer from cachexia, and it is estimated that cachexia is the cause of death in 30% of cancer patients. Unfortunately, there is no available treatment for cachexia. Bexarotene, a retinoid X receptor (RXR) agonist, is a FDA approved drug used to treat cancer and is able to induce myogenic differentiation in embryonic stem cells. In this study, we investigated the mechanism by which bexarotene enhances myogenic differentiation. The Akt signaling pathway is required for myogenesis and thus we examined its involvement in bexarotene-enhanced myogenic differentiation. We showed that bexarotene, through the activation of RXR signaling, regulates Akt2 expression to enhance myoblast differentiation and fusion. Additionally, we showed that Akt2, but neither Akt1 nor Akt3, is required for bexarotene-enhanced differentiation. Furthermore, we showed that the activation of RXR signaling by bexarotene correlates with a specific histone acetylation mark at the Akt2 locus. More importantly, we demonstrated that bexarotene is able to rescue myoblast differentiation in an in vitro cachexia system. Taken together, our data revealed the significance of Akt2 in bexarotene-enhanced myogenic differentiation and the potential of using bexarotene as a treatment for cachexia.
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Delman, Emily. "Effects of Synthetic Ligands onHeterodimer Pairs Regarding Full-Length Human PPARa, RXRa and LXRa." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1472204976.

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Books on the topic "RXRs"

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Lorna, Lawrence, ed. Thresholds to thriving: A power pack of practical Rx's. Napa, Calif: Realizations Inc., 1995.

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Wexler, Phillip S. The quest for service quality: Rxs for achieving excellence. Sandy, Utah: Maxcomm Associates, 1993.

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Shoemark, Pete. Yamaha RS/RXS 100 & 125 singles owners workshop manual. Sparkford: Haynes, 1992.

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Howard, Eisenberg, ed. It's never too late to date: Shirley and Howard's Rx's for dating and mating after 50. New York: ASJA Press, 2009.

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Atencio, Luis, and Paul P. Daniels. RxJS in Action. Manning Publications, 2017.

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Daniels, Paul, and Luis Atencio. RxJS in Action. Manning Publications Co. LLC, 2017.

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Rescuing American health care: Market Rx's. Washington, DC: The Foundation, 1991.

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Reactive programming with RxJS: Untangle your asynchronous Javascript code. 2015.

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Reactive Patterns with RxJS for Angular: A Practical Guide to Managing Your Angular Application's Data Reactively and Efficiently Using RxJS 7. Packt Publishing, Limited, 2022.

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Reactive Programming with RxJS 5: Untangle Your Asynchronous JavaScript Code. Pragmatic Bookshelf, 2018.

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Book chapters on the topic "RXRs"

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Gilardi, Federica, and Béatrice Desvergne. "RXRs: Collegial Partners." In Subcellular Biochemistry, 75–102. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9050-5_5.

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Allegretto, Elizabeth A. "Detection of RARs and RXRs in Cells and Tissues Using Specific Ligand-Binding Assays and Ligand-Binding lmmunoprecipitation Techniques." In Retinoid Protocols, 219–32. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1385/0-89603-438-0:219.

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Tauler Riera, Pedro, Maurizio Volterrani, Ferdinando Iellamo, Francesco Fallo, Andrea Ermolao, William J. Kraemer, Nicholas A. Ratamess, Avery Faigenbaum, Andrew Philp, and Keith Baar. "RXR." In Encyclopedia of Exercise Medicine in Health and Disease, 774. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2989.

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Clow, Mark. "RxJS with Angular." In Angular 5 Projects, 309–13. Berkeley, CA: Apress, 2018. http://dx.doi.org/10.1007/978-1-4842-3279-8_17.

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Clow, Mark. "Observers, Reactive Programming, and RxJS." In Angular 5 Projects, 291–307. Berkeley, CA: Apress, 2018. http://dx.doi.org/10.1007/978-1-4842-3279-8_16.

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Mey, Jörg. "RAR/RXR-Mediated Signaling." In Gene Regulation, Epigenetics and Hormone Signaling, 457–510. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527697274.ch16.

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Larsen, Henrik, Gijs van der Hoorn, and Andrzej Wąsowski. "Reactive Programming of Robots with RxROS." In Studies in Computational Intelligence, 55–83. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-75472-3_2.

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Barsony, Julia. "VDR and RXR Subcellular Trafficking." In Vitamin D, 153–73. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-303-9_6.

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Troć, R. "NpS: Resonant X-ray Magnetic Scattering (RXMS)." In Actinide Monochalcogenides, 651–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-47043-4_116.

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García Ruiz, Joaquín. "Local Geometry by XANES and RXS." In Springer Proceedings in Physics, 345–50. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73811-6_22.

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Conference papers on the topic "RXRs"

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Lotfi, Atieh, and Rajesh K. Gupta. "RxRE." In FPGA '17: The 2017 ACM/SIGDA International Symposium on Field-Programmable Gate Arrays. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3020078.3021797.

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Zhao, Tian, and Yonglun Li. "Semantics of RxJS." In REBLS '22: 9th ACM SIGPLAN International Workshop on Reactive and Event-Based Languages and Systems. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3563837.3568340.

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Alabor, Manuel, and Markus Stolze. "Debugging of RxJS-based applications." In SPLASH '20: Conference on Systems, Programming, Languages, and Applications, Software for Humanity. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3427763.3428313.

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Goldstein, Jonathan T., Craig Strathdee, Fujiko Duke, Juliann Shih, and Matthew Meyerson. "Abstract 3627: Validation of PPARG and RXRA as drivers of bladder cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3627.

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Sakai, Hiroyasu, Yohei Shirakami, and Masahito Shimizu. "Abstract 4052: The role of the phosphorylated RXRα on diethylnitrosamine-induced liver tumorigenesis in mice." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4052.

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Deng, Kaiyuan. "Research on Customer Satisfaction of Logistics Enterprises based on SPSS-Beijing RXRH Customs Co., Ltd." In The International Conference on Big Data Economy and Digital Management. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0011155200003440.

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Sakai, Hiroyasu, Yohei Shirakami, and Masahito Shimizu. "Abstract 2709: The role of the phosphorylated RXRα on cellular proliferation and liver tumorigenesis in mice." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2709.

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Morris, Jay, Vondina R. Brown, Kathleen V. Coleman, and Michal J. Wargovich. "Abstract A194: Epigenetic modification of RXRα in human colon carcinomas by the green tea polyphenol, EGCG." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a194.

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Kaneko, Yuhei, Maki Okube, Satoshi Sasaki, R. Garrett, I. Gentle, K. Nugent, and S. Wilkins. "Estimation of the Magnetic Electron-Density Distribution by RXMS at the Electronic Transition in Absorption Edge." In SRI 2009, 10TH INTERNATIONAL CONFERENCE ON RADIATION INSTRUMENTATION. AIP, 2010. http://dx.doi.org/10.1063/1.3463357.

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Cabang, April B., Jay L. Morris, and Michael J. Wargovich. "Abstract A03: Determining the role of Vitamin D Receptor (VDR) and Retinoid X Receptor Alpha (RXRα) in colitis." In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-a03.

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