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Journal articles on the topic 'Retinoid pathway gene expression'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Lefebvre, Bruno, Céline Brand, Sébastien Flajollet та Philippe Lefebvre. "Down-Regulation of the Tumor Suppressor Gene Retinoic Acid Receptor β2 through the Phosphoinositide 3-Kinase/Akt Signaling Pathway". Molecular Endocrinology 20, № 9 (2006): 2109–21. http://dx.doi.org/10.1210/me.2005-0321.

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Abstract The retinoic acid receptor β2 (RARβ2) is a potent, retinoid-inducible tumor suppressor gene, which is a critical molecular relay for retinoid actions in cells. Its down-regulation, or loss of expression, leads to resistance of cancer cells to retinoid treatment. Up to now, no primary mechanism underlying the repression of the RARβ2 gene expression, hence affecting cellular retinoid sensitivity, has been identified. Here, we demonstrate that the phosphoinositide 3-kinase/Akt signaling pathway affects cellular retinoid sensitivity, by regulating corepressor recruitment to the RARβ2 prom

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2

Mehta, Kapil, Teresa McQueen, Taghi Manshouri, Michael Andreeff, Steven Collins та Maher Albitar. "Involvement of Retinoic Acid Receptor-α–Mediated Signaling Pathway in Induction of CD38 Cell-Surface Antigen". Blood 89, № 10 (1997): 3607–14. http://dx.doi.org/10.1182/blood.v89.10.3607.

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Abstract Human leukocyte antigen CD38, a 45-kD single-chain, transmembrane glycoprotein, is a bifunctional ectoenzyme that participates in signal transduction pathways involved in the regulation of cell growth and differentiation. In this study, we demonstrate the nature of retinoid receptors involved in retinoic acid–induced expression of CD38 protein in the human myeloblastic leukemia cell line HL-60. We used a variant HL-60 cell line, HL-60R, in which retinoid receptor function has been abrogated by a trans-dominant negative mutation. We introduced the normal retinoic acid receptors (RAR)-α

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Mehta, Kapil, Teresa McQueen, Taghi Manshouri, Michael Andreeff, Steven Collins та Maher Albitar. "Involvement of Retinoic Acid Receptor-α–Mediated Signaling Pathway in Induction of CD38 Cell-Surface Antigen". Blood 89, № 10 (1997): 3607–14. http://dx.doi.org/10.1182/blood.v89.10.3607.3607_3607_3614.

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Human leukocyte antigen CD38, a 45-kD single-chain, transmembrane glycoprotein, is a bifunctional ectoenzyme that participates in signal transduction pathways involved in the regulation of cell growth and differentiation. In this study, we demonstrate the nature of retinoid receptors involved in retinoic acid–induced expression of CD38 protein in the human myeloblastic leukemia cell line HL-60. We used a variant HL-60 cell line, HL-60R, in which retinoid receptor function has been abrogated by a trans-dominant negative mutation. We introduced the normal retinoic acid receptors (RAR)-α, -β, and

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Murphy, Philip T., Gary Lynch, Stephen Bergin та ін. "Strong Correlation Between CTLA-4 and LEF1 Gene Expression Levels in CLL: Targeting of the Wnt/β-Catenin Pathway May Adversely Affect CTLA-4 Expression and Function". Blood 128, № 22 (2016): 5571. http://dx.doi.org/10.1182/blood.v128.22.5571.5571.

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Abstract Recently published clinical trials have confirmed the effectiveness of anti-CD38 monoclonal antibody therapy in myeloma. Furthermore, in vitro studies of chronic lymphocytic leukaemia (CLL) cells suggest that CD38 expression can be enhanced by treatment with retinoid derivatives and thus may enhance the cytotoxic effects of anti-CD38 therapy. However, retinoids have been shown to have diverse effects on cellular function and we have previously shown that the retinoid drug acitretin upregulates CD38 expression while also reducing cell homing to the chemokine CXCL12 in primary CLL cells

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Aydemir, Gamze, Marta Domínguez, Angel R. de Lera, Johanna Mihaly, Dániel Törőcsik, and Ralph Rühl. "Apo-14´-Carotenoic Acid Is a Novel Endogenous and Bioactive Apo-Carotenoid." Nutrients 11, no. 9 (2019): 2084. http://dx.doi.org/10.3390/nu11092084.

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Carotenoids can be metabolized to various apo-carotenoids and retinoids. Apo-15´-carotenoic acid (retinoic acid, RA) is a potent activator of the retinoic acid receptor (RAR) in its all-trans- (ATRA) and 9-cis- (9CRA) forms. In this study we show firstly, that apo-14´-carotenoic acid (A14CA), besides retinoic acids, is present endogenously and with increased levels in the human organism after carrot juice supplementation rich in β-carotene. All-trans-A14C (ATA14CA) is just a moderate activator of RAR-transactivation in reporter cell lines but can potently activate retinoic acid response elemen

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6

van der Wees, J., J. G. Schilthuis, C. H. Koster, et al. "Inhibition of retinoic acid receptor-mediated signalling alters positional identity in the developing hindbrain." Development 125, no. 3 (1998): 545–56. http://dx.doi.org/10.1242/dev.125.3.545.

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Retinoids regulate gene expression via nuclear retinoic acid receptors, the RARs and RXRs. To investigate the functions of retinoid receptors during early neural development, we expressed a dominant negative RARbeta in early Xenopus embryos. We obtained evidence that dominant negative RARbeta specifically inhibits RAR/RXR heterodimer-mediated, but not RXR homodimer-mediated, transactivation. Both all-trans- and 9-cis-RA-induced teratogenesis were, however, efficiently opposed by ectopic expression of dominant negative RARbeta, indicating that only RAR/RXR transactivation is required for retino

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Park, Dorothy J., Peter T. Vuong, Sven de Vos, Dan Douer та H. Phillip Koeffler. "Comparative analysis of genes regulated by PML/RARα and PLZF/RARα in response to retinoic acid using oligonucleotide arrays". Blood 102, № 10 (2003): 3727–36. http://dx.doi.org/10.1182/blood-2003-02-0412.

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Abstract Acute promyelocytic leukemia (APL) is associated with chromosomal translocations involving retinoic acid receptor α (RARα) and its fusion partners including promyelocytic leukemia (PML) and promyelocytic leukemia zinc finger (PLZF). Using oligonucleotide arrays, we examined changes in global gene expression mediated by the ectopic expression of either PML/RARα (retinoid-sensitive) or PLZF/RARα (retinoid-resistant) in U937 cells. Of more than 5000 genes analyzed, 16 genes were commonly up-regulated, and 57 genes were down-regulated by both fusion proteins suggesting their role in the A

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8

Quere, Ronan, Aurelie Baudet, Bruno Cassinat, et al. "Pharmacogenomic analysis of acute promyelocytic leukemia cells highlights CYP26 cytochrome metabolism in differential all-trans retinoic acid sensitivity." Blood 109, no. 10 (2007): 4450–60. http://dx.doi.org/10.1182/blood-2006-10-051086.

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AbstractDisease relapse sometimes occurs after acute promyelocytic leukemia (APL) therapy with all-trans retinoic acid (ATRA). Among the diagnostic parameters predicting relapse, heterogeneity in the in vitro differentiation rate of blasts is an independent factor. To identify biologic networks involved in resistance, we conducted pharmacogenomic studies in APL blasts displaying distinct ATRA sensitivities. Although the expression profiles of genes invested in differentiation were similarly modulated in low- and high-sensitive blasts, low-sensitive cells showed higher levels of transcription o

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Lehrke, Ingo, Matthias Schaier, Kerstin Schade, et al. "Retinoid receptor-specific agonists alleviate experimental glomerulonephritis." American Journal of Physiology-Renal Physiology 282, no. 4 (2002): F741—F751. http://dx.doi.org/10.1152/ajprenal.00026.2001.

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Retinoids are potent antiproliferative and anti-inflammatory compounds. We previously demonstrated that the natural pan-agonists all- trans retinoic acid (RA) and 13- cis RA efficiently preserve renal structure and function in rat mesangioproliferative glomerulonephritis. We examine effects of synthetic retinoid receptor-specific agonists 1) to identify common and receptor subtype-specific pathways in this model and 2) to characterize effects of retinoids on the renal endothelin (ET) system. Vehicle-injected control rats were compared with rats treated with daily subcutaneous injections of ago

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Hoffman, Lisa M., Kamal Garcha, Konstantina Karamboulas, et al. "BMP action in skeletogenesis involves attenuation of retinoid signaling." Journal of Cell Biology 174, no. 1 (2006): 101–13. http://dx.doi.org/10.1083/jcb.200604150.

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The bone morphogenetic protein (BMP) and growth and differentiation factor (GDF) signaling pathways have well-established and essential roles within the developing skeleton in coordinating the formation of cartilaginous anlagen. However, the identification of bona fide targets that underlie the action of these signaling molecules in chondrogenesis has remained elusive. We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activat

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Baleato, R. M., R. J. Aitken, and S. D. Roman. "244.Interaction between bone morphogenetic protein 4 and retinoid signalling in mouse spermatogenesis." Reproduction, Fertility and Development 16, no. 9 (2004): 244. http://dx.doi.org/10.1071/srb04abs244.

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Vitamin A (retinol, or ROL) is also essential for normal spermatogenesis in the rat and mouse. Vitamin A-deficient (VAD) rodents suffer various disorders including blindness and male infertility. The molecular mechanisms leading to infertility in vitamin A deficient rodents have never been fully elucidated. Following prolonged vitamin A withdrawal the only germ cells remaining in the VAD rodent testis are stem cell spermatogonia, type A1 spermatogonia, and a few preleptotene spermatocytes. Supplementing the diet of these animals with retinoic acid (RA) alleviates all symptoms of vitamin A defi

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Lattuada, Debora, Paola Viganó, Silvia Mangioni та ін. "Accumulation of Retinoid X Receptor-α in Uterine Leiomyomas Is Associated with a Delayed Ligand-Dependent Proteasome-Mediated Degradation and an Alteration of Its Transcriptional Activity". Molecular Endocrinology 21, № 3 (2007): 602–12. http://dx.doi.org/10.1210/me.2006-0206.

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Abstract An alteration of the retinoid pathway can influence the development of uterine leiomyomas in animal models, and retinoids have shown efficacy in inhibiting the growth of this benign tumor both in vitro and in vivo. However, the underlying mechanisms and biological implications are unclear. The present study was based on the demonstration of an accumulation of full-length retinoid X receptor α (RXRα) in leiomyomas that was not associated with a modification of its gene expression. This accumulation was shown to increase the transcription of the RXR-responsive gene cellular retinoic aci

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13

Jiao, Xiaoyang, Rang Liu, Jiali Huang, et al. "Cellular Retinoic-Acid Binding Protein 2 in Solid Tumor." Current Protein & Peptide Science 21, no. 5 (2020): 507–16. http://dx.doi.org/10.2174/1389203721666200203150721.

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The retinoic acid (RA) signaling pathway is crucial for many biological processes. The RA transporter, Cellular Retinoic-Acid Binding Protein 2 (CRABP2), is abnormally expressed in various tumor types. CRABP2 presents significant effects on tumorous behaviors and functions, including cell proliferation, apoptosis, invasion, migration, metastasis, and angiogenesis. The tumorigenesis mechanism of CRABP2, as both suppressor and promotor, is complicated, therefore, there remains the need for further investigation. Elucidating the regulating mechanisms in a specific stage of the tumor could facilit

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14

Benedetti, L., F. Grignani, BM Scicchitano, et al. "Retinoid-induced differentiation of acute promyelocytic leukemia involves PML-RARalpha-mediated increase of type II transglutaminase." Blood 87, no. 5 (1996): 1939–50. http://dx.doi.org/10.1182/blood.v87.5.1939.1939.

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Abstract All-trans retinoic acid (t-RA) administration leads to complete remission in acute promyelocytic leukemia (APL) patients by inducing growth arrest and differentiation of the leukemic clone. In the present study, we show that t-RA treatment dramatically induced type II transglutaminase (type II TGase) expression in cells carrying the t(15;17) translocation and expressing the PML-RARalpha product such as the APL-derived NB4 cell line and fresh leukemic cells from APL patients. This induction correlated with t-RA-induced growth arrest, granulocytic differentiation, and upregulation of th

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Benedetti, L., F. Grignani, BM Scicchitano, et al. "Retinoid-induced differentiation of acute promyelocytic leukemia involves PML-RARalpha-mediated increase of type II transglutaminase." Blood 87, no. 5 (1996): 1939–50. http://dx.doi.org/10.1182/blood.v87.5.1939.bloodjournal8751939.

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All-trans retinoic acid (t-RA) administration leads to complete remission in acute promyelocytic leukemia (APL) patients by inducing growth arrest and differentiation of the leukemic clone. In the present study, we show that t-RA treatment dramatically induced type II transglutaminase (type II TGase) expression in cells carrying the t(15;17) translocation and expressing the PML-RARalpha product such as the APL-derived NB4 cell line and fresh leukemic cells from APL patients. This induction correlated with t-RA-induced growth arrest, granulocytic differentiation, and upregulation of the leukocy

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16

Shao, Wenlin, Laura Benedetti, William W. Lamph, Clara Nervi та Wilson H. Miller. "A Retinoid-Resistant Acute Promyelocytic Leukemia Subclone Expresses a Dominant Negative PML-RARα Mutation". Blood 89, № 12 (1997): 4282–89. http://dx.doi.org/10.1182/blood.v89.12.4282.

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Abstract The unique t(15; 17) of acute promyelocytic leukemia (APL) fuses the PML gene with the retinoic acid receptor α (RARα) gene. Although retinoic acid (RA) inhibits cell growth and induces differentiation in human APL cells, resistance to RA develops both in vitro and in patients. We have developed RA-resistant subclones of the human APL cell line, NB4, whose nuclear extracts display altered RA binding. In the RA-resistant subclone, R4, we find an absence of ligand binding of PML-RARα associated with a point mutation changing a leucine to proline in the ligand-binding domain of the fusio

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ALVAREZ, Rosa, MaLuz CHECA, Sonia BRUN, et al. "Both retinoic-acid-receptor- and retinoid-X-receptor-dependent signalling pathways mediate the induction of the brown-adipose-tissue-uncoupling-protein-1 gene by retinoids." Biochemical Journal 345, no. 1 (1999): 91–97. http://dx.doi.org/10.1042/bj3450091.

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The intracellular pathways and receptors mediating the effects of retinoic acid (RA) on the brown-fat-uncoupling-protein-1 gene (ucp-1) have been analysed. RA activates transcription of ucp-1 and the RA receptor (RAR) is known to be involved in this effect. However, co-transfection of an expression vector for retinoid-X receptor (RXR) increases the action of 9-cis RA but not the effects of all-trans RA on the ucp-1 promoter in brown adipocytes. Either RAR-specific {p-[(E)-2-(5,6,7,8,-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl]benzoic acid} or RXR-specific [isopropyl-(E,E)-(R,S)-

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18

Tate, B. F., G. Allenby, R. Janocha, et al. "Distinct binding determinants for 9-cis retinoic acid are located within AF-2 of retinoic acid receptor alpha." Molecular and Cellular Biology 14, no. 4 (1994): 2323–30. http://dx.doi.org/10.1128/mcb.14.4.2323.

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Retinoids exert their physiological action by interacting with two families of nuclear receptors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs), which regulate gene expression by forming transcriptionally active heterodimeric RAR/RXR or homodimeric RXR/RXR complexes on DNA. Retinoid receptor activity resides in several regions, including the DNA and ligand binding domains, a dimerization interface, and both a ligand-independent (AF-1) and a ligand-dependent (AF-2) transactivation function. While 9-cis retinoic acid (RA) alone is the cognate ligand for the RXRs, both 9-

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Tate, B. F., G. Allenby, R. Janocha, et al. "Distinct binding determinants for 9-cis retinoic acid are located within AF-2 of retinoic acid receptor alpha." Molecular and Cellular Biology 14, no. 4 (1994): 2323–30. http://dx.doi.org/10.1128/mcb.14.4.2323-2330.1994.

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Retinoids exert their physiological action by interacting with two families of nuclear receptors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs), which regulate gene expression by forming transcriptionally active heterodimeric RAR/RXR or homodimeric RXR/RXR complexes on DNA. Retinoid receptor activity resides in several regions, including the DNA and ligand binding domains, a dimerization interface, and both a ligand-independent (AF-1) and a ligand-dependent (AF-2) transactivation function. While 9-cis retinoic acid (RA) alone is the cognate ligand for the RXRs, both 9-

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Shetty, Shoba, Maria A. Ramos-Roman, You-Ree Cho, et al. "Enhanced Fatty Acid Flux Triggered by Adiponectin Overexpression." Endocrinology 153, no. 1 (2012): 113–22. http://dx.doi.org/10.1210/en.2011-1339.

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Adiponectin overexpression in mice increases insulin sensitivity independent of adiposity. Here, we combined stable isotope infusion and in vivo measurements of lipid flux with transcriptomic analysis to characterize fatty acid metabolism in transgenic mice that overexpress adiponectin via the aP2-promoter (ADNTg). Compared with controls, fasted ADNTg mice demonstrated a 31% reduction in plasma free fatty acid concentrations (P = 0.008), a doubling of ketones (P = 0.028), and a 68% increase in free fatty acid turnover in plasma (15.1 ± 1.5 vs. 25.3 ± 6.8 mg/kg · min, P = 0.011). ADNTg mice had

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21

Ferlosio, Amedeo, Elena Doldo, Sara Agostinelli, et al. "Cellular retinol binding protein 1 transfection reduces proliferation and AKT-related gene expression in H460 non-small lung cancer cells." Molecular Biology Reports 47, no. 9 (2020): 6879–86. http://dx.doi.org/10.1007/s11033-020-05744-5.

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Abstract In recent years, new treatments with novel action mechanisms have been explored for advanced non-small cell lung cancer (NSCLC). Retinoids promote cancer cell differentiation and death and their trafficking and action is mediated from specific cytoplasmic and nuclear receptors, respectively. The purpose of this study was to investigate the effect of Cellular retinol binding protein-1 (CRBP-1) transfection in H460 human NSCLC cell line, normally not expressing CRBP-1. H460 cells were transfected by using a vector pTargeT Mammalian expression system carrying the whole sequence of CRBP-1

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Wertz, Karin, Nicole Seifert, Petra Buchwald Hunziker та ін. "β-Carotene interference with UVA-induced gene expression by multiple pathways". Pure and Applied Chemistry 78, № 8 (2006): 1539–50. http://dx.doi.org/10.1351/pac200678081539.

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UVA exposure causes skin photoaging by singlet oxygen (1O2)-mediated induction of matrix metalloproteases (MMPs). We assessed whether β-carotene, a carotenoid known as 1O2 quencher and retinoic acid (RA) precursor, interferes with UVA-induced gene regulation and prevents UVA-induced gene regulation in HaCaT human keratinocytes. HaCaT cells accumulated β-carotene in a time- and dose-dependent manner. UVA irradiation massively reduced the cellular β-carotene contents. β-Carotene suppressed UVA induction of MMP-1, MMP-3, and MMP-10 - three major MMPs involved in photoaging. HaCaT cells produced w

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Ross, Alexander W., Catriona A. Webster, Julian G. Mercer та ін. "Photoperiodic Regulation of Hypothalamic Retinoid Signaling: Association of Retinoid X Receptor γ with Body Weight". Endocrinology 145, № 1 (2004): 13–20. http://dx.doi.org/10.1210/en.2003-0838.

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Abstract This study reports novel events related to photoperiodic programming of the neuroendocrine hypothalamus. To investigate photoperiod-responsive genes, Siberian hamsters were maintained in long or short photoperiods that generate physiological states of obesity or leanness. Microarray expression analysis first identified CRBP1 as a photoperiod-responsive gene, and then further studies using in situ hybridization and immunocytochemistry revealed that expression levels of several related retinoid-signaling genes were modulated in response to photoperiod changes. Genes of the retinoid-sign

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Giannì, M., M. Terao, S. Sozzani, and E. Garattini. "Retinoic acid and cyclic AMP synergistically induce the expression of liver/bone/kidney-type alkaline phosphatase gene in L929 fibroblastic cells." Biochemical Journal 296, no. 1 (1993): 67–77. http://dx.doi.org/10.1042/bj2960067.

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In L929 mouse fibroblastic cells, liver/bone/kidney type alkaline phosphatase (L/B/K-ALP) enzymic activity is induced by all-trans-retinoic acid at concentrations between 10(-6) and 10(-5) M. At lower concentrations, retinoic acid is incapable of inducing this enzymic activity per se, but increases cyclic AMP (cAMP)-mediated induction. This effect is observed after incubation of the retinoid with dibutyryl cAMP, 8-bromo cAMP or forskolin. The synergism is dependent on the order of addition of retinoic acid and the activator of the cAMP pathway. Contemporaneous addition of the two agents, or ad

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Sanchez, Patricia Vanessa, Reid P. Bissonnette, Donald E. Tsai, and Martin Carroll. "Gene Expression Analysis of Bexarotene Differentiated Acute Myeloid Leukemias Identifies Known and Novel Gene Targets." Blood 112, no. 11 (2008): 1199. http://dx.doi.org/10.1182/blood.v112.11.1199.1199.

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Abstract Despite advances in understanding the molecular pathogenesis of acute myeloid leukemia (AML), therapy for relapsed disease remains inadequate with high mortalities. Clinicians at the University of Pennsylvania have demonstrated that the FDA approved retinoid X receptor (RXR) agonist bexarotene (Targretin™) stimulates leukemic cell differentiation in a subset patents with relapsed AML leading to clinical responses. This underscores the importance of identifying the mechanism by which bexarotene induces differentiation in AML in order to enhance the efficacy of this therapeutic approach

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Houle, Martin, Panagiotis Prinos, Angelo Iulianella, Nathalie Bouchard, and David Lohnes. "Retinoic Acid Regulation of Cdx1: an Indirect Mechanism for Retinoids and Vertebral Specification." Molecular and Cellular Biology 20, no. 17 (2000): 6579–86. http://dx.doi.org/10.1128/mcb.20.17.6579-6586.2000.

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ABSTRACT Retinoic acid (RA) is required for diverse developmental programs, including vertebral specification. Both RA receptor disruption and excess RA result in homeotic transformations of the axial skeleton. These effects are believed to occur through altered expression ofHox genes, several of which have been demonstrated to be direct RA targets. Members of the cdx (caudal) homeobox gene family are also implicated in regulating Hoxexpression. Disruption of cdx1 results in vertebral homeotic transformations and alteration of Hox expression boundaries; similar homeosis is also observed in cdx

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Levi, Liraz, Tamar Ziv, Arie Admon, Berta Levavi-Sivan, and Esther Lubzens. "Insight into molecular pathways of retinal metabolism, associated with vitellogenesis in zebrafish." American Journal of Physiology-Endocrinology and Metabolism 302, no. 6 (2012): E626—E644. http://dx.doi.org/10.1152/ajpendo.00310.2011.

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Retinal is the main retinoid stored in oviparous eggs of fish, amphibians, and reptiles, reaching the oocytes in association with vitellogenins, the yolk precursor proteins. During early presegmentation stages of zebrafish embryos, retinal is metabolized to retinoic acid (RA), which regulates genes involved in cell proliferation, differentiation, and tissue function and is therefore essential for normal embryonic development. While synthesis of vitellogenin and its regulation by 17β-estradiol (E2) were extensively investigated, pathways for retinal synthesis remain obscure. We determined the e

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Everaert, Bert R., Steven J. Van Laere, Robrecht Lembrechts, Vicky Y. Hoymans, Jean-Pierre Timmermans, and Christiaan J. Vrints. "Identification of Macrophage Genotype and Key Biological Pathways in Circulating Angiogenic Cell Transcriptome." Stem Cells International 2019 (May 2, 2019): 1–12. http://dx.doi.org/10.1155/2019/9545261.

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Background. Circulating angiogenic cells (CAC) have been identified as important regulators of vascular biology. However, there is still considerable debate about the genotype and function of CAC. Methods and Results. Data from publicly available gene expression data sets were used to analyse the transcriptome of in vitro cultured CAC (CACiv). Genes and pathways of interest were further evaluated using qPCR comparing CACiv versus CD14+ monocytic cells. The CACiv transcriptome strongly related to tissue macrophages, and more specifically to regulatory M2c macrophages. The cytokine expression pr

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Nakanishi, Tsuyoshi, Jun-ichi Nishikawa, Youhei Hiromori, et al. "Trialkyltin Compounds Bind Retinoid X Receptor to Alter Human Placental Endocrine Functions." Molecular Endocrinology 19, no. 10 (2005): 2502–16. http://dx.doi.org/10.1210/me.2004-0397.

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Abstract Retinoid X receptor (RXR) is a nuclear receptor that plays important and multiple roles in mammalian development and homeostasis. We previously reported that, in human choriocarcinoma cells, tributyltin chloride and triphenyltin hydroxide, which are typical environmental contaminants and cause masculinization in female mollusks, are potent stimulators of human chorionic gonadotropin production and aromatase activity, which play key endocrine functions in maintaining pregnancy and fetal development. However, the molecular mechanism through which these compounds stimulate these endocrin

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Ruberte, E., V. Friederich, P. Chambon, and G. Morriss-Kay. "Retinoic acid receptors and cellular retinoid binding proteins. III. Their differential transcript distribution during mouse nervous system development." Development 118, no. 1 (1993): 267–82. http://dx.doi.org/10.1242/dev.118.1.267.

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We have studied the transcript distribution of the retinoic acid receptors (RARs) and the cytoplasmic retinoid binding proteins during embryonic development of the mouse nervous system. Of the three retinoic acid receptors, only RAR-gamma was not expressed in developing neural structures. RAR-beta and RAR-alpha both showed rostral limits of expression in the medulla oblongata equivalent to their patterns of expression in the neuroepithelium of the early hindbrain neural tube. Within their expression domains in the spinal cord and brain, RAR-alpha was ubiquitously expressed, whereas RAR-beta tr

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Bland, R., R. L. Sammons, M. C. Sheppard, and G. R. Williams. "Thyroid hormone, vitamin D and retinoid receptor expression and signalling in primary cultures of rat osteoblastic and immortalised osteosarcoma cells." Journal of Endocrinology 154, no. 1 (1997): 63–74. http://dx.doi.org/10.1677/joe.0.1540063.

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Abstract 3,5,3′-Tri-iodothyronine (T3), 1α,25(OH)2-vitamin D3 (D3) and retinoids activate related nuclear receptors which interact by heterodimerisation to regulate gene expression. Actions of each hormone are discrete and may be specified by changes in the relative concentrations of their receptors (T3R, vitamin D receptor (VDR), retinoic acid receptor (RAR), retinoid X receptor (RXR)). T3, D3 and retinoids are essential for skeletal development and maintenance and we have previously shown complex interactions amongst their signalling pathways in osteosarcoma cells. In these studies we demons

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Xue, J. C., E. J. Schwarz, A. Chawla, and M. A. Lazar. "Distinct stages in adipogenesis revealed by retinoid inhibition of differentiation after induction of PPARgamma." Molecular and Cellular Biology 16, no. 4 (1996): 1567–75. http://dx.doi.org/10.1128/mcb.16.4.1567.

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Retinoic acid (RA) inhibits adipocyte differentiation of 3T3-L1 preadipocytes but is effective only early in adipogenesis. RA prevented induction of the adipogenic factors PPARgamma and C/EBPalpha. Using receptor-specific ligands, we determined that the effects of RA were mediated by liganded RA receptors (RARs) rather than retinoid X receptors. Preadipocytes expressed primarily RARalpha and RARgamma; during adipocyte differentiation, RARalpha gene expression was nearly constant, whereas RARgamma1 mRNA and protein levels dramatically decreased. Ectopic expression of RARgamma1 extended the peri

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Bissonnette, R. P., T. Brunner, S. B. Lazarchik, et al. "9-cis retinoic acid inhibition of activation-induced apoptosis is mediated via regulation of fas ligand and requires retinoic acid receptor and retinoid X receptor activation." Molecular and Cellular Biology 15, no. 10 (1995): 5576–85. http://dx.doi.org/10.1128/mcb.15.10.5576.

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T-cell hybridomas, thymocytes, and T cells can be induced to undergo apoptotic cell death by activation through the T-cell receptor. This process requires macromolecular synthesis and thus gene expression, and it has been shown to be influenced by factors regulating transcription. Recently, activation, T-cell hybridomas rapidly express the Fas/CD95 receptor and its ligand, Fas ligand (FasL), which interact to transduce the death signal in the activated cell. Retinoids, the active metabolites of vitamin A, modulate expression of specific target genes by binding to two classes of intracellular r

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Aranda, Ana, and Angel Pascual. "Nuclear Hormone Receptors and Gene Expression." Physiological Reviews 81, no. 3 (2001): 1269–304. http://dx.doi.org/10.1152/physrev.2001.81.3.1269.

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The nuclear hormone receptor superfamily includes receptors for thyroid and steroid hormones, retinoids and vitamin D, as well as different “orphan” receptors of unknown ligand. Ligands for some of these receptors have been recently identified, showing that products of lipid metabolism such as fatty acids, prostaglandins, or cholesterol derivatives can regulate gene expression by binding to nuclear receptors. Nuclear receptors act as ligand-inducible transcription factors by directly interacting as monomers, homodimers, or heterodimers with the retinoid X receptor with DNA response elements of

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Anchan, Raymond M., Daniel P. Drake, Charles F. Haines, Elizabeth A. Gerwe, and Anthony-Samuel LaMantia. "Disruption of local retinoid-mediated gene expression accompanies abnormal development in the mammalian olfactory pathway." Journal of Comparative Neurology 379, no. 2 (1997): 171–84. http://dx.doi.org/10.1002/(sici)1096-9861(19970310)379:2<171::aid-cne1>3.0.co;2-0.

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MacDonald, P. N., D. R. Dowd, S. Nakajima, et al. "Retinoid X receptors stimulate and 9-cis retinoic acid inhibits 1,25-dihydroxyvitamin D3-activated expression of the rat osteocalcin gene." Molecular and Cellular Biology 13, no. 9 (1993): 5907–17. http://dx.doi.org/10.1128/mcb.13.9.5907.

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The vitamin D receptor (VDR) binds the vitamin D-responsive element (VDRE) as a heterodimer with an unidentified receptor auxiliary factor (RAF) present in mammalian cell nuclear extracts. VDR also interacts with the retinoid X receptors (RXRs), implying that RAF may be related to the RXRs. Here we demonstrate that highly purified HeLa cell RAF contained RXR beta immunoreactivity and that both activities copurified and precisely coeluted in high-resolution hydroxylapatite chromatography. Furthermore, an RXR beta-specific antibody disrupted VDR-RAF-VDRE complexes in mobility shift assays. These

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MacDonald, P. N., D. R. Dowd, S. Nakajima, et al. "Retinoid X receptors stimulate and 9-cis retinoic acid inhibits 1,25-dihydroxyvitamin D3-activated expression of the rat osteocalcin gene." Molecular and Cellular Biology 13, no. 9 (1993): 5907–17. http://dx.doi.org/10.1128/mcb.13.9.5907-5917.1993.

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The vitamin D receptor (VDR) binds the vitamin D-responsive element (VDRE) as a heterodimer with an unidentified receptor auxiliary factor (RAF) present in mammalian cell nuclear extracts. VDR also interacts with the retinoid X receptors (RXRs), implying that RAF may be related to the RXRs. Here we demonstrate that highly purified HeLa cell RAF contained RXR beta immunoreactivity and that both activities copurified and precisely coeluted in high-resolution hydroxylapatite chromatography. Furthermore, an RXR beta-specific antibody disrupted VDR-RAF-VDRE complexes in mobility shift assays. These

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Boddicker, Rebecca L., Xueju Wang, Surendra Dasari, et al. "Retinoic Acid Receptor Alpha Expression Drives Cell-Cycle Progression and Is Associated with Increased Sensitivity to Retinoids in Peripheral T-Cell Lymphoma." Blood 128, no. 22 (2016): 1749. http://dx.doi.org/10.1182/blood.v128.22.1749.1749.

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Abstract Background: Peripheral T-cell lymphomas (PTCLs) are aggressive non-Hodgkin lymphomas with marked clinical, pathological, and molecular heterogeneity. Outcomes following standard therapy generally are poor; however, few candidate therapeutic targets have been identified for precision medicine approaches. Retinoic acid receptor alpha (RARA) is a transcription factor that modulates cell growth and differentiation in response to natural or synthetic retinoids. Retinoids have been used successfully to treat acute promyelocytic leukemia and some cutaneous T-cell lymphomas (CTCLs). However,

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Glasow, Annegret, Angela Barrett, Rajeev Gupta та ін. "Expression of ATRA Inducible RARα2 Isoform Is Deregulated in AML." Blood 106, № 11 (2005): 1204. http://dx.doi.org/10.1182/blood.v106.11.1204.1204.

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Abstract Retinoids exert a variety of effects on both normal and malignant hematopoietic cells. To date, three different retinoic acid receptor (RAR) and retinoid X receptor (RXR) genes have been characterized, each encoding multiple N-terminal protein isoforms. RXRs serve as co-regulators for RARs, and many other nuclear receptors integrating different signalling pathways. All-trans-retinoic acid (ATRA) signaling pathway is of critical importance for optimal myelomonocytic differentiation and its disruption by translocations of the RARα gene leads to acute promyelocytic leukemia (APL). APL as

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Han, Minjae, and Pyung Cheon Lee. "Microbial Production of Bioactive Retinoic Acid Using Metabolically Engineered Escherichia coli." Microorganisms 9, no. 7 (2021): 1520. http://dx.doi.org/10.3390/microorganisms9071520.

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Microbial production of bioactive retinoids, including retinol and retinyl esters, has been successfully reported. Previously, there are no reports on the microbial biosynthesis of retinoic acid. Two genes (blhSR and raldhHS) encoding retinoic acid biosynthesis enzymes [β-carotene 15,15′-oxygenase (Blh) and retinaldehyde dehydrogenase2 (RALDH2)] were synthetically redesigned for modular expression. Co-expression of the blhSR and raldhHS genes on the plasmid system in an engineered β-carotene-producing Escherichia coli strain produced 0.59 ± 0.06 mg/L of retinoic acid after flask cultivation. D

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Mey, Jörg. "Retinoic Acid as a Regulator of Cytokine Signaling after Nerve Injury." Zeitschrift für Naturforschung C 56, no. 3-4 (2001): 163–76. http://dx.doi.org/10.1515/znc-2001-3-401.

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Abstract After an injury of the central nervous system it is of foremost clinical concern to prevent nerve cell degeneration and to develop strategies for the support of axonal regeneration. This requires an understanding of traumatic processes in the nervous system and their regulation by intercellular cytokine signaling. Although injury-induced temporal changes in gene expression of many cytokines have been described in this context, much less is known about their regulation. This review proposes a role of retinoic acid (RA) as transcriptional regulator in nerve regeneration. Four lines of e

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Richards, Burt, Jon Karpilow, Christine Dunn, et al. "Genetic Selection for Modulators of a Retinoic-Acid-Responsive Reporter in Human Cells." Genetics 163, no. 3 (2003): 1047–60. http://dx.doi.org/10.1093/genetics/163.3.1047.

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Abstract We used a genetic screening methodology, a human cell line bearing a retinoic-acid-responsive enhanced GFP reporter, and a flow sorter to recover dominant modulators of reporter expression. Four inducers and three suppressors that were fused to the C terminus of a protein scaffold for stability were isolated and their mechanisms of action studied. Mutagenesis experiments indicated that six of these dominant agents exerted their effects at the protein level. The single cDNA coding fragment that was isolated comprised the central 64-amino-acid section of human cyclophilin B, which conta

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Cheung, Cecilia Y., Debra F. Anderson, Marion Rouzaire, Loïc Blanchon, Vincent Sapin, and Robert A. Brace. "Retinoic Acid Pathway Regulation of Vascular Endothelial Growth Factor in Ovine Amnion." Reproductive Sciences 26, no. 10 (2018): 1351–59. http://dx.doi.org/10.1177/1933719118765979.

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Vascular endothelial growth factor (VEGF) has been proposed as an important regulator of amniotic fluid absorption across the amnion into the fetal vasculature on the surface of the placenta. However, the activators of VEGF expression and action in the amnion have not been identified. Using the pregnant sheep model, we aimed to investigate the presence of the retinoic acid (RA) pathway in ovine amnion and to determine its effect on VEGF expression. Further, we explored relationships between RA receptors and VEGF and tested the hypothesis that RA modulates intramembranous absorption (IMA) throu

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Niu, Haixia, Gayla Hadwiger, Hideji Fujiwara, and John S. Welch. "Pathways of Retinoid Synthesis in Mouse Bone Marrow-Derived Macrophages and Hematopoietic Progenitors." Blood 126, no. 23 (2015): 1009. http://dx.doi.org/10.1182/blood.v126.23.1009.1009.

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Abstract Introduction: Retinoid receptors are nuclear hormone receptors which are dynamically regulated during terminal myeloid maturation. Retinoic acid receptor α (RARA) is the target of at least ten fusion proteins that lead to acute promyelocytic leukemia (APL). All trans-retinoic acid (ATRA) has been thought to be the principle natural ligand for RARs and it has been used for the treatment of patients with APL. However, the enzymatic pathways that regulate natural retinoids metabolism in hematopoietic cells have not been well defined. ATRA is synthesized from vitamin A through two sequent

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Viswakarma, Navin, Yuzhi Jia, Liang Bai, et al. "Coactivators in PPAR-Regulated Gene Expression." PPAR Research 2010 (2010): 1–21. http://dx.doi.org/10.1155/2010/250126.

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Peroxisome proliferator-activated receptor (PPAR)α,β(also known asδ), andγfunction as sensors for fatty acids and fatty acid derivatives and control important metabolic pathways involved in the maintenance of energy balance. PPARs also regulate other diverse biological processes such as development, differentiation, inflammation, and neoplasia. In the nucleus, PPARs exist as heterodimers with retinoid X receptor-αbound to DNA with corepressor molecules. Upon ligand activation, PPARs undergo conformational changes that facilitate the dissociation of corepressor molecules and invoke a spatiotemp

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Nones, Katia, Yvonne E. M. Dommels, Sheridan Martell, et al. "The effects of dietary curcumin and rutin on colonic inflammation and gene expression in multidrug resistance gene-deficient (mdr1a−/−) mice, a model of inflammatory bowel diseases." British Journal of Nutrition 101, no. 2 (2008): 169–81. http://dx.doi.org/10.1017/s0007114508009847.

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Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have antioxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Multidrug resistance gene-deficient (mdr1a− / − ) mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet–gene interact

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Rottman, J. N., R. L. Widom, B. Nadal-Ginard, V. Mahdavi, and S. K. Karathanasis. "A retinoic acid-responsive element in the apolipoprotein AI gene distinguishes between two different retinoic acid response pathways." Molecular and Cellular Biology 11, no. 7 (1991): 3814–20. http://dx.doi.org/10.1128/mcb.11.7.3814.

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The gene coding for apolipoprotein AI, a plasma protein involved in the transport of cholesterol and other lipids in the plasma, is expressed predominantly in liver and intestine. Previous work in our laboratory has shown that hepatocyte-specific expression is determined by synergistic interactions between transcription factors bound to three separate sites, sites A (-214 to -192), B (-169 to -146), and C (-134 to -119), within a powerful liver-specific enhancer located in the region -222 to -110 nucleotides upstream of the apolipoprotein AI gene transcription start site (+1). In this study, i

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Rottman, J. N., R. L. Widom, B. Nadal-Ginard, V. Mahdavi, and S. K. Karathanasis. "A retinoic acid-responsive element in the apolipoprotein AI gene distinguishes between two different retinoic acid response pathways." Molecular and Cellular Biology 11, no. 7 (1991): 3814–20. http://dx.doi.org/10.1128/mcb.11.7.3814-3820.1991.

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The gene coding for apolipoprotein AI, a plasma protein involved in the transport of cholesterol and other lipids in the plasma, is expressed predominantly in liver and intestine. Previous work in our laboratory has shown that hepatocyte-specific expression is determined by synergistic interactions between transcription factors bound to three separate sites, sites A (-214 to -192), B (-169 to -146), and C (-134 to -119), within a powerful liver-specific enhancer located in the region -222 to -110 nucleotides upstream of the apolipoprotein AI gene transcription start site (+1). In this study, i

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Rodriguez, A., L. J. Royo, F. Goyache, et al. "249BOVINE GRANULOSA CELLS MRNA EXPRESSION OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-± AND THE PROTO-ONCOGENE C-FOS." Reproduction, Fertility and Development 16, no. 2 (2004): 245. http://dx.doi.org/10.1071/rdv16n1ab249.

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PPARα and c-Fos are involved in regulation of gene expression and are known to be dependent on retinoic acid (RA), which in turn influences oocyte growth and developmental competence (Duque et al., 2002 Hum. Reprod. 17, 2706–2714; Hidalgo et al., 2003. Reproduction 125, 409–416), probably acting in part through granulosa cells. Peroxisome proliferator-activated receptor-α (PPARα) heterodimerizes with the retinoid receptor X (RXR), while c-Jun/c-Fos heterodimerizes with liganded retinoic acid receptors (RARs), then preventing formation of transcription factor activator protein 1 (AP-1) complexe

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Kugita, Masanori, Kazuhiro Nishii, Miwa Morita, et al. "Global gene expression profiling in early-stage polycystic kidney disease in the Han:SPRD Cy rat identifies a role for RXR signaling." American Journal of Physiology-Renal Physiology 300, no. 1 (2011): F177—F188. http://dx.doi.org/10.1152/ajprenal.00470.2010.

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Han:SPRD Cy is a spontaneous rat model of polycystic kidney disease (PKD) caused by a missense mutation in Pkdr1. Cystogenesis in this model is not clearly understood. In the current study, we performed global gene expression profiling in early-stage PKD cyst development in Cy/Cy kidneys and normal (+/+) kidneys at 3 and 7 days of postnatal age. Expression profiles were determined by microarray analysis, followed by validation with real-time RT-PCR. Genes were selected with over 1.5-fold expression changes compared with age-matched +/+ kidneys for canonical pathway analysis. We found nine path

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