Journal articles: 'COUP-TF1'

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Yu, Xianming, and Janet E. Mertz. "Distinct Modes of Regulation of Transcription of Hepatitis B Virus by the Nuclear Receptors HNF4α and COUP-TF1." Journal of Virology 77, no. 4 (February 15, 2003): 2489–99. http://dx.doi.org/10.1128/jvi.77.4.2489-2499.2003.

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ABSTRACT To study the effects of the nuclear receptors (NRs) HNF4α and COUP-TF1 on the life cycle of hepatitis B virus (HBV), the human hepatoma cell line Huh7 was transiently cotransfected with plasmids containing the HBV genome and encoding these two NRs. Overexpression of HNF4α and COUP-TF1 led to a 9-fold increase and a 7- to 10-fold decrease, respectively, in viral DNA synthesis. These two NRs also exhibited distinct modes of regulation of viral transcription. Overexpression of HNF4α led to a more-than-10-fold increase in synthesis of the pregenomic RNA but to only a 2- to 3-fold increase in synthesis of the pre-C and S RNAs. Moreover, the NR response element within the pre-C promoter, NRREpreC, played the major role in activation of pregenomic RNA synthesis by HNF4α. On the other hand, overexpression of COUP-TF1 led to an over-10-fold repression of synthesis of both pre-C and pregenomic RNAs mediated through either NRREpreC or NRREenhI. HNF4α and COUP-TF1 antagonized each other's effects on synthesis of pregenomic RNA and viral DNA when they were co-overexpressed. A naturally occurring HBV variant which allows for binding by HNF4α but not COUP-TF1 in its NRREpreC exhibited significantly higher levels of synthesis of pregenomic RNA and viral DNA than wild-type HBV in coexpression experiments. Last, deletion analysis revealed that non-NRRE sequences located within both the C and pre-S1 regions are also essential for maximum activation of the pregenomic promoter by HNF4α but not for repression by COUP-TF1. Thus, HNF4α and COUP-TF1 function through different mechanisms to regulate expression of the HBV genes.

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Liu, Yan-Yun, Teruyo Nakatani, Takahiko Kogai, Kaizeen Mody, and Gregory A. Brent. "Thyroid Hormone and COUP-TF1 Regulate Kallikrein-Binding Protein (KBP) Gene Expression." Endocrinology 152, no. 3 (March 1, 2011): 1143–53. http://dx.doi.org/10.1210/en.2010-0580.

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Kallikrein-binding protein (KBP) is a component of the kallikrein-kinin system that mediates vasodilation and inhibits tumor growth by antagonizing vascular endothelial growth factor-mediated angiogenesis. We demonstrate that KBP gene expression is repressed by T3 and modulated by the orphan nuclear receptor, chicken ovalbumin upstream promoter transcription factor 1 (COUP-TF1). In hypothyroid mice, KBP mRNA expression in the testis was increased 2.1-fold compared with euthyroid mice. We have identified two negative thyroid hormone response elements (nTREs) in the mouse KBP gene, nTRE1 located in the 5′ flanking region (−53 to −29) and nTRE2, located in the first intron (104–132). We used functional assays, cofactor knockdown, and chromatin immunoprecipitation assays to characterize nTRE1 and nTRE2 in hepatic (HepG2) and testes (GC-1spg) cell lines. Reporter expression directed by both elements was enhanced with addition of thyroid hormone receptor and repressed with the addition of T3. COUP-TF1 enhanced basal expression of both elements but blunted unliganded thyroid hormone receptor enhancement and T3 repression of nTRE1 but not nTRE2. Both nTREs bound nuclear corepressor and binding increased in response to T3. Nuclear corepressor knockdown resulted in loss of T3 repression of both nTRE1 and nTRE2. COUP-TF1, which usually represses T3 induction of positive thyroid hormone response elements, reverses T3 repression mediated by nTRE1 in the mouse KBP gene. Endogenous KBP expression is repressed by T3 and two functional nTREs, both of which are required, have been characterized in the KBP gene. COUP-TF1 may be an important factor to modulate expression of genes that are repressed by T3.

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Miller, Myrna M., Keith W. Jarosinski, and Karel A. Schat. "Negative modulation of the chicken infectious anemia virus promoter by COUP-TF1 and an E box-like element at the transcription start site binding δEF1." Journal of General Virology 89, no. 12 (December 1, 2008): 2998–3003. http://dx.doi.org/10.1099/vir.0.2008/003103-0.

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Expression of enhanced green fluorescent protein (EGFP) under control of the promoter-enhancer of chicken infectious anemia virus (CAV) is increased in an oestrogen receptor-enhanced cell line when treated with oestrogen and the promoter-enhancer binds unidentified proteins that recognize a consensus oestrogen response element (ERE). Co-transfection assays with the CAV promoter and the nuclear receptor chicken ovalbumin upstream promoter transcription factor 1 (COUP-TF1) showed that expression of EGFP was decreased by 50 to 60 % in DF-1 and LMH cells. The CAV promoter that included sequences at and downstream of the transcription start point had less expression than a short promoter construct. Mutation of a putative E box at this site restored expression levels. Electromobility shift assays showed that the transcription regulator delta-EF1 (δEF1) binds to this E box region. These findings indicate that the CAV promoter activity can be affected directly or indirectly by COUP-TF1 and δEF1.

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Power, S. C., and S. Cereghini. "Positive regulation of the vHNF1 promoter by the orphan receptors COUP-TF1/Ear3 and COUP-TFII/Arp1." Molecular and Cellular Biology 16, no. 3 (March 1996): 778–91. http://dx.doi.org/10.1128/mcb.16.3.778.

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vHNF1 (also termed HNF1 beta) is a member of the hepatocyte nuclear fa ctor 1 (HNF1; also termed HNF1 alpha) family of homeodomain-containing transcription factors that interact with a sequence motif found in the regulatory regions of a large number of genes expressed mainly in the liver. It has been suggested that vHNF1 plays a role in early differentiation of specialized epithelia of several endoderm- and mesoderm-derived organs, with HNF1 playing a role in later stages. In support of this idea, expression of vHNF1 but not HNF1 is induced upon treatment of the embryonal carcinoma cell line F9 with retinoic acid. We have cloned and analyzed the vHNF1 promoter to gain a better understanding of the regulation of vHNF1 expression and how it relates to the expression of HNF1. We have identified five sites of DNA-protein interaction within the first 260 bp upstream of the transcription start site, which involve at least three different families of transcription factors. Two sites, a distal DR-1 motif and a proximal octamer motif, are the most important for promoter activity. The DR-1 motif interacts with several members of the steroid hormone receptor superfamily including HNF4, COUP-TFI/Ear3, COUP-TFII/Arp1, and RAR alpha/RXR alpha heterodimers. The vHNF1 promoter is transactivated by COUP-TFI/Ear3 and COUP-TFII/Arp1 and, unlike the HNF1 promoter, is virtually unaffected by HNF4. Interestingly, the proximal octamer site and not the DR-1 site is required for COUP-TFI/Ear3 and COUP-TFII/Arp1 transactivation of the vHNF1 promoter. COUP-TFI/Ear3 does not bind directly to this proximal octamer site. We present evidence of an interaction between COUP-TFI/Ear3 and the octamer-binding proteins in vitro and in the cell, suggesting that COUP-TFI and COUP-TFII activate the vHNF1 promoter via an indirect mechanism.

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COMPE, Emmanuel, Georges de SOUSA, Kamel FRANCÇOIS, Régis ROCHE, Roger RAHMANI, Janine TORRESANI, Michel RAYMONDJEAN, and Richard PLANELLS. "Spot 14 protein interacts and co-operates with chicken ovalbumin upstream promoter-transcription factor 1 in the transcription of the L-type pyruvate kinase gene through a specificity protein 1 (Sp1) binding site." Biochemical Journal 358, no. 1 (August 8, 2001): 175–83. http://dx.doi.org/10.1042/bj3580175.

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In hepatocytes, the amount of the Spot 14 (S14) protein is closely related to the full expression of enzymes involved in the glycolytic and lipogenic pathways. In the present study we address the role played by this protein in the control of transcription of the L-type pyruvate kinase (L-PK) gene in primary hepatocytes. We show that human S14, which by itself does not bind to the L-PK promoter, physically interacts with the human chicken ovalbumin upstream promoter-transcription factor 1 (COUP-TF1) and induces the switch of this factor from a repressor to an activator. However, the enhancing activity of S14 and COUP-TF1 depends on the presence of a proximal GC-rich box (the L0 element) that specifically binds nuclear proteins from the livers of rats fed a glucose-rich diet. Moreover, the L0 element, which strongly binds dephosphorylated specificity protein 1 (Sp1), loses all affinity when this factor is phosphorylated by cAMP-dependent protein kinase. Mutations that affect binding of Sp1 and nuclear proteins to the L0 box also decrease basal transcription and impair glucose responsiveness of the promoter. These results therefore shed light on the mechanism by which the S14 protein, whose concentration rapidly rises after glucose intake, contributes to the full activity of the L-PK promoter.

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Galson, D. L., T. Tsuchiya, D. S. Tendler, L. E. Huang, Y. Ren, T. Ogura, and H. F. Bunn. "The orphan receptor hepatic nuclear factor 4 functions as a transcriptional activator for tissue-specific and hypoxia-specific erythropoietin gene expression and is antagonized by EAR3/COUP-TF1." Molecular and Cellular Biology 15, no. 4 (April 1995): 2135–44. http://dx.doi.org/10.1128/mcb.15.4.2135.

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The erythropoietin (Epo) gene is regulated by hypoxia-inducible cis-acting elements in the promoter and in a 3' enhancer, both of which contain consensus hexanucleotide hormone receptor response elements which are important for function. A group of 11 orphan nuclear receptors, transcribed and translated in vitro, were screened by the electrophoretic mobility shift assay. Of these, hepatic nuclear factor 4 (HNF-4), TR2-11, ROR alpha 1, and EAR3/COUP-TF1 bound specifically to the response elements in the Epo promoter and enhancer and, except for ROR alpha 1, formed DNA-protein complexes that had mobilities similar to those observed in nuclear extracts of the Epo-producing cell line Hep3B. Moreover, both anti-HNF-4 and anti-COUP antibodies were able to supershift complexes in Hep3B nuclear extracts. Like Epo, HNF-4 is expressed in kidney, liver, and Hep3B cells but not in HeLa cells. Transfection of a plasmid expressing HNF-4 into HeLa cells enabled an eightfold increase in the hypoxic induction of a luciferase reporter construct which contains the minimal Epo enhancer and Epo promoter, provided that the nuclear hormone receptor consensus DNA elements in both the promoter and the enhancer were intact. The augmentation by HNF-4 in HeLa cells could be abrogated by cotransfection with HNF-4 delta C, which retains the DNA binding domain of HNF-4 but lacks the C-terminal activation domain. Moreover, the hypoxia-induced expression of the endogenous Epo gene was significantly inhibited in Hep3B cells stably transfected with HNF-4 delta C. On the other hand, cotransfection of EAR3/COUP-TF1 and the Epo reporter either with HNF-4 into HeLa cells or alone into Hep3B cells suppressed the hypoxia induction of the Epo reporter. These electrophoretic mobility shift assay and functional experiments indicate that HNF-4 plays a critical positive role in the tissue-specific and hypoxia-inducible expression of the Epo gene, whereas the COUP family has a negative modulatory role.

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Angelova, Meglena, Radoslav Minkov, Vanya Goranova, Stoyan Pavlov, Vesselina Michaleva, and Anton B. Tonchev. "Expression of Transcription Factor Coup-TF1 (NR2F1) in Developing Occipital Cortex in Humans." Scripta Scientifica Medica 47, no. 1 (March 20, 2015): 53. http://dx.doi.org/10.14748/ssm.v47i1.851.

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8

Borello, Ugo, Mayur Madhavan, Ilya Vilinsky, Andrea Faedo, Alessandra Pierani, John Rubenstein, and Kenneth Campbell. "Sp8 and COUP-TF1 Reciprocally Regulate Patterning and Fgf Signaling in Cortical Progenitors." Cerebral Cortex 24, no. 6 (January 10, 2013): 1409–21. http://dx.doi.org/10.1093/cercor/bhs412.

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9

Guo, Lei, Jeffrey Lynch, Kimitoshi Nakamura, Larry Fliegel, Hideko Kasahara, Seigo Izumo, Issei Komuro, Luis B. Agellon, and Marek Michalak. "COUP-TF1 Antagonizes Nkx2.5-mediated Activation of the Calreticulin Gene during Cardiac Development." Journal of Biological Chemistry 276, no. 4 (December 5, 2000): 2797–801. http://dx.doi.org/10.1074/jbc.c000822200.

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10

Fischer, Silke F. "Genotype-dependent activation or repression of HBV enhancer II by transcription factor COUP-TF1." World Journal of Gastroenterology 12, no. 37 (2006): 6054. http://dx.doi.org/10.3748/wjg.v12.i37.6054.

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11

Schoorlemmer, J., A. van Puijenbroek, M. van Den Eijnden, L. Jonk, C. Pals, and W. Kruijer. "Characterization of a negative retinoic acid response element in the murine Oct4 promoter." Molecular and Cellular Biology 14, no. 2 (February 1994): 1122–36. http://dx.doi.org/10.1128/mcb.14.2.1122-1136.1994.

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Expression of Oct4 in embryonic stem cells is controlled by a distal upstream stem cell-specific enhancer that is deactivated during retinoic acid (RA)-induced differentiation by an indirect mechanism not involving binding of RA receptors (H. Okazawa, K. Okamoto, F. Ishino, T. Ishino-Kaneko, S. Takeda, Y. Toyoda, M. Muramatsu, and H. Hamada, EMBO J. 10:2997-3005, 1991). Here we report that in RA-treated P19 embryonal carcinoma cells the Oct4 promoter is also subject to negative regulation by RA. The minimal Oct4 promoter sequence mediating repression consists of a promoter-proximal sequence containing a GC-rich SP1 consensus-like sequence and several hormone response element half-sites that can be arranged into direct repeats with different spacing. The GC box binds a nuclear factor that is invariably present in undifferentiated and RA-treated differentiated P19 cells. By contrast, the hormone response element-containing sequence binds factors that are induced following RA treatment. Mutational analysis and competition experiments show that the functional entity binding the RA-induced factor is a direct repeat sequence with a spacing of one nucleotide, previously shown to be a binding site for COUP transcription factors (COUP-TFs). Cotransfected orphan receptors COUP-TF1, ARP-1, and EAR-2 were able to repress the activity of Oct4 promoter-driven reporters in P19 EC cells, albeit with different efficiencies. Furthermore, the negative transcriptional effect of COUP-TFs is dominant over the activating effect of the Oct4 embryonic stem cell-specific enhancer. These results show that negative regulation of Oct4 expression during RA-induced differentiation of embryonic stem cells is controlled by two different mechanisms, including deactivation of the embryonic stem cell-specific enhancer and promoter silencing by orphan nuclear hormone receptors.

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12

Schoorlemmer, J., A. van Puijenbroek, M. van Den Eijnden, L. Jonk, C. Pals, and W. Kruijer. "Characterization of a negative retinoic acid response element in the murine Oct4 promoter." Molecular and Cellular Biology 14, no. 2 (February 1994): 1122–36. http://dx.doi.org/10.1128/mcb.14.2.1122.

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Expression of Oct4 in embryonic stem cells is controlled by a distal upstream stem cell-specific enhancer that is deactivated during retinoic acid (RA)-induced differentiation by an indirect mechanism not involving binding of RA receptors (H. Okazawa, K. Okamoto, F. Ishino, T. Ishino-Kaneko, S. Takeda, Y. Toyoda, M. Muramatsu, and H. Hamada, EMBO J. 10:2997-3005, 1991). Here we report that in RA-treated P19 embryonal carcinoma cells the Oct4 promoter is also subject to negative regulation by RA. The minimal Oct4 promoter sequence mediating repression consists of a promoter-proximal sequence containing a GC-rich SP1 consensus-like sequence and several hormone response element half-sites that can be arranged into direct repeats with different spacing. The GC box binds a nuclear factor that is invariably present in undifferentiated and RA-treated differentiated P19 cells. By contrast, the hormone response element-containing sequence binds factors that are induced following RA treatment. Mutational analysis and competition experiments show that the functional entity binding the RA-induced factor is a direct repeat sequence with a spacing of one nucleotide, previously shown to be a binding site for COUP transcription factors (COUP-TFs). Cotransfected orphan receptors COUP-TF1, ARP-1, and EAR-2 were able to repress the activity of Oct4 promoter-driven reporters in P19 EC cells, albeit with different efficiencies. Furthermore, the negative transcriptional effect of COUP-TFs is dominant over the activating effect of the Oct4 embryonic stem cell-specific enhancer. These results show that negative regulation of Oct4 expression during RA-induced differentiation of embryonic stem cells is controlled by two different mechanisms, including deactivation of the embryonic stem cell-specific enhancer and promoter silencing by orphan nuclear hormone receptors.

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13

Teng, Xiaochun, Yan-Yun Liu, Weiping Teng, and Gregory A. Brent. "COUP-TF1 Modulates Thyroid Hormone Action in an Embryonic Stem-Cell Model of Cortical Pyramidal Neuronal Differentiation." Thyroid 28, no. 5 (May 2018): 667–78. http://dx.doi.org/10.1089/thy.2017.0256.

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Tambyrajah, Winston S., Elena Doran, Jeffrey D. Wood, and John D. McGivan. "The pig CYP2E1 promoter is activated by COUP-TF1 and HNF-1 and is inhibited by androstenone." Archives of Biochemistry and Biophysics 431, no. 2 (November 2004): 252–60. http://dx.doi.org/10.1016/j.abb.2004.08.016.

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Perets, Ruth, Tommy Kaplan, Ilan Stein, Guy Hidas, Shay Tayeb, Eti Avraham, Yinon Ben-Neriah, Itamar Simon, and Eli Pikarsky. "Genome-Wide Analysis of Androgen Receptor Targets Reveals COUP-TF1 as a Novel Player in Human Prostate Cancer." PLoS ONE 7, no. 10 (October 4, 2012): e46467. http://dx.doi.org/10.1371/journal.pone.0046467.

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Bietti, Lucas M. "The commemoration of March 24th, 1976." Journal of Language and Politics 10, no. 3 (October 31, 2011): 347–71. http://dx.doi.org/10.1075/jlp.10.3.03bie.

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In December 2001, Argentina underwent the worst socio-economic crisis in its history. Strong criticisms were raised by society against almost all the social injustices encouraged by the policies promoted by the former governments. Forgiveness of the crimes committed by the dictatorship during the “Dirty War” which took place in the late 70’s, and reconciliation between the members of the dictatorship and society, was the position held by the post-dictatorship governments. However, the official discourse has radically changed since 2003, because of the administration of elected president Nestor Kirchner (2003–2007). The aim of this paper is to explore some of the changes in relation to the creation of two time-frames (TF1/TF2) to represent actors from the past and the present, and reinforce the current exceptionality of Néstor Kirchner’s political stance. To do this, I will analyse four political speeches given by ex- president Néstor Kirchner to commemorate the anniversary of the coup d’état of March 24th, 1976, the date which marks the beginning of the 1976–1983 military dictatorship.

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Zhuang, Yong, and Lorraine J. Gudas. "Overexpression of COUP-TF1 in murine embryonic stem cells reduces retinoic acid-associated growth arrest and increases extraembryonic endoderm gene expression." Differentiation 76, no. 7 (September 2008): 760–71. http://dx.doi.org/10.1111/j.1432-0436.2007.00258.x.

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Lethimonier, Christèle, Gilles Flouriot, Olivier Kah, and Bernadette Ducouret. "The Glucocorticoid Receptor Represses the Positive Autoregulation of the Trout Estrogen Receptor Gene by Preventing the Enhancer Effect of a C/EBPβ-Like Protein." Endocrinology 143, no. 8 (August 1, 2002): 2961–74. http://dx.doi.org/10.1210/endo.143.8.8958.

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Abstract Stress and cortisol are known to have negative effects on vitellogenesis in oviparous species. This provides a physiological context in which to explore in more detail the molecular mechanisms involved in transcriptional interferences between two steroids receptors, the estradiol receptor (ER) and the glucocorticoid receptor (GR). We have previously shown that the cortisol inhibitory effect on rainbow trout (rt) vitellogenesis is the result of a repression of the estradiol-induced ER-positive autoregulation by activated GR. In the present study, we demonstrate that the GR repression involves a proximal region of the rtER promoter that is unable to bind GR. This inhibition is counteracted in part by the orphan receptor COUP-TF1 that has been previously shown to cooperate with ERs on the same promoter. A detailed analysis allowed us to identify a C/EBPβ-like protein that is implicated in both the maximal stimulatory effect of estradiol and the GR repression. Indeed, GR, through its DNA-binding domain, suppresses the binding of C/EBPβ on the rtER promoter by protein-protein interactions and thereby prevents the enhancer effect of this transcription factor.

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Wagner, Andrea, Anja Doerks, Mordechai Aboud, Angel Alonso, Takashi Tokino, Rolf M. Flügel, and Martin Löchelt. "Induction of Cellular Genes Is Mediated by the Bel1 Transactivator in Foamy Virus-Infected Human Cells." Journal of Virology 74, no. 10 (May 15, 2000): 4441–47. http://dx.doi.org/10.1128/jvi.74.10.4441-4447.2000.

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ABSTRACT To gain insight into human foamy virus (HFV; also called spumaretrovirus)-induced alterations of cellular genes, the expression profiles of defined genes in HFV-infected primary human cells were analyzed by cDNA array assays. Several distinct cellular genes activated by HFV infection were identified; the identities of the cellular genes were confirmed by RNA blot analyses. Compared with mock-infected controls, the concentrations of cellular Kip2, Egr-1, COUP-TF1, insulin-like growth factor II (IGF-II), and EphB3 mRNAs were significantly increased in HFV-infected cells and showed a gene-specific and time-dependent induction. Immunoblot analyses with antibodies against some of the cellular gene products revealed increased levels of the corresponding proteins. To investigate mechanisms of HFV-induced alterations in cellular gene expression, the capacity of known HFV genes to increase expression of defined cellular genes was analyzed by transient expression experiments. Plasmids that encode the HFV Bel1 transcriptional transactivator were necessary and sufficient to strongly increase expression of p57Kip2, IGF-II, and EphB3 genes in 293T cells. Potential mechanisms and consequences of activation of cellular genes during HFV infection and Bel1 transactivation of the Kip2 gene are discussed.

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Cardozo, Mônica, Kelly Furtado, Aline De Conti, Fábia de Oliveira Andrade, Laura Fernandes, Adriana Campos, Clarissa Scolastici, and Fernando Moreno. "The chemopreventive activity of β-ionone involves modulation of Rxrα, Rarβ and Coup-Tf1 expression in liver pre-neoplastic lesions in rats." Current Drug Targets 16, no. 999 (October 1, 2015): 1. http://dx.doi.org/10.2174/1389450116666151001110507.

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21

Ochi, Shohei, Shyu Manabe, Takako Kikkawa, and Noriko Osumi. "Thirty Years’ History since the Discovery of Pax6: From Central Nervous System Development to Neurodevelopmental Disorders." International Journal of Molecular Sciences 23, no. 11 (May 30, 2022): 6115. http://dx.doi.org/10.3390/ijms23116115.

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Pax6 is a sequence-specific DNA binding transcription factor that positively and negatively regulates transcription and is expressed in multiple cell types in the developing and adult central nervous system (CNS). As indicated by the morphological and functional abnormalities in spontaneous Pax6 mutant rodents, Pax6 plays pivotal roles in various biological processes in the CNS. At the initial stage of CNS development, Pax6 is responsible for brain patterning along the anteroposterior and dorsoventral axes of the telencephalon. Regarding the anteroposterior axis, Pax6 is expressed inversely to Emx2 and Coup-TF1, and Pax6 mutant mice exhibit a rostral shift, resulting in an alteration of the size of certain cortical areas. Pax6 and its downstream genes play important roles in balancing the proliferation and differentiation of neural stem cells. The Pax6 gene was originally identified in mice and humans 30 years ago via genetic analyses of the eye phenotypes. The human PAX6 gene was discovered in patients who suffer from WAGR syndrome (i.e., Wilms tumor, aniridia, genital ridge defects, mental retardation). Mutations of the human PAX6 gene have also been reported to be associated with autism spectrum disorder (ASD) and intellectual disability. Rodents that lack the Pax6 gene exhibit diverse neural phenotypes, which might lead to a better understanding of human pathology and neurodevelopmental disorders. This review describes the expression and function of Pax6 during brain development, and their implications for neuropathology.

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Dressel, Uwe, Dorit Thormeyer, Boran Altincicek, Achim Paululat, Martin Eggert, Sandra Schneider, Stephan P. Tenbaum, Rainer Renkawitz, and Aria Baniahmad. "Alien, a Highly Conserved Protein with Characteristics of a Corepressor for Members of the Nuclear Hormone Receptor Superfamily." Molecular and Cellular Biology 19, no. 5 (May 1, 1999): 3383–94. http://dx.doi.org/10.1128/mcb.19.5.3383.

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ABSTRACT Some members of nuclear hormone receptors, such as the thyroid hormone receptor (TR), silence gene expression in the absence of the hormone. Corepressors, which bind to the receptor’s silencing domain, are involved in this repression. Hormone binding leads to dissociation of corepressors and binding of coactivators, which in turn mediate gene activation. Here, we describe the characteristics of Alien, a novel corepressor. Alien interacts with TR only in the absence of hormone. Addition of thyroid hormone leads to dissociation of Alien from the receptor, as shown by the yeast two-hybrid system, glutathioneS-transferase pull-down, and coimmunoprecipitation experiments. Reporter assays indicate that Alien increases receptor-mediated silencing and that it harbors an autonomous silencing function. Immune staining shows that Alien is localized in the cell nucleus. Alien is a highly conserved protein showing 90% identity between human and Drosophila. Drosophila Alien shows similar activities in that it interacts in a hormone-sensitive manner with TR and harbors an autonomous silencing function. Specific interaction of Alien is seen with Drosophila nuclear hormone receptors, such as the ecdysone receptor and Seven-up, the Drosophila homologue of COUP-TF1, but not with retinoic acid receptor, RXR/USP, DHR 3, DHR 38, DHR 78, or DHR 96. These properties, taken together, show that Alien has the characteristics of a corepressor. Thus, Alien represents a member of a novel class of corepressors specific for selected members of the nuclear hormone receptor superfamily.

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Tarumoto, Takahisa, Shigehiko Imagawa, Ken Ohmine, Tadashi Nagai, Masato Higuchi, Nobuo Imai, Norio Suzuki, Masayuki Yamamoto, and Keiya Ozawa. "NG-monomethyl-l-arginine inhibits erythropoietin gene expression by stimulating GATA-2." Blood 96, no. 5 (September 1, 2000): 1716–22. http://dx.doi.org/10.1182/blood.v96.5.1716.

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Abstract NG-monomethyl-l-arginine (L-NMMA) has been reported to be elevated in uremic patients. Based on the hypothesis that the pathogenesis of the anemia of renal disease might be due to the perturbation of transcription factors of the erythropoietin (Epo) gene by L-NMMA, the present study was designed to investigate the effect of L-NMMA on Epo gene expression through the GATA transcription factor. L-NMMA caused decreased levels of NO, cyclic guanosine monophosphate (cGMP), and Epo protein in Hep3B cells. L-NAME (analogue of L-NMMA) also inhibited Epo production in anemic mice. Transfection of the Epo promoter-luciferase gene into Hep3B cells revealed that L-NMMA inhibited the Epo promoter activity. However, L-NMMA did not inhibit the Epo promoter activity when mutated Epo promoter (GATA to TATA) was transfected, and L-NMMA did not affect the enhancer activity. Electrophoretic mobility shift assays demonstrated the stimulation of GATA binding activity by L-NMMA. However, L-NMMA had no effect on the binding activity of hepatic nuclear factor-4, COUP-TF1, hypoxia-inducing factor-1, or NF-κB. Furthermore, cGMP inhibited the L-NMMA–induced GATA binding activity. L-NMMA also increased GATA-2 messenger RNA expression. These results demonstrate that L-NMMA suppresses Epo gene expression by up-regulation of the GATA transcription factor and support the hypothesis that L-NMMA is one of the candidate substances that underlie the pathogenesis of renal anemia.

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Tarumoto, Takahisa, Shigehiko Imagawa, Ken Ohmine, Tadashi Nagai, Masato Higuchi, Nobuo Imai, Norio Suzuki, Masayuki Yamamoto, and Keiya Ozawa. "NG-monomethyl-l-arginine inhibits erythropoietin gene expression by stimulating GATA-2." Blood 96, no. 5 (September 1, 2000): 1716–22. http://dx.doi.org/10.1182/blood.v96.5.1716.h8001716_1716_1722.

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NG-monomethyl-l-arginine (L-NMMA) has been reported to be elevated in uremic patients. Based on the hypothesis that the pathogenesis of the anemia of renal disease might be due to the perturbation of transcription factors of the erythropoietin (Epo) gene by L-NMMA, the present study was designed to investigate the effect of L-NMMA on Epo gene expression through the GATA transcription factor. L-NMMA caused decreased levels of NO, cyclic guanosine monophosphate (cGMP), and Epo protein in Hep3B cells. L-NAME (analogue of L-NMMA) also inhibited Epo production in anemic mice. Transfection of the Epo promoter-luciferase gene into Hep3B cells revealed that L-NMMA inhibited the Epo promoter activity. However, L-NMMA did not inhibit the Epo promoter activity when mutated Epo promoter (GATA to TATA) was transfected, and L-NMMA did not affect the enhancer activity. Electrophoretic mobility shift assays demonstrated the stimulation of GATA binding activity by L-NMMA. However, L-NMMA had no effect on the binding activity of hepatic nuclear factor-4, COUP-TF1, hypoxia-inducing factor-1, or NF-κB. Furthermore, cGMP inhibited the L-NMMA–induced GATA binding activity. L-NMMA also increased GATA-2 messenger RNA expression. These results demonstrate that L-NMMA suppresses Epo gene expression by up-regulation of the GATA transcription factor and support the hypothesis that L-NMMA is one of the candidate substances that underlie the pathogenesis of renal anemia.

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Messager, M., C. Carrière, X. Bertagna, and Y. de Keyzer. "RT-PCR analysis of corticotroph-associated genes expression in carcinoid tumours in the ectopic-ACTH syndrome." European Journal of Endocrinology 154, no. 1 (January 2006): 159–66. http://dx.doi.org/10.1530/eje.1.02077.

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Objective: ACTH is frequently produced in non-pituitary tumours, leading to the ectopic-ACTH syndrome, but the molecular mechanisms of its expression remain obscure. This study was aimed at understanding the transcription mechanisms of the ACTH-precursor gene in carcinoid tumours of the lung or thymus. Design: Transcripts coding for a series of corticotroph-associated transcription factor genes were detected, together with markers of the corticotroph phenotype. We studied a series of 41 carcinoid tumours including 15 with proven ectopic-ACTH syndrome. Methods: Specific RT-PCR reactions were designed for each gene including alternatively spliced isoforms. Results: The markers of the corticotroph phenotype were detected in all ACTH-positive tumours. Expression of the Tpit and Pitx1 genes were not restricted to ACTH-positive tumours but were also detected in many ACTH-negative carcinoids. Only a subset of ACTH-negative tumours expressed NAK-1/Nur77, and NeuroD1 expression was detected in <50% of the tumours regardless of their secretory status. The glucocorticoid receptor alpha was detected in every tumour in contrast to its beta isoform detectable in a few tumours only. Chicken ovalbumin upstream promoter-transcription factor 1 (COUP-TF1) and peroxisome proliferator-activated receptor (PPAR) γ2 were expressed in 50% of the tumours of each group whereas PPARγ1 was expressed in almost every tumour. Conclusions: ACTH-positive carcinoids do not share a characteristic expression pattern of the corticotroph-associated transcription factor genes, suggesting that the transcriptional mechanisms of the ACTH-precursor gene differ from those in normal pituitary corticotrophs. Expression of Tpit and Pitx1 genes in most carcinoids suggests that some aspects of the pituitary corticotroph phenotype may belong to general carcinoid differentiation.

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Rodriguez-Tirado, Carolina, Nupura Kale, Maria Jose Carlini, Nitisha Shrivastava, Alcina Rodrigues, Bassem Khalil, Jose Javier Bravo-Cordero, Melissa Alexander, Jiayi Ji, and Maria Soledad Sosa. "Abstract P3-06-03: NR2F1 is a barrier to dissemination of early-evolved mammary cancer cells." Cancer Research 82, no. 4_Supplement (February 15, 2022): P3–06–03—P3–06–03. http://dx.doi.org/10.1158/1538-7445.sabcs21-p3-06-03.

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Abstract Pre-malignant cells disseminate during very early and sometimes asymptomatic stages of tumor progression. Once settled in permissive environments at secondary organs, they can act as a source for metastasis (e.g. in breast, pancreatic, colon, melanoma and lung carcinomas), thus emerging as important players in future prognosis. Granted that biological barriers to tumorigenesis exist, there must also be limiting steps to early dissemination in pre-malignant cells, all of which remain largely unknown. We report that the orphan nuclear receptor NR2F1/COUP-TF1, downstream of Her2 signaling via p38alpha serves as a barrier to early dissemination in pre-malignant breast cells. Our work shows that NR2F1 expression is positively regulated by p38α-MAPK pathway and inhibited by HER2 oncogenic signaling pathway. Furthermore, NR2F1 downregulation in human and murine pre-malignant cell lines led to a partial epithelial-to-mesenchymal transition characterized by decreased E-cadherin expression and β-catenin membrane localization, disorganized laminin 5 deposition, and increased expression of CK14, TWIST1, ZEB1 and PRRX1, thus explaining an increased motility and dissemination of early cells upon loss of NR2F1. Interestingly, NR2F1 lost also maintained epithelial markers (like CK18), suggesting an hybrid luminal-mesenchymal phenotype that could favor cellular plasticity to adapt to distant sites. We also showed that NR2F1 blocked b-catenin nuclear localization via a WNT-dependent pathway. Significantly, downregulation of NR2F1 increased the in vivo dissemination potential of pre-malignant cells to lungs in a HER2-dependent manner. Lastly, Nr2f1 expression was downregulated in non-invasive DCIS biopsies when compared to benign adjacent tissue, and its expression was inversely correlated to Prrx1 levels. The inverse correlation between Nr2f1 and Prrx1 levels was lost in genetically evolved primary tumors, which suggests that a unique inhibitory mechanism of dissemination dominates at early stages of tumor progression. Overall, our data suggest the existence of an inhibitory mechanism of dissemination regulated by NR2F1 downstream of HER2 signaling in premalignant breast cells and propose that therapeutic strategies that aim to maintain NR2F1 expression could reduce dissemination of premalignant cells and delay relapses. Citation Format: Carolina Rodriguez-Tirado, Nupura Kale, Maria Jose Carlini, Nitisha Shrivastava, Alcina Rodrigues, Bassem Khalil, Jose Javier Bravo-Cordero, Melissa Alexander, Jiayi Ji, Maria Soledad Sosa. NR2F1 is a barrier to dissemination of early-evolved mammary cancer cells [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P3-06-03.

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Entin, Igor A., and Scott C. Kogan. "Discovery of Genes Involved in Experimental Pre-Leukemia to Leukemia Transition in Mice Using Expression Arrays." Blood 104, no. 11 (November 16, 2004): 1109. http://dx.doi.org/10.1182/blood.v104.11.1109.1109.

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Abstract Acute myeloid leukemia (AML) is characterized by a block in differentiation of myeloid cells accompanied by suppression of normal production of blood cells and dissemination of immature cells from their normal hematopoietic environment. In order to gain insight into the mechanisms governing these features of leukemia, we have examined mRNA expression patterns in transgenic mice that express PML-RARA (associated with human acute promyelocytic leukemia, APL) and BCL2. Such mice represent a model system in which these genetic changes combine to initially arrest differentiation in a pre-leukemic state, with acute leukemia arising only upon the acquisition of additional genetic changes. In the present study we identified the set of genes whose transcription is altered in pre-leukemic and leukemic bone marrow in comparison to bone marrow from normal mice. We generated and analyzed three sets of gene expression data from cDNA microarrays: (1) PRE-LEUKEMIA vs. NORMAL (6600 substances), (2) LEUKEMIA vs. NORMAL (6677 substances) and (3) PRE-LEUKEMIA vs. LEUKEMIA (3762 substances). Greater than 90% of substances showed similar expression in the pre-leukemic and leukemic samples. Sixty unique genes were differentially expressed, in a statistically significant manner, with two-fold or more difference in expression, and presenting in all three datasets. Comparison of these 60 revealed genes to a published human AML expression dataset (Bullinger et al., N Engl J Med, 350:1605, 2004) identified eight genes with the same pattern of expression in our mouse model and in human APL, and four common genes with opposite expression. For mouse pre-leukemia vs. leukemia as compared to all human AMLs vs. APL, the eight genes that showed a similar change were: COL1A2, COL5A2, EIF5A, LAMR1, LGALS1, NOTCH2, SNN, and ACP5. Of particular interest to our laboratory are two genes: LGALS1 and NOTCH2. Among the identified genes the first is most over-expressed, and the second is most under-expressed in human APL. Next, we identified genes in our dataset co-expressed with LGALS1 or NOTCH2 (correlation coefficient >0.85). Among discovered genes were revealed transcription factors (NKX6-1, GTF3A, ZFP95, SOX11, HOXA4 and more), translation factors (EIF3S6, EIF5A, EIF4A1 and more), differentiation factors (RQCD1, NEUROD2, CREBBP/EP300 inhibitory protein 1 and more), oncogenes (Ski, COUP-TF1 and more) and others. We are currently seeking to identify which of these changes may contribute to AML pathogenesis. Gene profiling using such a comparative approach for analysis will allow better understanding of leukemogenesis, and can also be applied for studies of tumor progression in other malignancies.

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Wang, Q. H., J. Y. Chen, K. N. Guo, X. B. Zheng, Q. Wu, H. Wei, and Y. Liu. "A correlation study of Boar taint-related genes, Boar tant substances and sex hormones in Bama miniature pigs at defferent ages." Indian Journal of Animal Research, OF (October 29, 2015). http://dx.doi.org/10.18805/ijar.5962.

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The Bama miniature pig (Sus scrofa domestica), endemic in China,which is characterized by its small size and specific meat flavor. The evaluation of pork quality is closely related to boar taint. However, there are no published studies of boar taint in Bama miniature pigs. In this study, the correlation between mRNA expression of boar taint-related genes,boar taint substances (androstenone and skatole) and sex hormones (testosterone, estradiol) of Bama miniature pigs at consecutive ages were examined. We found a gradual increase of mRNA (CYP2E1, CYP2A19, CYP2C34, and COUP-TF1) expression in the livers of pigs aged from birth to 6 months of age. The mRNA expression of COUP-TF1 and CYP2C34 peaked at 12 months old. However, the mRNA expression of CYP2E1 and CYP2A19 declined after 6 months age. The mRNA expression of CYP11A1, CYP17A1, StAR, and COUP-TF1 was stable over time in the testicle of Bama miniature pig. However, a substantial increase in their relative expression levels was observed before sexual maturity. Boar age was positively correlated to sex hormone (testosterone, estradiol) and boar taint substances (androstenone, skatole). There is in vivo gene regulation in boars that controls the relationship between boar taint substances and sex hormones. In addition, CYP11A1, CYP17A1, StAR, and sex hormones (testosterone, estradiol) can be used as markers for low boar taint study. Our study elucidated the correlation of boar taint-related genes,boar taint substances and sex hormones. These results have provided reference for applied research using Bama miniature pigs as a model for livestock production.

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Rodriguez-Tirado, Carolina, Nupura Kale, Maria J. Carlini, Nitisha Shrivastava, Alcina A. Rodrigues, Bassem Khalil, Jose J. Bravo-Cordero, et al. "NR2F1 is a barrier to dissemination of early stage breast cancer cells." Cancer Research, April 26, 2022. http://dx.doi.org/10.1158/0008-5472.can-21-4145.

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Abstract Cancer cells can disseminate during very early and sometimes asymptomatic stages of tumor progression. Though biological barriers to tumorigenesis have been identified and characterized, the mechanisms that limit early dissemination remain largely unknown. We report here that the orphan nuclear receptor NR2F1/COUP-TF1 serves as a barrier to early dissemination. NR2F1 expression was decreased in patient ductal carcinoma in situ (DCIS) samples. High-resolution intravital imaging of HER2+ early stage cancer cells revealed that loss of function of NR2F1 increased in vivo dissemination and was accompanied by decreased E-cadherin expression, activation of WNT-dependent β-catenin signaling, disorganized laminin 5 deposition, and increased expression of EMT genes such as TWIST1, ZEB1, and PRRX1. Furthermore, downregulation of NR2F1 promoted a hybrid luminal/basal phenotype. NR2F1 expression was positively regulated by p38α signaling and repressed by HER2 and WNT4 pathways. Lastly, early cancer cells with NR2F1LOW/PRRX1HIGH staining were observed in DCIS samples. Together, these findings reveal the existence of an inhibitory mechanism of dissemination regulated by NR2F1 in early stage breast cancer cells.

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Rodriguez-Tirado, Carolina, Nupura Kale, Maria J. Carlini, Nitisha Shrivastava, Alcina A. Rodrigues, Bassem Khalil, Jose J. Bravo-Cordero, et al. "NR2F1 is a barrier to dissemination of early stage breast cancer cells." Cancer Research, April 26, 2022. http://dx.doi.org/10.1158/0008-5472.can-21-4145.

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Abstract Cancer cells can disseminate during very early and sometimes asymptomatic stages of tumor progression. Though biological barriers to tumorigenesis have been identified and characterized, the mechanisms that limit early dissemination remain largely unknown. We report here that the orphan nuclear receptor NR2F1/COUP-TF1 serves as a barrier to early dissemination. NR2F1 expression was decreased in patient ductal carcinoma in situ (DCIS) samples. High-resolution intravital imaging of HER2+ early stage cancer cells revealed that loss of function of NR2F1 increased in vivo dissemination and was accompanied by decreased E-cadherin expression, activation of WNT-dependent β-catenin signaling, disorganized laminin 5 deposition, and increased expression of EMT genes such as TWIST1, ZEB1, and PRRX1. Furthermore, downregulation of NR2F1 promoted a hybrid luminal/basal phenotype. NR2F1 expression was positively regulated by p38α signaling and repressed by HER2 and WNT4 pathways. Lastly, early cancer cells with NR2F1LOW/PRRX1HIGH staining were observed in DCIS samples. Together, these findings reveal the existence of an inhibitory mechanism of dissemination regulated by NR2F1 in early stage breast cancer cells.

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31

Krebs, Joachim. "The Influence of Thyroid Hormone on Ca2+ Signaling Pathways during Embryonal Development." Current Topics in Medicinal Chemistry 21 (June 3, 2021). http://dx.doi.org/10.2174/1568026621666210603155653.

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: Thyroid hormones influence brain development through regulation of gene expression. Ca2+-dependent gene expression is a major pathway controlled by the Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) which in turn is induced by the thyroid hormone T3 as also demonstrated in a mouse embryonic stem cell line. In addition, T3 is controlling the expression of neurexin, synaptotagmin2 (SYT2), synaptotagmin-related gene1 (SRG1) and a number of other genes, involved in neurotransmitter release in a Ca2+-dependent manner. It has been noticed that the development of dopaminergic neurons by evoking significant calcium entry occurs through TRPC calcium channels. It also was demonstrated that the T3-mediated development of an early neuronal network is characteristic for depolarizing GABAergic neurons concomitant with intracellular calcium transients. An important aspect of T3-dependent regulation of gene expression in the developing brain is its modulation by the transcription activator COUP-TF1. Regulation of alternative splicing by CaMKIV is another important aspect for embryonal neural development since it can lead to the expression of PMCA1a, the neuronal specific isoform of the plasma membrane calcium pump. Maternal hypothyroidism or CaMKIV deficiency can have a severe influence on fetal brain development.

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Rodgers, Krista M., Jared T. Ahrendsen, Frank A. Strnad, Joan C. Yonchek, Wendy B. Macklin, Richard J. Traystman, and Paco S. Herson. "Abstract 70: Neurogenesis in the Pediatric Brain Following Ischemic Stroke: a Potential Target for Endogenous Regeneration and Repair." Stroke 47, suppl_1 (February 2016). http://dx.doi.org/10.1161/str.47.suppl_1.70.

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Introduction: Following stroke, neurons are seriously damaged or die, impairing local brain function and contributing to long-term disability. Mounting evidence suggests that stroke recovery in children is enhanced compared to adults. Neurogenesis, a process involving the generation of functionally integrated neurons from progenitor cells, may play a role in enhanced plasticity and neuronal repair. Stroke-induced neurogenesis in adults involves massive proliferation and migration of newborn neurons, however these newborn neurons go on to die, never repopulating areas of damage. We tested the hypothesis that neurogenesis in the young brain effectively repopulates injured regions following ischemia. Methods: Stroke was induced in adult (2-3 mo, n=21) and pediatric (P20-25, n=21) mice by 45-min right middle cerebral artery occlusion (MCAo). Bromodeoxyuridine (BrdU) was injected on days 3 and 4, and mice sacrificed at 24 hr, 7 d or 30 d after recovery from MCAo. Immunohistochemistry was performed to assess cellular proliferation and neurogenesis. Results: The results revealed extensive neuronal cell death in the striatum of both pediatric and adult mice at 24 hr and 7 d after stroke. Remarkably, significant numbers of healthy, mature neurons (NeuN+) were observed in the striatum of pediatric mice at 30 d post-injury. Birth-dating with BrdU demonstrated robust, ischemia-induced proliferation of neural progenitor cells in both adult and pediatric brain. Consistent with previous reports, we observed very few mature NeuN+ neurons double labeled with BrdU in the injured adult brain. In contrast, significant numbers of BrdU+NeuN cells were observed in the pediatric brain 30 d after MCAo, indicative of mature neurons and most importantly, with COUP-TF1-interacting protein 2 (Ctip2) expression, a marker of medium spiny striatal neurons. Conclusion: Our results indicate that cerebral ischemia in pediatric mice increases neurogenesis and migration to sites of damage, and supports the possibility of true neuronal replacement in the pediatric brain. These findings have exciting implications for heightened restorative processes in the pediatric brain microenvironment.

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Journal articles on the topic 'COUP-TF1'

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