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1
Mastick, G. S., and S. B. Scholnick. "Repression and activation of the Drosophila dopa decarboxylase gene in glia." Molecular and Cellular Biology 12, no. 12 (December 1992): 5659–66. http://dx.doi.org/10.1128/mcb.12.12.5659.
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Glial expression of the Drosophila dopa decarboxylase gene (Ddc) is repressed by a regulatory region located approximately 1 kb upstream of the transcriptional start site. We have used in vitro mutagenesis and germ line transformation to determine which elements within the Ddc promoter mediate repression. Our evidence suggests that the hypodermal cell activator elements IIA and IIB play a major role in the transcriptional regulation of Ddc in glial cells. A variety of mutations demonstrate that element IIA is a strong glial activator element and that element IIB is necessary for glial repression. Although these two regulatory elements are nearly identical in sequence, our data suggest that they are not redundant. Altering the wild-type number and spacing of elements IIA and IIB indicates that the wild-type arrangement of this repeat is critical for repression. We conclude that these key elements of the Ddc promoter regulate both activation and repression in glia.
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Mastick, G. S., and S. B. Scholnick. "Repression and activation of the Drosophila dopa decarboxylase gene in glia." Molecular and Cellular Biology 12, no. 12 (December 1992): 5659–66. http://dx.doi.org/10.1128/mcb.12.12.5659-5666.1992.
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Glial expression of the Drosophila dopa decarboxylase gene (Ddc) is repressed by a regulatory region located approximately 1 kb upstream of the transcriptional start site. We have used in vitro mutagenesis and germ line transformation to determine which elements within the Ddc promoter mediate repression. Our evidence suggests that the hypodermal cell activator elements IIA and IIB play a major role in the transcriptional regulation of Ddc in glial cells. A variety of mutations demonstrate that element IIA is a strong glial activator element and that element IIB is necessary for glial repression. Although these two regulatory elements are nearly identical in sequence, our data suggest that they are not redundant. Altering the wild-type number and spacing of elements IIA and IIB indicates that the wild-type arrangement of this repeat is critical for repression. We conclude that these key elements of the Ddc promoter regulate both activation and repression in glia.
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Fedoroff, N. "The heritable activation of cryptic Suppressor-mutator elements by an active element." Genetics 121, no. 3 (March 1, 1989): 591–608. http://dx.doi.org/10.1093/genetics/121.3.591.
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Abstract A weakly active maize Suppressor-mutator (Spm-omega) element is able to heritably activate cryptic Spm elements in the maize genome. The spontaneous activation frequency, which is 1-5 x 10(-5) in the present genetic background, increases by about 100-fold in the presence of an Spm-omega and remains an order of magnitude above the background level a generation after removal of the activating Spm-omega. Sectorial somatic reactivation of cryptic elements can be detected phenotypically in kernels. Selection of such kernels constitutes an efficient selection for plants with reactivated Spm elements. Analysis of the reactivation process reveals that it is gradual and proceeds through genetically metastable intermediates that exhibit different patterns of element expression during plant development. Newly reactivated elements tend to return to an inactive form. However, the probability that an element will remain in a heritably active state increases when the element is maintained in the presence of an active Spm element for several generations.
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Dilchert, Katharina, Thorsten Scherpf, and Viktoria H. Gessner. "Carbenoid‐Mediated Formation and Activation of Element‐Element and Element–Hydrogen Bonds." European Journal of Inorganic Chemistry 2020, no. 43 (November 5, 2020): 4111–15. http://dx.doi.org/10.1002/ejic.202000860.
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Aoki, Yutaka, Thomas Braun, David Davies, Odile Eisenstein, Ian Fairlamb, Natalie Fey, Mike George, et al. "Understanding unusual element-element bond formation and activation: general discussion." Faraday Discussions 220 (2019): 376–85. http://dx.doi.org/10.1039/c9fd90071c.
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Frost, Bess E., Wenyan Sun, Hanie Samimi, and Habil Zare. "JUMP AROUND, JUMP AROUND: TRANSPOSABLE ELEMENT ACTIVATION IN NEURODEGENERATIVE TAUOPATHY." Innovation in Aging 3, Supplement_1 (November 2019): S587. http://dx.doi.org/10.1093/geroni/igz038.2178.
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Abstract Transposable elements, or “jumping genes,” constitute ~45% of the human genome. We have identified transposable element activation as a key mediator of neurodegeneration in tauopathies, a group of disorders that are pathologically defined by deposits of tau protein in the brain. Cellular defenses that limit transposable element mobilization include 1) formation of silencing heterochromatin and 2) generation of piwi-interacting RNAs (piRNAs) that clear transposable element transcripts. Using genetic approaches in Drosophila models of tauopathy, we find evidence for a causal relationship between tau-induced heterochromatin decondensation and piRNA depletion, transposable element mobilization, and neurodegeneration. 3TC, an FDA-approved inhibitor of reverse transcriptase, suppresses transposable element mobilization and neuronal death in tau transgenic Drosophila. We detect a significant increase in transcripts of the human endogenous retrovirus class of transposable elements in postmortem human Alzheimer’s disease brains. Our data identify transposable element activation as a conserved, pharmacologically targetable driver of neurodegeneration in tauopathy.
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Drazinic, C. M., J. B. Smerage, M. C. López, and H. V. Baker. "Activation mechanism of the multifunctional transcription factor repressor-activator protein 1 (Rap1p)." Molecular and Cellular Biology 16, no. 6 (June 1996): 3187–96. http://dx.doi.org/10.1128/mcb.16.6.3187.
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Transcriptional activation in eukaryotic organisms normally requires combinatorial interactions of multiple transcription factors. In most cases, the precise role played by each transcription factor is not known. The upstream activating sequence (UAS) elements of glycolytic enzyme genes in Saccharomyces cerevisiae are excellent model systems for the study of combinatorial interactions. The yeast protein known as Rap1p acts as both a transcriptional repressor and an activator, depending on sequence context. Rap1p-binding sites are found adjacent to Gcr1p-binding sites in the UAS elements of glycolytic enzyme genes. These UAS elements constitute some of the strongest activating sequences known in S. cerevisiae. In this study, we have investigated the relationship between Rap1p- and Gcr1p-binding sites and the proteins that bind them. In vivo DNA-binding studies with rap1ts mutant strains demonstrated that the inability of Rap1p to bind at its site resulted in the inability of Gcr1p to bind at adjacent binding sites. Synthetic oligonucleotides, modeled on the UAS element of PYK1, in which the relative positions of the Rap1p- and Gcr1p-binding sites were varied prepared and tested for their ability to function as UAS elements. The ability of the oligonucleotides to function as UAS elements was dependent not only on the presence of both binding sites but also on the relative distance between the binding sites. In vivo DNA-binding studies showed that the ability of Rap1p bind its site was independent of Gcr1p but that the ability of Gcr1p to bind its site was dependent on the presence of an appropriately spaced and bound Rap1p-binding site. In vitro binding studies showed Rap1p-enhanced binding of Gcr1p on oligonucleotides modeled after the native PYK1 UAS element but not when the Rap1p- and Gcr1p-binding sites were displaced by 5 nucleotides. This work demonstrates that the role of the Rap1p in the activation of glycolytic enzyme genes is to bind in their UAS elements and to facilitate the binding of Gcr1p at adjacent binding sites.
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Wu, T. J., G. Monokian, D. F. Mark, and C. R. Wobbe. "Transcriptional activation by herpes simplex virus type 1 VP16 in vitro and its inhibition by oligopeptides." Molecular and Cellular Biology 14, no. 5 (May 1994): 3484–93. http://dx.doi.org/10.1128/mcb.14.5.3484.
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VP16 is a herpes simplex virus (HSV)-encoded transcriptional activator protein that is essential for efficient viral replication and as such may be a target for novel therapeutic agents directed against viral gene expression. We have reconstituted transcriptional activation by VP16 in an in vitro system that is dependent on DNA sequences from HSV immediate-early gene promoters and on protein-protein interactions between VP16 and Oct-1 that are required for VP16 activation in vivo. Activation increased synergistically with the number of TAATGARAT elements (the cis-acting element for VP16 activation in vivo) upstream of the core promoter, and mutations of this element that reduce Oct-1 or VP16 DNA binding reduced transactivation in vitro. A VP16 insertion mutant unable to interact with Oct-1 was inactive, but, surprisingly, a deletion mutant lacking the activation domain was approximately 65% as active as the full-length protein. The activation domains of Oct-1 were necessary for activation in reactions containing the VP16 deletion mutant, and they contributed significantly to activation by full-length VP16. Addition of a GA-rich element present in many HSV immediate-early gene enhancers synergistically stimulated VP16-activated transcription. Finally, oligopeptides that are derived from a region of VP16 thought to contact a cellular factor known as HCF (host cell factor) and that inhibit efficient VP16 binding to the TAATGARAT element also specifically inhibited VP16-activated, but not basal, transcription. Amino acid substitutions in one of these peptides identified three residues that are absolutely required for inhibition and presumably for interaction of VP16 with HCF.
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Wu, T. J., G. Monokian, D. F. Mark, and C. R. Wobbe. "Transcriptional activation by herpes simplex virus type 1 VP16 in vitro and its inhibition by oligopeptides." Molecular and Cellular Biology 14, no. 5 (May 1994): 3484–93. http://dx.doi.org/10.1128/mcb.14.5.3484-3493.1994.
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VP16 is a herpes simplex virus (HSV)-encoded transcriptional activator protein that is essential for efficient viral replication and as such may be a target for novel therapeutic agents directed against viral gene expression. We have reconstituted transcriptional activation by VP16 in an in vitro system that is dependent on DNA sequences from HSV immediate-early gene promoters and on protein-protein interactions between VP16 and Oct-1 that are required for VP16 activation in vivo. Activation increased synergistically with the number of TAATGARAT elements (the cis-acting element for VP16 activation in vivo) upstream of the core promoter, and mutations of this element that reduce Oct-1 or VP16 DNA binding reduced transactivation in vitro. A VP16 insertion mutant unable to interact with Oct-1 was inactive, but, surprisingly, a deletion mutant lacking the activation domain was approximately 65% as active as the full-length protein. The activation domains of Oct-1 were necessary for activation in reactions containing the VP16 deletion mutant, and they contributed significantly to activation by full-length VP16. Addition of a GA-rich element present in many HSV immediate-early gene enhancers synergistically stimulated VP16-activated transcription. Finally, oligopeptides that are derived from a region of VP16 thought to contact a cellular factor known as HCF (host cell factor) and that inhibit efficient VP16 binding to the TAATGARAT element also specifically inhibited VP16-activated, but not basal, transcription. Amino acid substitutions in one of these peptides identified three residues that are absolutely required for inhibition and presumably for interaction of VP16 with HCF.
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Pan, Y. B., and P. A. Peterson. "Spontaneous Activation of Quiescent Uq Transposable Elements during Endosperm Development in Zea Mays." Genetics 119, no. 2 (June 1, 1988): 457–64. http://dx.doi.org/10.1093/genetics/119.2.457.
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Abstract This study addresses the question of the activation of quiescent transposable elements in maize breeding lines. The a-ruq reporter allele of the Uq transposable element system expresses Uq activity (spots or sectors of spots in otherwise colorless aleurone tissue) when exposed to various genotypes of assorted maize inbred lines lacking any active Uq element. This activation of quiescent Uq elements occurs randomly during the growth of the endosperm. It is concluded that there are components in the genome that enhance the rare activation of quiescent Uq elements. Further, it seems that this activation occurs in the absence of any stress-inducing treatment, but that normal growth conditions provide sufficient stimulus for such activation.
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Orwig, Kyle E., and Michael J. Soares. "Transcriptional Activation of the Decidual/Trophoblast Prolactin-Related Protein Gene1." Endocrinology 140, no. 9 (September 1, 1999): 4032–39. http://dx.doi.org/10.1210/endo.140.9.6954.
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Abstract The decidual/trophoblast PRL-related protein (d/tPRP) is dually expressed by decidual and trophoblast cells during pregnancy. We have characterized the proximal d/tPRP promoter responsible for directing d/tPRP expression in decidual and trophoblast cells. We have demonstrated that the proximal 93 bp of d/tPRP 5′-flanking DNA are sufficient to direct luciferase gene expression in primary decidual and Rcho-1 trophoblast cells, but not in fibroblast, undifferentiated uterine stromal cells or trophoblast cells of a labyrinthine lineage. The 93-bp d/tPRP promoter was also sufficient to direct differentiation-dependent expression in trophoblast giant cells. Mutational analysis demonstrated the differential importance of activating protein-1 and Ets regulatory elements (located within the proximal 93 bp of d/tPRP 5′-flanking DNA) for activation of the d/tPRP promoter in decidual vs. trophoblast cells. Disruption of the activating protein-1 regulatory element inhibited d/tPRP promoter activity by more than 95% in decidual cells, and approximately 80% trophoblast cells. Disruption of the Ets regulatory element reduced d/tPRP promoter activity by approximately 50% in decidual cells, while inactivating the d/tPRP promoter in trophoblast cells. Protein interactions with the trophoblast Ets regulatory element were shown to be cell type specific and to change during trophoblast giant cell formation. In conclusion, a 93-bp region of the d/tPRP promoter is shown to contain regulatory elements sufficient for gene activation in decidual and trophoblast cells.
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Kong, Xingzhong, Shangbin Hu, Jingkang Yang, and Yongchang Wang. "Activation cross sections for the element rhenium." Journal of Radioanalytical and Nuclear Chemistry 218, no. 1 (April 1997): 127–29. http://dx.doi.org/10.1007/bf02033989.
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Kafala, S. I., and T. D. Macmahon. "Neutron activation analysis without multi-element standards." Journal of Radioanalytical and Nuclear Chemistry Articles 169, no. 1 (March 1993): 187–99. http://dx.doi.org/10.1007/bf02046793.
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Odic, Darko, and Jay Pratt. "Solving the Correspondence Problem within the Ternus Display: The Differential-Activation Theory." Perception 37, no. 12 (January 1, 2008): 1790–804. http://dx.doi.org/10.1068/p5670.
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The Ternus display produces a bistable illusion of motion: at very short interstimulus intervals (ISIs; < 30 ms) observers perceive element motion while at longer ISIs (> 30 ms) observers perceive group motion. In experiment 1, however, we find that, when the Ternus display's ISI contains an occluding box, group motion is mostly eliminated. These results do not fit the predictions made by the short-range/long-range two-process theory [Braddick and Adlard, 1978, in Visual Psychophysics and Psychology (New York: Academic Press)]. We propose that the differential-activation theory (Gilroy et al, 2001 Perception & Psychophysics63 847–861) accounts for our results. We then extend the differential-activation theory as an explanatory mechanism for the Ternus display in experiment 2 by selectively placing an occluder over the first, second, or third Ternus display element. As predicted by the differential-activation theory, the occlusion of the far-left element produced a normal distribution of group motion increasing with ISI, while the occlusion of the other two elements produced an illusion of occluded elements remaining stationary throughout the display. Furthermore, as predicted by the differential-activation theory, each moving element was assigned to its nearest neighbour, producing, in the case of second and third element occlusion, a novel Ternus display motion illusion where only two out of three elements are perceived as moving.
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Quincey, R. V., and R. E. Godfrey. "Upstream activation of ribosomal RNA biosynthesis in Saccharomyces cerevisiae." Biochemical Journal 232, no. 1 (November 15, 1985): 205–9. http://dx.doi.org/10.1042/bj2320205.
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Yeast was transformed with eight recombinants that contained an rRNA minigene and upstream elements of rDNA in different orientations in the multi-copy yeast-Escherichia coli shuttle vector, pJDB207. The effect of these elements of upstream rDNA on the initiation of transcription of the minigene at the site for rRNA biosynthesis was determined by using an S1 nuclease mapping procedure to measure the abundance of the minigene transcript in RNA from the yeast transformants. Transcription of the minigene was enhanced 3-fold by DNA within a 2.2 kb element more than 1.5 kb upstream from the initiation site. Inversion of the 2.2 kb element decreased expression of the minigene by 40%. This 2.2 kb element contained approx. 500 bp from the 25S rRNA coding region at the 3′ end of the preceding rRNA gene and 1 kb of adjacent nontranscribed spacer rDNA. The enhancing activity was independent of interference from readthrough that might have contributed to the 7-fold decrease in minigene expression caused by removing all rDNA upstream from −209 bp.
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HERRERO, Pilar, Leticia FLORES, Tamara de la CERA, and Fernando MORENO. "Functional characterization of transcriptional regulatory elements in the upstream region of the yeast GLK1 gene." Biochemical Journal 343, no. 2 (October 8, 1999): 319–25. http://dx.doi.org/10.1042/bj3430319.
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The glucokinase gene GLK1 of the yeast Saccharomyces cerevisiae is transcriptionally regulated in response to the carbon source of the growth medium. Northern-blot analysis shows that the GLK1 gene is expressed at a basal level in the presence of glucose, de-repressed more than 6-fold under conditions of sugar limitation and more than 25-fold under conditions of ethanol induction. lacZ fusions of the GLK1 gene promoter were constructed and a deletion analysis was performed in order to identify the cis-acting regulatory elements of the promoter that controls GLK1 gene expression. First, the expression seemed to be mediated mainly by one GCR1 and three stress-responsive element (STRE) activating elements. Secondly, an ethanol repression autoregulation (ERA)/twelve-fold TA repeat (TAB) repressor element was identified within the promoter region of the GLK1 gene. A specific and differential protein binding to the STRE was observed with extracts from de-repressed and repressed cells. No differential binding to the GCR1 or ERA/TAB elements was observed with extracts from de-repressed and repressed cells, but, in both cases, the binding was competed for by an excess of the unlabelled GLK1GCR1 andGLK1ERA sequence. The transcription factors Msn2 and Msn4, which bind to the GLK1 upstream region through the STRE, contribute to inductive activation. The transcription factor Gcr1, which binds through the GCR1 element, contributes to constitutive activation. In order to achieve the severe glucose repression of GLK1, constitutive repressor factors acting through the ERA/TAB element must counteract constitutive activation generated by Gcr1 binding to the GCR1 element. Full expression of the GLK1 gene is produced by inductive activation of three STRE when Msn2 and Msn4 proteins are translocated to the nucleus by covalent modification. The combinatorial effect of the entire region leads to the regulated transcription of GLK1, i.e., silent in media with glucose and other preferred carbon sources, such as fructose or mannose, and increased levels of expression upon glucose depletion.
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Faris, Mary, Kevin M. Latinis, Stephan J. Kempiak, Gary A. Koretzky, and Andre Nel. "Stress-Induced Fas Ligand Expression in T Cells Is Mediated through a MEK Kinase 1-Regulated Response Element in the Fas Ligand Promoter." Molecular and Cellular Biology 18, no. 9 (September 1, 1998): 5414–24. http://dx.doi.org/10.1128/mcb.18.9.5414.
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ABSTRACT T lymphocytes undergo apoptosis in response to a variety of stimuli, including exposure to UV radiation and γ-irradiation. While the mechanism by which stress stimuli induce apoptosis is not well understood, we have previously shown that the induction of Fas ligand (FasL) gene expression by environmental stress stimuli is dependent on c-Jun N-terminal kinase (JNK) activation. Using inducible dominant-active (DA) JNK kinase kinase (MEKK1) expression in Jurkat cells, we map a specific MEKK1-regulated response element to positions −338 to −316 of the Fas ligand (FasL) promoter. Mutation of that response element abrogated MEKK1-mediated FasL promoter activation and interfered in stress-induced activation of that promoter. Using electrophoretic mobility shift assays, we demonstrate that activator protein 1 (AP-1) binding proteins, namely, activating transcription factor 2 (ATF2) and c-Jun, bind to the MEKK1 response element. Transient transfection of interfering c-Jun and ATF2 mutants, which lack the consensus JNK phosphorylation sites, abrogated the transcriptional activation of the FasL promoter, demonstrating the involvement of these transcription factors in the regulation of the FasL promoter. Taken together, our data indicate that MEKK1 and transcription factors regulated by the JNK pathway play a role in committing lymphocytes to undergo apoptosis by inducing FasL expression via a novel response element in the promoter of that gene.
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Zhu, Ming, Hyounggee Baek, Ruiwu Liu, Aimin Song, Kit Lam, and Derick Lau. "LAS0811: From Combinatorial Chemistry to Activation of Antioxidant Response Element." Journal of Biomedicine and Biotechnology 2009 (2009): 1–8. http://dx.doi.org/10.1155/2009/420194.
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The antioxidant response element (ARE) and its transcription factor, nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), are potential targets for cancer chemoprevention. We sought to screen small molecules synthesized with combinatorial chemistry for activation of ARE. By high-throughput screening of 9400 small molecules from 10 combinatorial chemical libraries using HepG2 cells with an ARE-driven reporter, we have identified a novel small molecule, 1,2-dimethoxy-4,5-dinitrobenzene (LAS0811), as an activator of the ARE. LAS0811 upregulated the activity of NAD(P)H:quinone oxidoreductase 1 (NQO1), a representative antioxidative enzyme regulated by ARE. It enhanced production of an endogenous reducing agent, glutathione (GSH). In addition, LAS0811 induced expression of heme oxygenase 1 (HO1), which is an ARE-regulated enzyme with anti-inflammatory activity. Furthermore, LAS0811 reduced cell death due to the cytotoxic stress of a strong oxidant, t-butyl hydroperoxide (t-BOOH). Mechanistically, LAS0811 upregulated the expression of Nrf2 and promoted its translocation into the nuclei leading to subsequent ARE activation. Taken together, LAS0811 is a novel activator of the ARE and its associated detoxifying genes and, thus, a potential agent for cancer chemoprevention.
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Peng, Nan, Qiu Xia, Zhengjun Chen, Yun Xiang Liang, and Qunxin She. "An upstream activation element exerting differential transcriptional activation on an archaeal promoter." Molecular Microbiology 74, no. 4 (October 8, 2009): 928–39. http://dx.doi.org/10.1111/j.1365-2958.2009.06908.x.
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BANKS, Eric B., James F. CRISH, Jean F. WELTER, and Richard L. ECKERT. "Characterization of human involucrin promoter distal regulatory region transcriptional activator elements–a role for Sp1 and AP1 binding sites." Biochemical Journal 331, no. 1 (April 1, 1998): 61–68. http://dx.doi.org/10.1042/bj3310061.
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Human involucrin (hINV) is an important precursor of the keratinocyte cornified envelope that is specifically expressed in the suprabasal layers of stratifying epithelia. Previous truncation and mutagenesis experiments have shown that an activator protein 1 (Ap1) site, AP1–5, located 2100 bp upstream of the transcription start site, is required for optimal promoter activity. These previous studies suggest that AP1–5 is part of a distal regulatory region spanning nucleotides -2473 to -2088. In the present report, we study the distal regulatory region (DRR), which surrounds AP1–5. Our studies show that this region contains weak and strong activator elements spanning nucleotides -2473/-2216 and -2140/-2088, respectively. The strong activator element contains AP1–5 and an adjacent specificity protein 1 (Sp1) site. The AP1–5 site is absolutely required for DRR activity, as its mutation reduces transcription to basal levels. Mutagenesis studies of the AP1–5 and Sp1 sites in the presence or absence of the weak activator element indicate that the Sp1 site and the weak activator element synergistically activate the AP1–5 site-dependent transcription. The cooperation between the Sp1 and AP1–5 sites is also observed in the context of the full-length promoter. Gel mobility shift and supershift studies show that Sp1, but not Sp2, Sp3 or Sp4 binds to the Sp1 site. When the Sp1 site is mutated or the distance between the AP1–5 and Sp1 site is increased, the binding of AP1 factors to AP1–5 is markedly reduced. Surprisingly, gel shift studies suggest that activation does not require the formation of a stable AP1/Sp1/DNA ternary complex. These studies suggest that the AP1–5 site is absolutely required for transcriptional activation, that the weak activator element and Sp1 sites serve to enhance this activation, and that the Sp1 site is required for optimal AP1 factor binding at the AP1–5 site.
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Peng, Nan, Xiang Ao, Yun Xiang Liang, and Qunxin She. "Archaeal promoter architecture and mechanism of gene activation." Biochemical Society Transactions 39, no. 1 (January 19, 2011): 99–103. http://dx.doi.org/10.1042/bst0390099.
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Sulfolobus solfataricus and Sulfolobus islandicus contain several genes exhibiting D-arabinose-inducible expression and these systems are ideal for studying mechanisms of archaeal gene expression. At sequence level, only two highly conserved cis elements are present on the promoters: a regulatory element named ara box directing arabinose-inducible expression and the basal promoter element TATA, serving as the binding site for the TATA-binding protein. Strikingly, these promoters possess a modular structure that allows an essentially inactive basal promoter to be strongly activated. The invoked mechanisms include TFB (transcription factor B) recruitment by the ara-box-binding factor to activate gene expression and modulation of TFB recruitment efficiency to yield differential gene expression.
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Stargell, L. A., and K. Struhl. "A new class of activation-defective TATA-binding protein mutants: evidence for two steps of transcriptional activation in vivo." Molecular and Cellular Biology 16, no. 8 (August 1996): 4456–64. http://dx.doi.org/10.1128/mcb.16.8.4456.
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Using a genetic screen, we isolated four TATA-binding protein (TBP) mutants that are specifically defective in vivo for the response to acidic activators. In contrast to previously described activation-defective TBP mutants, these TBP derivatives are not specifically defective for interactions with TATA elements or TFIIA. Three of these derivatives interact normally with a TATA element, TFIIA, TFIIB, or an acidic activation domain; presumably, they affect another protein-protein interaction important for transcriptional activation. The remaining derivative (with F-237 replaced by D) binds a TATA element with wild-type affinity, but the TBP-TATA complex has an altered electrophoretic mobility and interacts poorly with TFIIA and TFIIB; this suggests that the conformation of the TBP-TATA element complex plays a role in transcriptional activation. To determine the step at which the TBP derivatives were unable to activate transcription, we utilized an artificial recruitment assay in which TBP is targeted to the promoter via fusion to the LexA DNA-binding domain. Consistent with previous evidence that acidic activators can increase recruitment of TBP to the promoter in vivo, the activation defect of some of these TBP derivatives can be corrected by artificial recruitment. In contrast, the activation defect of the other TBP derivatives is not bypassed by artificial recruitment. Thus, these TBP mutants define two steps in the process of transcriptional stimulation by acidic activators: efficient recruitment to the TATA element and a postrecruitment interaction with a component(s) of the initiation complex.
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Jackson, S. M., C. A. Keech, D. J. Williamson, and A. Gutierrez-Hartmann. "Interaction of basal positive and negative transcription elements controls repression of the proximal rat prolactin promoter in nonpituitary cells." Molecular and Cellular Biology 12, no. 6 (June 1992): 2708–19. http://dx.doi.org/10.1128/mcb.12.6.2708.
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The proximal rat prolactin (rPRL) promoter contains three cell-specific elements, designated footprints I, III, and IV, which restrict rPRL gene expression to anterior pituitary lactotroph cells. Footprint II (-130 to -120) binds a factor, which we have termed F2F, present in pituitary and nonpituitary cell types. Here we demonstrate that a key role of the footprint II site is to inhibit rPRL promoter activity in nonpituitary cells, specifically, by interfering with the basal activating function of a vicinal element. Gene transfer analysis revealed 20-fold activation of the rPRL promoter in nonpituitary cell types when footprint II was either deleted or specifically mutated. Similar activation of the intact rPRL promoter was obtained by in vivo F2F titration studies. In GH4 rat pituitary cells, the footprint II inhibitory activity was masked by the redundant, positively acting cell-specific elements and was inhibitory only if the two upstream sites, footprints III and IV, were deleted. Deletion of the -112 to -80 region in the footprint II site-specific mutant background resulted in complete loss of rPRL promoter activity in both pituitary and nonpituitary cell types, mapping a basal activating element that is operative irrespective of cell type to this region. While the basal activating element imparted an activating function in a heterologous promoter assay, the footprint II sequence did not display any inherent repressor function and actually induced several minimal heterologous promoters. However, the inhibitory activity of the footprint II site was detected only if it was in context with the basal activating element. These data underscore the importance of ubiquitous activating and inhibitory factors in establishing cell-specific gene expression and further emphasize the complexity of the molecular mechanisms which restrict gene expression to specific cell types. We provide a novel paradigm to study rPRL promoter function and hormone responsiveness independently of lactotroph cell-specific requirements.
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Jackson, S. M., C. A. Keech, D. J. Williamson, and A. Gutierrez-Hartmann. "Interaction of basal positive and negative transcription elements controls repression of the proximal rat prolactin promoter in nonpituitary cells." Molecular and Cellular Biology 12, no. 6 (June 1992): 2708–19. http://dx.doi.org/10.1128/mcb.12.6.2708-2719.1992.
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The proximal rat prolactin (rPRL) promoter contains three cell-specific elements, designated footprints I, III, and IV, which restrict rPRL gene expression to anterior pituitary lactotroph cells. Footprint II (-130 to -120) binds a factor, which we have termed F2F, present in pituitary and nonpituitary cell types. Here we demonstrate that a key role of the footprint II site is to inhibit rPRL promoter activity in nonpituitary cells, specifically, by interfering with the basal activating function of a vicinal element. Gene transfer analysis revealed 20-fold activation of the rPRL promoter in nonpituitary cell types when footprint II was either deleted or specifically mutated. Similar activation of the intact rPRL promoter was obtained by in vivo F2F titration studies. In GH4 rat pituitary cells, the footprint II inhibitory activity was masked by the redundant, positively acting cell-specific elements and was inhibitory only if the two upstream sites, footprints III and IV, were deleted. Deletion of the -112 to -80 region in the footprint II site-specific mutant background resulted in complete loss of rPRL promoter activity in both pituitary and nonpituitary cell types, mapping a basal activating element that is operative irrespective of cell type to this region. While the basal activating element imparted an activating function in a heterologous promoter assay, the footprint II sequence did not display any inherent repressor function and actually induced several minimal heterologous promoters. However, the inhibitory activity of the footprint II site was detected only if it was in context with the basal activating element. These data underscore the importance of ubiquitous activating and inhibitory factors in establishing cell-specific gene expression and further emphasize the complexity of the molecular mechanisms which restrict gene expression to specific cell types. We provide a novel paradigm to study rPRL promoter function and hormone responsiveness independently of lactotroph cell-specific requirements.
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LI, FAN, HONGGENG LI, WEI HU, SICHENG SU, and BINGYU WANG. "SIMULATION OF MUSCLE ACTIVATION WITH COUPLED NONLINEAR FE MODELS." Journal of Mechanics in Medicine and Biology 16, no. 06 (September 2016): 1650082. http://dx.doi.org/10.1142/s0219519416500822.
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Muscle activation plays an important role in head–neck dynamic response in vehicle accidents, especially in low speed impacts. The aim of the present study was to analyze the mechanical characteristics and dynamic stability of the muscle using coupled non-linear finite element model, which could be further applied for biomechanical study of head–neck system in car crash accidents. A rabbit tibialis anterior (TA) geometry model was developed. Two finite element models of TA were developed with coupled constitutive models. One coupled model was developed combining quasi-linear viscoelastic (QLV) elements and Hill type elements, and the other was developed combining hyperelastic rubber elements and Hill type elements, representing the passive behavior and active behavior, respectively. The models were validated via eccentric contractions tests under different strain rates published by Myers et al. Isometric Contraction and axial compression were also simulated via both models to evaluate the computational stability. The results showed that the coupled constitutive muscle models had a good biofidelity for the simulation of muscle activation. Both muscle models can fulfill the requirement of neck muscle system modeling for biomechanical study.
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Szent-Gyorgyi, C. "A bipartite operator interacts with a heat shock element to mediate early meiotic induction of Saccharomyces cerevisiae HSP82." Molecular and Cellular Biology 15, no. 12 (December 1995): 6754–69. http://dx.doi.org/10.1128/mcb.15.12.6754.
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Although key genetic regulators of early meiotic transcription in Saccharomyces cerevisiae have been well characterized, the activation of meiotic genes is still poorly understood in terms of cis-acting DNA elements and their associated factors. I report here that induction of HSP82 is regulated by the early meiotic IME1-IME2 transcriptional cascade. Vegetative repression and meiotic induction depend on interactions of the promoter-proximal heat shock element (HSE) with a nearby bipartite repression element, composed of the ubiquitous early meiotic motif, URS1 (upstream repression sequence 1), and a novel ancillary repression element. The ancillary repression element is required for efficient vegetative repression, is spatially separable from URS1, and continues to facilitate repression during sporulation. In contrast, URS1 also functions as a vegetative repression element but is converted early in meiosis into an HSE-dependent activation element. An early step in this transformation may be the antagonism of URS1-mediated repression by IME1. The HSE also nonspecifically supports a second major mode of meiotic activation that does not require URS1 but does require expression of IME2 and concurrent starvation. Interestingly, increased rather than decreased URS1-mediated vegetative transcription can be artificially achieved by introducing rare point mutations into URS1 or by deleting the UME6 gene. These lesions offer insight into mechanisms of URS-dependent repression and activation. Experiments suggest that URS1-bound factors functionally modulate heat shock factor during vegetative transcription and early meiotic induction but not during heat shock. The loss of repression and activation observed when the IME2 activation element, T4C, is substituted for the HSE suggests specific requirements for URS1-upstream activation sequence interactions.
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Hagan, Christy R., and Charles M. Rudin. "Mobile Genetic Element Activation and Genotoxic Cancer Therapy." American Journal of PharmacoGenomics 2, no. 1 (2002): 25–35. http://dx.doi.org/10.2165/00129785-200202010-00003.
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Barlow, Christy A., Arti Shukla, Brooke T. Mossman, and Karen M. Lounsbury. "Oxidant-Mediated cAMP Response Element Binding Protein Activation." American Journal of Respiratory Cell and Molecular Biology 34, no. 1 (January 2006): 7–14. http://dx.doi.org/10.1165/rcmb.2005-0153oc.
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Keuong, Yann Waye, Jan Halvor Nordlien, Sachiko Ono, and Kemal Nisancioglu. "Electrochemical Activation of Aluminum by Trace Element Lead." Journal of The Electrochemical Society 150, no. 11 (2003): B547. http://dx.doi.org/10.1149/1.1615996.
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Graver, Brit, Anne M. Pedersen, and Kemal Nisancioglu. "Anodic Activation of Aluminum by Trace Element Tin." ECS Transactions 16, no. 52 (December 18, 2019): 55–69. http://dx.doi.org/10.1149/1.3229955.
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Lavi, N., E. Neeman, and Y. Nir-El. "Neutron activation analysis for environmental trace element research." Journal of Radioanalytical and Nuclear Chemistry Articles 163, no. 2 (December 1992): 307–12. http://dx.doi.org/10.1007/bf02034804.
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Avino, Pasquale, Geraldo Capannesi, Francesco Lopez, and Alberto Rosada. "Determination of Interesting Toxicological Elements in PM2.5by Neutron and Photon Activation Analysis." Scientific World Journal 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/458793.
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Human activities introduce compounds increasing levels of many dangerous species for environment and population. In this way, trace elements in airborne particulate have a preeminent position due to toxic element presence affecting the biological systems. The main problem is the analytical determination of such species at ultratrace levels: a very specific methodology is necessary with regard to the accuracy and precision and contamination problems. Instrumental Neutron Activation Analysis and Instrumental Photon Activation Analysis assure these requirements. A retrospective element analysis in airborne particulate collected in the last 4 decades has been carried out for studying their trend. The samples were collected in urban location in order to determine only effects due to global aerosol circulation; semiannual samples have been used to characterize the summer/winter behavior of natural and artificial origin. The levels of natural origin element are higher than those in other countries owing to geological and meteorological factors peculiar to Central Italy. The levels of artificial elements are sometimes less than those in other countries, suggesting a less polluted general situation for Central Italy. However, for a few elements (e.g., Pb) the levels measured are only slight lower than those proposed as air ambient standard.
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Erclik, Mary S., and Jane Mitchell. "Activation of the insulin-like growth factor binding protein-5 promoter by parathyroid hormone in osteosarcoma cells requires activation of an activated protein-2 element." Journal of Molecular Endocrinology 34, no. 3 (June 2005): 713–22. http://dx.doi.org/10.1677/jme.1.01741.
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We have previously shown that parathyroid hormone (PTH) stimulates the expression of insulin-like growth factor binding protein-5 (IGFBP-5) transcript levels in the osteosarcoma cell-line, UMR106–01 cells. In the present study we examined the molecular basis for the PTH induction of IGFBP-5 mRNA in these cells. PTH had no effect on the half-life of the IGFBP-5 transcript but did stimulate the transactivation of the proximal 889 base pairs of the rat IGFBP 5′ flanking region in a luciferase fusion construct, suggesting that PTH stimulates transcript levels through transcriptional mechanisms. Progressive 5′ deletions to −59 base pairs of the proximal promoter region had no effect on PTH induction of transactivation, indicating that an element existed within the first −59 base pairs upstream of the transcription start site that was responsive to PTH. Within the −59 base pairs there are CCAAT/enhancer binding protein (C/EBP), E-box, nuclear factor-1 (NF-1) and activator protein-2 (AP-2) elements. Mutation of the C/EBP, E-box or NF-1 elements had no effect on the ability of PTH to induce the transactivation of the IGFBP-5 promoter. Mutation of the AP-2 element resulted in a 40% reduction of PTH-stimulated luciferase activity. When three tandem repeats of the AP-2 consensus sequence were fused to a luciferase reporter, PTH stimulated a 25% increase in reporter activity. Electrophoretic mobility shift assays using UMR106–01 cell nuclear extracts showed that PTH caused a prominent shifted band in a probe spanning the region containing all four elements. The shifted band was almost completely absent when the probe contained a mutated AP-2 element. These results suggest that the AP-2 element functions in the PTH induction of IGFBP-5 gene expression.
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Bylino, Oleg V., Airat N. Ibragimov, and Yulii V. Shidlovskii. "Evolution of Regulated Transcription." Cells 9, no. 7 (July 12, 2020): 1675. http://dx.doi.org/10.3390/cells9071675.
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The genomes of all organisms abound with various cis-regulatory elements, which control gene activity. Transcriptional enhancers are a key group of such elements in eukaryotes and are DNA regions that form physical contacts with gene promoters and precisely orchestrate gene expression programs. Here, we follow gradual evolution of this regulatory system and discuss its features in different organisms. In eubacteria, an enhancer-like element is often a single regulatory element, is usually proximal to the core promoter, and is occupied by one or a few activators. Activation of gene expression in archaea is accompanied by the recruitment of an activator to several enhancer-like sites in the upstream promoter region. In eukaryotes, activation of expression is accompanied by the recruitment of activators to multiple enhancers, which may be distant from the core promoter, and the activators act through coactivators. The role of the general DNA architecture in transcription control increases in evolution. As a whole, it can be seen that enhancers of multicellular eukaryotes evolved from the corresponding prototypic enhancer-like regulatory elements with the gradually increasing genome size of organisms.
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Maruyama, K., K. D. Schoor, and D. L. Hartl. "Identification of nucleotide substitutions necessary for trans-activation of mariner transposable elements in Drosophila: analysis of naturally occurring elements." Genetics 128, no. 4 (August 1, 1991): 777–84. http://dx.doi.org/10.1093/genetics/128.4.777.
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Abstract Six copies of the mariner element from the genomes of Drosophila mauritiana and Drosophila simulans were chosen at random for DNA sequencing and functional analysis and compared with the highly active element Mos1 and the inactive element peach. All elements were 1286 base pairs in length, but among them there were 18 nucleotide differences. As assayed in Drosophila melanogaster, three of the elements were apparently nonfunctional, two were marginally functional, and one had moderate activity that could be greatly increased depending on the position of the element in the genome. Both molecular (site-directed mutagenesis) and evolutionary (cladistic analysis) techniques were used to analyze the functional effects of nucleotide substitutions. The nucleotide sequence of the element is the primary determinant of function, though the activity level of elements is profoundly influenced by position effects. Cladistic analysis of the sequences has identified a T----A transversion at position 1203 (resulting in a Phe----Leu amino acid replacement in the putative transposase) as being primarily responsible for the low activity of the barely functional elements. Use of the sequences from the more distantly related species, Drosophila yakuba and Drosophila teissieri, as outside reference species, indicates that functional mariner elements are ancestral and argues against their origination by a novel mutation or by recombination among nonfunctional elements.
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Guertin, M., H. LaRue, D. Bernier, O. Wrange, M. Chevrette, M. C. Gingras, and L. Bélanger. "Enhancer and promoter elements directing activation and glucocorticoid repression of the alpha 1-fetoprotein gene in hepatocytes." Molecular and Cellular Biology 8, no. 4 (April 1988): 1398–407. http://dx.doi.org/10.1128/mcb.8.4.1398.
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Mutations were introduced in 7 kilobases of 5'-flanking rat alpha 1-fetoprotein (AFP) genomic DNA, linked to the chloramphenicol acetyltransferase gene. AFP promoter activity and its repression by a glucocorticoid hormone were assessed by stable and transient expression assays. Stable transfection assays were more sensitive and accurate than transient expression assays in a Morris 7777 rat hepatoma recipient (Hepa7.6), selected for its strong AFP repression by dexamethasone. The segment of DNA encompassing a hepatocyte-constitutive chromatin DNase I-hypersensitive site at -3.7 kilobases and a liver developmental stage-specific site at -2.5 kilobases contains interacting enhancer elements sufficient for high AFP promoter activity in Hepa7.6 or HepG2 cells. Deletions and point mutations define an upstream promoter domain of AFP gene activation, operating with at least three distinct promoter-activating elements, PEI at -65 base pairs, PEII at -120 base pairs, and DE at -160 base pairs. PEI and PEII share homologies with albumin promoter sequences, PEII is a near-consensus nuclear factor I recognition sequence, and DE overlaps a glucocorticoid receptor recognition sequence. An element conferring glucocorticoid repression of AFP gene activity is located in the upstream AFP promoter domain. Receptor-binding assays indicate that this element is the glucocorticoid receptor recognition sequence which overlaps with promoter-activating element DE.
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Guertin, M., H. LaRue, D. Bernier, O. Wrange, M. Chevrette, M. C. Gingras, and L. Bélanger. "Enhancer and promoter elements directing activation and glucocorticoid repression of the alpha 1-fetoprotein gene in hepatocytes." Molecular and Cellular Biology 8, no. 4 (April 1988): 1398–407. http://dx.doi.org/10.1128/mcb.8.4.1398-1407.1988.
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Mutations were introduced in 7 kilobases of 5'-flanking rat alpha 1-fetoprotein (AFP) genomic DNA, linked to the chloramphenicol acetyltransferase gene. AFP promoter activity and its repression by a glucocorticoid hormone were assessed by stable and transient expression assays. Stable transfection assays were more sensitive and accurate than transient expression assays in a Morris 7777 rat hepatoma recipient (Hepa7.6), selected for its strong AFP repression by dexamethasone. The segment of DNA encompassing a hepatocyte-constitutive chromatin DNase I-hypersensitive site at -3.7 kilobases and a liver developmental stage-specific site at -2.5 kilobases contains interacting enhancer elements sufficient for high AFP promoter activity in Hepa7.6 or HepG2 cells. Deletions and point mutations define an upstream promoter domain of AFP gene activation, operating with at least three distinct promoter-activating elements, PEI at -65 base pairs, PEII at -120 base pairs, and DE at -160 base pairs. PEI and PEII share homologies with albumin promoter sequences, PEII is a near-consensus nuclear factor I recognition sequence, and DE overlaps a glucocorticoid receptor recognition sequence. An element conferring glucocorticoid repression of AFP gene activity is located in the upstream AFP promoter domain. Receptor-binding assays indicate that this element is the glucocorticoid receptor recognition sequence which overlaps with promoter-activating element DE.
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Cheriyath, Venugopalan, Carl D. Novina, and Ananda L. Roy. "TFII-I Regulates Vβ Promoter Activity through an Initiator Element." Molecular and Cellular Biology 18, no. 8 (August 1, 1998): 4444–54. http://dx.doi.org/10.1128/mcb.18.8.4444.
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ABSTRACT In our effort to understand the transcriptional regulation of naturally occurring TATA-less but initiator (Inr)-containing genes, we have employed the murine T-cell receptor Vβ 5.2 promoter as a model. Here we show by transient-transfection assays that the Inr binding transcription factor TFII-I is required for efficient expression of the Vβ promoter in vivo. Mutations in the Inr element that reduced binding of TFII-I also abolished the Vβ promoter activity by ectopic TFII-I. We further biochemically identified a protease-resistant N-terminal DNA binding fragment of TFII-I, p70. When ectopically expressed, recombinant p70 bound to the Vβ Inr element with a specificity similar to that of wild-type TFII-I. More importantly, p70, which lacks independent activation functions, behaved as a dominant negative mutant that inhibited Inr-specific function of wild-type TFII-I. However, the activation functions of p70 were restored when fused to the heterologous activation domain of the yeast activator protein GAL4. Taken together, these data suggest that TFII-I functions in vivo require an intact Inr element and that the Inr-specific transcriptional functions of TFII-I are solely dictated by its N-terminal DNA binding domain and do not require its own C-terminal activation domain.
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Hendy, Oliver, John Campbell, Jocelyn D. Weissman, Daniel R. Larson, and Dinah S. Singer. "Differential context-specific impact of individual core promoter elements on transcriptional dynamics." Molecular Biology of the Cell 28, no. 23 (November 7, 2017): 3360–70. http://dx.doi.org/10.1091/mbc.e17-06-0408.
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Eukaryotic transcription occurs in bursts that vary in size and frequency, but the contribution of individual core promoter elements to transcriptional bursting is not known. Here we analyze the relative contributions to bursting of the individual core promoter elements—CCAAT, TATAA-like, Sp1BS, and Inr—of an MHC class I gene in primary B-cells during both basal and activated transcription. The TATAA-like, Sp1BS, and Inr elements all function as negative regulators of transcription, and each was found to contribute differentially to the overall bursting pattern of the promoter during basal transcription. Whereas the Sp1BS element regulates burst size, the Inr element regulates burst frequency. The TATAA-like element contributes to both. Surprisingly, each element has a distinct role in bursting during transcriptional activation by γ-interferon. The CCAAT element does not contribute significantly to the constitutive transcriptional dynamics of primary B-cells, but modulates both burst size and frequency in response to γ-interferon activation. The ability of core promoter elements to modulate transcriptional bursting individually allows combinatorial fine-tuning of the level of MHC class I gene expression in response to intrinsic and extrinsic signals.
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Xu, Weiling, Suzy A. A. Comhair, Shuo Zheng, Shan C. Chu, Joanna Marks-Konczalik, Joel Moss, S. Jaharul Haque, and Serpil C. Erzurum. "STAT-1 and c-Fos interaction in nitric oxide synthase-2 gene activation." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 1 (July 2003): L137—L148. http://dx.doi.org/10.1152/ajplung.00441.2002.
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Interferon-γ (IFN-γ) is required for induction of the human nitric oxide synthase-2 ( NOS2) gene in lung epithelium. Although the human NOS2 promoter region contains many cytokine-responsive elements, the molecular basis of induction is only partially understood. Here, the major cis-regulatory elements that control IFN-γ-inducible NOS2 gene transcription in human lung epithelial cells are identified as composite response elements that bind signal transducer and activator of transcription 1 (STAT-1) and activator protein 1 (AP-1), which is comprised of c-Fos, Fra-2, c-Jun, and JunD. Notably, IFN-γ activation of the human NOS2 promoter is shown to require functional AP-1 regulatory region(s), suggesting a role for AP-1 activation/binding in the IFN-γ induction of genes. We show that c-Fos interacts with STAT-1 after IFN-γ activation and the c-Fos/STAT-1 complex binds to the γ-activated site (GAS) element in close proximity to AP-1 sites located at 4.9 kb upstream of the transcription start site. Taken together, our findings support a model in which a physical interaction between c-Fos and STAT-1 participates in NOS2 gene transcriptional activation.
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Susperregui, Antonio R. G., Cristina Gamell, Edgardo Rodríguez-Carballo, Maria José Ortuño, Ramon Bartrons, José Luis Rosa, and Francesc Ventura. "Noncanonical BMP Signaling Regulates Cyclooxygenase-2 Transcription." Molecular Endocrinology 25, no. 6 (June 1, 2011): 1006–17. http://dx.doi.org/10.1210/me.2010-0515.
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Abstract Activation of p38 MAPK has been shown to be relevant for a number of bone morphogenetic protein (BMP) physiological effects. We report here the involvement of noncanonical phosphorylated mothers against decapentaplegic (Smad) signaling in the transcriptional induction of Cox2 (Ptgs2) by BMP-2 in mesenchymal cells and organotypic calvarial cultures. We demonstrate that different regulatory elements are required for regulation of Cox2 expression by BMP-2: Runt-related transcription factor-2 and cAMP response element sites are essential, whereas a GC-rich Smad binding element is important for full responsiveness. Efficient transcriptional activation requires cooperation between transcription factors because mutation of any element results in a strong decrease of BMP-2 responsiveness. BMP-2 activation of p38 leads to increased recruitment of activating transcription factor-2, Runx2, Smad, and coactivators such as p300 at the responsive sites in the Cox2 proximal promoter. We demonstrate, by either pharmacological or genetic analysis, that maximal BMP-2 effects on Cox2 and JunB expression require the function of p38 and its downstream effector mitogen/stress-activated kinase 1. Altogether our results strongly suggest that cooperative effects between canonical and noncanonical BMP signaling allow the fine-tuning of BMP transcriptional responses on specific target genes.
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Chen, Hong-Chi, and Edward P. Feener. "MEK1,2 response element mediates angiotensin II—stimulated plasminogen activator inhibitor-1 promoter activation." Blood 103, no. 7 (April 1, 2004): 2636–44. http://dx.doi.org/10.1182/blood-2003-05-1737.
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Abstract The MEK1,2 (MAPK/ERK kinase 1 and 2) pathway mediates the up-regulation of plasminogen activator inhibitor-1 (PAI-1) expression in vascular smooth muscle cells by a variety of hormones, including angiotensin II. Transfection of constitutively active MEKK-1, an upstream activator of the mitogen-activated protein (MAP) kinase pathways, was used to isolate an enhancer element located between -89 and -50 bp in PAI-1 promoter that was activated by MEKK-1 and selectively blocked by the MEK1,2 inhibitor PD98059. Mutational analysis revealed that the MEKK-1 response element (MRE) contained 2 cis-acting Sp1- and AP-1—like sequences, located between -75 to -70 and -63 to -52 bp, respectively. Overexpression of Sp1 enhanced MEKK-1—induced MRE promoter activity and a dominant-negative c-Fos blocked this Sp1 response. The combination of Sp1 and c-Jun or c-Fos was required to activate this MRE. Angiotensin II (Ang II) stimulation increased c-Fos, c-Jun, and Sp1 binding to the MRE by 100-, 4.9-, and 1.9-fold, respectively, and these responses were inhibited by PD98059 and AT1 receptor antagonist candesartan. Intravenous Ang II infusion in rats increased aortic c-Fos binding to the MRE. This MRE sequence mediated a 4-fold increase of MEK1,2-dependent PAI-1/luciferase mRNA expression by angiotensin II stimulation. This report identifies the MEK1,2 response element that mediates angiotensin II—stimulated PAI-1 promoter activation and shows that activation of this element requires Sp1 and AP-1 co-activation.
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Melnikova, L. S., Е. A. Pomerantseva, V. V. Molodina, and P. G. Georgiev. "Mapping the D.melanogaster En1A Enhancer Modules Responsible for Transcription Activation and LongDistance Enhancer-Promoter Interactions." Acta Naturae 9, no. 1 (March 15, 2017): 99–104. http://dx.doi.org/10.32607/20758251-2017-9-1-99-104.
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The structure of the new enhancer En1A of the 1A region of the X chromosome of D. melanogaster was investigated. Two distinct regulatory elements were found. The first element is responsible for transcription activation, and the second element provides specific interaction with the promoter of the yellow gene. The findings support the hypothesis of a modular structure for enhancers, including certain sequences that bind transcription activators and special communication elements providing long-distance enhancer-promoter interaction.
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Barbu, Mihai Constantin Răzvan, George Bogdan Burcea, Dragoş Laurenţiu Diaconescu, Marius Cătălin Popescu, Leonardo Daniel Păsărin, and Paula Apostu. "The Role of Social Media on Sponsorship Activation." Studia Universitatis Babeş-Bolyai Educatio Artis Gymnasticae 66, no. 1 (March 30, 2021): 111–26. http://dx.doi.org/10.24193/subbeag.66(1).11.
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"ABSTRACT. Globally, sponsorship has grown impressive over the last 30 years, receiving an increased importance in the communication mix of companies. Sport organizations have understood the importance and the role sponsorship it plays for the financial support they need. Sponsorship is the material support of an event, activity or organization by an unaffiliated partner. It is a good way to increase brand awareness, which helps to generate consumer preferences and promote brand loyalty and also improves the brand image. Brands play an important role in the development of companies because they bring a number of benefits to them. The paper ""Innovation’s impact on sponsorship activation"" aims to present a series of theoretical elements of activating sponsorship, as well as the element of innovation in this process, an element represented by the social media presence in our lives and in the last part of the paper is presented a study based on a survey on our topic."
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Wesoly, Joanna, Zofia Szweykowska-Kulinska, and Hans A. R. Bluyssen. "STAT activation and differential complex formation dictate selectivity of interferon responses." Acta Biochimica Polonica 54, no. 1 (March 9, 2007): 27–38. http://dx.doi.org/10.18388/abp.2007_3266.
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Interferons (IFNs) induce gene expression by phosphorylating latent transcription factors belonging to the signal transducer and activator of transcription (STAT) family, mediated by janus kinases (Jaks). STAT dimers directly activate genes containing the IFNgamma activation site (GAS) DNA element, with different STAT proteins displaying slightly different intrinsic DNA binding specificities. The combinatorial association of STATs with the additional DNA binding adaptor protein interferon regulatory factor (IRF)9 expands the range of enhancer elements that can be targeted by the JAK-STAT pathway to interferon-stimulated response element (ISRE) and IRF response element (IRE). Based on the amino-acid sequence similarity within the IRF family and functional overlap with the STAT family, in this paper we hypothesize that other IRF members could serve as adapter proteins for the STATs during IFN responses to redirect them to subsets of ISRE, GAS and/or IRE-containing IFN-stimulated genes (ISGs). In addition, the fact that STAT2 homodimers are not capable of binding consensus GAS sites leaves the possibility for a novel type of DNA-binding site bound by STAT2 homodimers and potentially other STAT complexes.
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LUCIAKOVA, Katarina, Zdenek HODNY, Peter BARATH, and B. Dean NELSON. "In vivo mapping of the human adenine nucleotide translocator-2 (ANT2) promoter provides support for regulation by a pair of proximal Sp1-activating sites and an upstream silencer element." Biochemical Journal 352, no. 2 (November 24, 2000): 519–23. http://dx.doi.org/10.1042/bj3520519.
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Regulatory factors bound to the human adenine nucleotide translocator-2 (ANT2) promoter have been mapped in HeLa cells by in vivo DNase I protection and ligation-mediated PCR amplification. Protein binding was detected at only three sites within the extended promoter region (to nt -703). One, starting at nt -61 and covering the TATA box and transcription start, most probably represents occupation by the transcription-initiation machinery. A repeated Sp1 element determined by in vitro studies to be the major activation element for the promoter was also protected in vivo on nucleotides responsible for strong binding to the zinc fingers. Occupation of two additional upstream Sp1 elements was not observed. The third site occupied in vivo was identified previously by in vitro studies as a unique silencer element. Treatment of cells with trichostatin A to induce hyperacetylation released the silencer-binding protein after 1h, but had no effect on the Sp1-activating elements. Prolonged treatment (24h) displaced Sp1 from the activating elements. These findings confirm and extend in vitro studies indicating that regulation of the ANT2 promoter is most probably exerted through a single pair of proximal Sp1-activating elements and an upstream silencer, and that chromatin organization plays a role in the interaction between the two.
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Lee, M., and K. Struhl. "Mutations on the DNA-binding surface of TATA-binding protein can specifically impair the response to acidic activators in vivo." Molecular and Cellular Biology 15, no. 10 (October 1995): 5461–69. http://dx.doi.org/10.1128/mcb.15.10.5461.
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The TATA-binding protein (TBP) contains a concave surface that interacts specifically with TATA promoter elements and a convex surface that mediates protein-protein interactions with general and gene-specific transcription factors. Biochemical experiments suggest that interactions between activator proteins and TBP are important in stimulating transcription by the RNA polymerase II machinery. To gain insight into the role of TBP in mediating transcriptional activation in vivo, we implemented a genetic strategy in Saccharomyces cerevisiae that involved the use of a TBP derivative with altered specificity for TATA elements. By genetically screening a set of TBP mutant libraries that were biased to the convex surface that mediates protein-protein interactions, we identified TBP derivatives that are impaired in the response to three acidic activators (Gcn4, Gal4, and Ace1) but appear normal for constitutive polymerase II transcription. A genetic complementation assay indicates that the activation-defective phenotypes reflect specific functional properties of the TBP derivatives rather than an indirect effect on transcription. Surprisingly, three of the four activation-defective mutants affect residues that directly contact DNA. Moreover, all four mutants are defective for TATA element binding, but they interact normally with an acidic activation domain and TFIIB. In addition, we show that a subset of TBP derivatives with mutations on the DNA-binding surface of TBP are also compromised in their responses to acidic activators in vivo. These observations suggest that interactions at the TBP-TATA element interface can specifically affect the response to acidic activator proteins in vivo.
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La Vista-Picard, N., P. D. Hobbs, M. Pfahl, M. I. Dawson, and M. Pfahl. "The receptor-DNA complex determines the retinoid response: a mechanism for the diversification of the ligand signal." Molecular and Cellular Biology 16, no. 8 (August 1996): 4137–46. http://dx.doi.org/10.1128/mcb.16.8.4137.
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To obtain insights into the principles governing the complex biological responses to retinoids, we have analyzed the ligand sensitivities of various retinoid receptor-DNA complexes. We find that different retinoid receptor heterodimers show distinct activation patterns with various response elements while a given heterodimer can be activated at different retinoic acid concentrations on different response elements. In vitro binding experiments suggest that the same retinoic acid receptor-retinoid X receptor (RAR-RXR) heterodimer can have different ligand affinities, depending on the response element it is bound to. The differential responses of a particular receptor heterodimer with various retinoic acid responsive elements can be enhanced through the use of conformationally restricted retinoids. RAR- and RXR-selective retinoids can also synergistically activate the receptor heterodimers, indicating that both partners in the heterodimer can contribute to ligand-induced transcriptional activation. However, the relative influence of the RAR or RXR partner is specific for each response element. Together, our data demonstrate that it is the receptor-DNA complex and not the receptor alone that determines the ligand response. This flexibility allows for a highly pleiotropic retinoid response. Furthermore, conformationally restricted retinoids can accentuate the differential responses and exhibit a certain degree of gene selectivity by differentially activating the RAR or RXR component in the context of a given response element.
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Stoflet, E. S., L. J. Schmidt, P. K. Elder, G. M. Korf, D. N. Foster, A. R. Strauch, and M. J. Getz. "Activation of a muscle-specific actin gene promoter in serum-stimulated fibroblasts." Molecular Biology of the Cell 3, no. 10 (October 1992): 1073–83. http://dx.doi.org/10.1091/mbc.3.10.1073.
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Treatment of AKR-2B mouse fibroblasts with serum growth factors or inhibitors of protein synthesis, such as cycloheximide, results in a stimulation of cytoskeletal beta-actin transcription but has no effect on transcription of muscle-specific isotypes, such as the vascular smooth muscle (VSM) alpha-actin gene. Deletion mapping and site-specific mutagenesis studies demonstrated that a single "CArG" element of the general form CC(A/T)6GG was necessary and possibly sufficient to impart serum and cycloheximide-inducibility to the beta-actin promoter. Although the VSM alpha-actin promoter exhibits at least three similar sequence elements, it remained refractory to serum and cycloheximide induction. However, deletion of a 33 base pair sequence between -191 and -224 relative to the transcription start site resulted in the transcriptional activation of this muscle-specific promoter in rapidly growing or serum-stimulated fibroblasts. Although the activity of this truncated promoter was potentiated by cycloheximide in a manner indistinguishable from that of the beta-actin promoter, this was dependent on a more complex array of interacting elements. These included at least one CArG box and a putative upstream activating element closely associated with the -191 to -224 inhibitory sequences. These results demonstrate that the expression of a muscle-specific actin gene in fibroblasts is suppressed by a cis-acting negative control element and that in the absence of this element, the promoter is responsive to growth factor-induced signal transduction pathways.
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HARRIS, Laura R., Olli-Pekka KAMARAINEN, Minna SEVAKIVI, Gwen C. MILLER, James W. CLARKE, Jennifer L. POTTER, and Laura C. BRIDGEWATER. "A novel retinoic acid-response element requires an enhancer element mediator for transcriptional activation." Biochemical Journal 383, no. 1 (September 24, 2004): 37–43. http://dx.doi.org/10.1042/bj20040715.
Full textAbstract:
The Col11a2 gene codes for α2(XI), a subunit of type XI collagen that is a critical component of the cartilage extracellular matrix. The 5′ regulatory region of Col11a2 was subjected to deletional analysis to detect any regulatory element in addition to the two known chondrocyte-specific enhancer elements B/C and D/E. Deletion of the region from −342 to −242 bp reduced transcriptional activity to less than 50% of wild-type, but the sequence showed no independent ability to increase transcription from a minimal promoter. When cloned downstream of the D/E enhancer, however, a subsection of the sequence nearly doubled transcriptional activity and produced an additional 3-fold activation in response to RA (retinoic acid). A 6-bp direct repeat, separated by 4 bp (a DR-4 element) near the 5′-end of this region, was found to be essential for its activity, and was further shown to bind the RA X receptor β in electrophoretic mobility-shift assays. The present study has revealed a novel RA-response element in Col11a2 that does not interact directly with the promoter, but instead requires the D/E enhancer to mediate transcriptional activation. Proteins bound at the enhancer, therefore, would be expected to affect the transcriptional response to RA. Such a system of regulation, particularly if found to be operating in other cartilage genes, could explain the conflicting responses RA produces in chondrocytes under different experimental conditions.