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Articoli di riviste sul tema "Transcriptional interference"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 maggio 2024

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1

O’Callaghan, Chris, Da Lin, and Thomas K. Hiron. "Intragenic transcriptional interference regulates the human immune ligand MICA." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 109.23. http://dx.doi.org/10.4049/jimmunol.200.supp.109.23.

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Abstract Regulation of MICA expression is incompletely understood, but human MICA can be upregulated in cancer cells, virus-infected cells and rapidly proliferating cells. Binding of MICA to the activating NKG2D receptor on cytotoxic immune cells promotes elimination of the cell expressing MICA. We noted that MICA has tandem promoters that drive overlapping forward transcription. We show that the MICA gene contains a conserved upstream promoter that expresses a non coding transcript. Transcription from the upstream promoter represses transcription from the standard downstream MICA promoter in

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2

Fang, Zhiming, Zhongming Zhao, Valsamma Eapen, and Raymond A. Clarke. "siRNA Mediate RNA Interference Concordant with Early On-Target Transient Transcriptional Interference." Genes 12, no. 8 (August 23, 2021): 1290. http://dx.doi.org/10.3390/genes12081290.

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Exogenous siRNAs are commonly used to regulate endogenous gene expression levels for gene function analysis, genotype–phenotype association studies and for gene therapy. Exogenous siRNAs can target mRNAs within the cytosol as well as nascent RNA transcripts within the nucleus, thus complicating siRNA targeting specificity. To highlight challenges in achieving siRNA target specificity, we targeted an overlapping gene set that we found associated with a familial form of multiple synostosis syndrome type 4 (SYSN4). In the affected family, we found that a previously unknown non-coding gene TOSPEAK

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3

Ingelbrecht, I., P. Breyne, K. Vancompernolle, A. Jacobs, M. Van Montagu, and A. Depicker. "Transcriptional interference in transgenic plants." Gene 109, no. 2 (December 1991): 239–42. http://dx.doi.org/10.1016/0378-1119(91)90614-h.

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4

SHEARWIN, K., B. CALLEN, and J. EGAN. "Transcriptional interference – a crash course." Trends in Genetics 21, no. 6 (June 2005): 339–45. http://dx.doi.org/10.1016/j.tig.2005.04.009.

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5

Hu, Xiao, Susan Eszterhas, Nicolas Pallazzi, Eric E. Bouhassira, Jennifer Fields, Osamu Tanabe, Scott A. Gerber та ін. "Transcriptional interference among the murine β-like globin genes". Blood 109, № 5 (31 жовтня 2006): 2210–16. http://dx.doi.org/10.1182/blood-2006-06-029868.

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Abstract Mammalian β-globin loci contain multiple genes that are activated at different developmental stages. Studies have suggested that the transcription of one gene in a locus can influence the expression of the other locus genes. The prevalent model to explain this transcriptional interference is that all potentially active genes compete for locus control region (LCR) activity. To investigate the influence of transcription by the murine embryonic genes on transcription of the other β-like genes, we generated mice with deletions of the promoter regions of Ey and βh1 and measured transcripti

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Palmer, Adam C., J. Barry Egan, and Keith E. Shearwin. "Transcriptional interference by RNA polymerase pausing and dislodgement of transcription factors." Transcription 2, no. 1 (January 2011): 9–14. http://dx.doi.org/10.4161/trns.2.1.13511.

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7

Ard, Ryan, and Robin C. Allshire. "Transcription-coupled changes to chromatin underpin gene silencing by transcriptional interference." Nucleic Acids Research 44, no. 22 (September 8, 2016): 10619–30. http://dx.doi.org/10.1093/nar/gkw801.

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8

Chan, H., S. Hartung, and M. Breindl. "Retrovirus-induced interference with collagen I gene expression in Mov13 fibroblasts is maintained in the absence of DNA methylation." Molecular and Cellular Biology 11, no. 1 (January 1991): 47–54. http://dx.doi.org/10.1128/mcb.11.1.47-54.1991.

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We have studied the role of DNA methylation in repression of the murine alpha 1 type I collagen (COL1A1) gene in Mov13 fibroblasts. In Mov13 mice, a retroviral provirus has inserted into the first intron of the COL1A1 gene and blocks its expression at the level of transcriptional initiation. We found that regulatory sequences in the COL1A1 promoter region that are involved in the tissue-specific regulation of the gene are unmethylated in collagen-expressing wild-type fibroblasts and methylated in Mov13 fibroblasts, confirming and extending earlier observations. To directly assess the role of D

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9

Chan, H., S. Hartung, and M. Breindl. "Retrovirus-induced interference with collagen I gene expression in Mov13 fibroblasts is maintained in the absence of DNA methylation." Molecular and Cellular Biology 11, no. 1 (January 1991): 47–54. http://dx.doi.org/10.1128/mcb.11.1.47.

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We have studied the role of DNA methylation in repression of the murine alpha 1 type I collagen (COL1A1) gene in Mov13 fibroblasts. In Mov13 mice, a retroviral provirus has inserted into the first intron of the COL1A1 gene and blocks its expression at the level of transcriptional initiation. We found that regulatory sequences in the COL1A1 promoter region that are involved in the tissue-specific regulation of the gene are unmethylated in collagen-expressing wild-type fibroblasts and methylated in Mov13 fibroblasts, confirming and extending earlier observations. To directly assess the role of D

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10

Jorgensen, Victoria, Jingxun Chen, Helen Vander Wende, Devon E. Harris, Alicia McCarthy, Shane Breznak, Siu Wah Wong-Deyrup, et al. "Tunable Transcriptional Interference at the Endogenous Alcohol Dehydrogenase Gene Locus in Drosophila melanogaster." G3: Genes|Genomes|Genetics 10, no. 5 (March 25, 2020): 1575–83. http://dx.doi.org/10.1534/g3.119.400937.

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Neighboring sequences of a gene can influence its expression. In the phenomenon known as transcriptional interference, transcription at one region in the genome can repress transcription at a nearby region in cis. Transcriptional interference occurs at a number of eukaryotic loci, including the alcohol dehydrogenase (Adh) gene in Drosophila melanogaster. Adh is regulated by two promoters, which are distinct in their developmental timing of activation. It has been shown using transgene insertion that when the promoter distal from the Adh start codon is deleted, transcription from the proximal p

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11

Fogagnolo, Carolinne T., Daniela S. Mizobuti, and Marcio C. Bajgelman. "Abstract A010: Assay development to assess the efficiency and stability of candidate molecules for transcriptional gene silencing of FOXP3, using a human tumor-derived cell line." Cancer Immunology Research 11, no. 12_Supplement (December 1, 2023): A010. http://dx.doi.org/10.1158/2326-6074.tumimm23-a010.

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Abstract Regulatory T cells play an important role to modulate the balance between immunotolerance and immunosurveillance. These cells have the property of inhibiting effector lymphocytes and may antagonize antitumor immunity. Regulatory T cells are originated in the thymus, or even converted from peripheral lymphocytes by factors produced in the tumor microenvironment. Clinical data suggests that regulatory T cell infiltration correlates with poor prognosis in the treatment of solid tumors. The FOXP3 transcription factor is considered a master key to control the phenotype of regulatory T cell

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12

Karin, M., and L. Chang. "AP-1--glucocorticoid receptor crosstalk taken to a higher level." Journal of Endocrinology 169, no. 3 (June 1, 2001): 447–51. http://dx.doi.org/10.1677/joe.0.1690447.

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More than a decade ago our view of gene regulation by glucocorticoids (GC) and other steroid hormones underwent a dramatic change with the discovery of negative crosstalk (transcriptional interference) between the GC receptor (GCR) and transcription factor AP-1 (Jun:Fos). It was initially observed that induction of the collagenase type 1 gene, which is mediated through activation of AP-1 by growth factors and inflammatory cytokines, is repressed by GC. This repression was attributed to mutual negative interactions between AP-1 and GCR. Although the exact molecular mechanism underlying this par

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13

Buetti‐Dinh, Antoine, Rosemarie Ungricht, János Z. Kelemen, Chetak Shetty, Prasuna Ratna, and Attila Becskei. "Control and signal processing by transcriptional interference." Molecular Systems Biology 5, no. 1 (January 2009): 300. http://dx.doi.org/10.1038/msb.2009.61.

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14

Saatcioglu, F., P. Bartunek, T. Deng, M. Zenke, and M. Karin. "A conserved C-terminal sequence that is deleted in v-ErbA is essential for the biological activities of c-ErbA (the thyroid hormone receptor)." Molecular and Cellular Biology 13, no. 6 (June 1993): 3675–85. http://dx.doi.org/10.1128/mcb.13.6.3675-3685.1993.

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The thyroid hormone (T3) receptor type alpha, the c-ErbA alpha proto-oncoprotein, stimulates transcription of T3-dependent promoters, interferes with AP-1 activity, and induces erythroid differentiation in a ligand-dependent manner. The v-ErbA oncoprotein does not bind hormone and has lost all of these activities. Using c-ErbA/v-ErbA chimeras, we found that a deletion of 9 amino acids, conserved among many members of the nuclear receptor superfamily, which are located at the extreme carboxy terminus of c-ErbA alpha is responsible for loss of both transactivation and transcriptional interferenc

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Saatcioglu, F., P. Bartunek, T. Deng, M. Zenke, and M. Karin. "A conserved C-terminal sequence that is deleted in v-ErbA is essential for the biological activities of c-ErbA (the thyroid hormone receptor)." Molecular and Cellular Biology 13, no. 6 (June 1993): 3675–85. http://dx.doi.org/10.1128/mcb.13.6.3675.

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The thyroid hormone (T3) receptor type alpha, the c-ErbA alpha proto-oncoprotein, stimulates transcription of T3-dependent promoters, interferes with AP-1 activity, and induces erythroid differentiation in a ligand-dependent manner. The v-ErbA oncoprotein does not bind hormone and has lost all of these activities. Using c-ErbA/v-ErbA chimeras, we found that a deletion of 9 amino acids, conserved among many members of the nuclear receptor superfamily, which are located at the extreme carboxy terminus of c-ErbA alpha is responsible for loss of both transactivation and transcriptional interferenc

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16

Hao, Nan, Adam C. Palmer, Ian B. Dodd, and Keith E. Shearwin. "Directing traffic on DNA—How transcription factors relieve or induce transcriptional interference." Transcription 8, no. 2 (March 1, 2017): 120–25. http://dx.doi.org/10.1080/21541264.2017.1285851.

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17

Schwer, Beate, Angad Garg, Agata Jacewicz, and Stewart Shuman. "Genetic screen for suppression of transcriptional interference identifies a gain-of-function mutation in Pol2 termination factor Seb1." Proceedings of the National Academy of Sciences 118, no. 33 (August 13, 2021): e2108105118. http://dx.doi.org/10.1073/pnas.2108105118.

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The system of long noncoding RNA (lncRNA)–mediated transcriptional interference that represses fission yeast phosphate homoeostasis gene pho1 provides a sensitive readout of genetic influences on cotranscriptional 3′-processing and termination and a tool for discovery of regulators of this phase of the Pol2 transcription cycle. Here, we conducted a genetic screen for relief of transcriptional interference that unveiled a mechanism by which Pol2 termination is enhanced via a gain-of-function mutation, G476S, in the RNA-binding domain of an essential termination factor, Seb1. The genetic and phy

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18

Snyder, M., R. J. Sapolsky, and R. W. Davis. "Transcription interferes with elements important for chromosome maintenance in Saccharomyces cerevisiae." Molecular and Cellular Biology 8, no. 5 (May 1988): 2184–94. http://dx.doi.org/10.1128/mcb.8.5.2184-2194.1988.

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Transcription directed into a Saccharomyces cerevisiae autonomously replicating sequence (ARS) causes high-frequency loss of minichromosomes. Conditionally stable artificial yeast chromosomes were constructed that contain an inducible GAL promoter upstream of ARS1. Under growth conditions in which the promoter was inactive, these chromosomes were mitotically stable; however, when the GAL promoter was induced, the chromosomes became extremely unstable as a result of transcriptional impairment of ARS function. This interference by the GAL promoter occurred only in cis but can occur from either s

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Snyder, M., R. J. Sapolsky, and R. W. Davis. "Transcription interferes with elements important for chromosome maintenance in Saccharomyces cerevisiae." Molecular and Cellular Biology 8, no. 5 (May 1988): 2184–94. http://dx.doi.org/10.1128/mcb.8.5.2184.

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Transcription directed into a Saccharomyces cerevisiae autonomously replicating sequence (ARS) causes high-frequency loss of minichromosomes. Conditionally stable artificial yeast chromosomes were constructed that contain an inducible GAL promoter upstream of ARS1. Under growth conditions in which the promoter was inactive, these chromosomes were mitotically stable; however, when the GAL promoter was induced, the chromosomes became extremely unstable as a result of transcriptional impairment of ARS function. This interference by the GAL promoter occurred only in cis but can occur from either s

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Tavernarakis, Nektarios, and George Thireos. "Transcriptional interference caused by GCN4 overexpression reveals multiple interactions mediating transcriptional activation." Molecular and General Genetics MGG 247, no. 5 (September 1995): 571–78. http://dx.doi.org/10.1007/bf00290348.

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21

Schweizer, Sophie, Christoph Harms, Heike Lerch, Jennifer Flynn, Jochen Hecht, Ferah Yildirim, Andreas Meisel, and Stefanie Märschenz. "Inhibition of Histone Methyltransferases SUV39H1 and G9a Leads to Neuroprotection in an in vitro Model of Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 35, no. 10 (May 13, 2015): 1640–47. http://dx.doi.org/10.1038/jcbfm.2015.99.

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Cerebral ischemia induces a complex transcriptional response with global changes in gene expression. It is essentially regulated by transcription factors as well as epigenetic players. While it is well known that the inhibition of transcriptionally repressive histone deacetylases leads to neuroprotection, the role of histone methyltransferases in the postischemic transcriptional response remains elusive. We investigated the effects of inhibition of the repressive H3K9 histone methyltransferases SUV39H1 and G9a on neuronal survival, H3K9 promoter signatures and gene expression. Their inhibition

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22

Mortlock, Douglas P., Zhi-Ming Fang, Kelly J. Chandler, Yue Hou, Lissett R. Bickford, Charles E. de Bock, Valsamma Eapen, and Raymond A. Clarke. "Transcriptional Interference Regulates the Evolutionary Development of Speech." Genes 13, no. 7 (July 4, 2022): 1195. http://dx.doi.org/10.3390/genes13071195.

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The human capacity to speak is fundamental to our advanced intellectual, technological and social development. Yet so very little is known regarding the evolutionary genetics of speech or its relationship with the broader aspects of evolutionary development in primates. In this study, we describe a large family with evolutionary retrograde development of the larynx and wrist. The family presented with severe speech impairment and incremental retrograde elongations of the pisiform in the wrist that limited wrist rotation from 180° to 90° as in primitive primates. To our surprise, we found that

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23

Racanelli, Alexandra C., Fiona B. Turner, Lin-Ying Xie, Shirley M. Taylor, and Richard G. Moran. "A Mouse Gene That Coordinates Epigenetic Controls and Transcriptional Interference To Achieve Tissue-Specific Expression." Molecular and Cellular Biology 28, no. 2 (November 12, 2007): 836–48. http://dx.doi.org/10.1128/mcb.01088-07.

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ABSTRACT The mouse fpgs gene uses two distantly placed promoters to produce functionally distinct isozymes in a tissue-specific pattern. We queried how the P1 and P2 promoters were differentially controlled. DNA methylation of the CpG-sparse P1 promoter occurred only in tissues not initiating transcription at this site. The P2 promoter, which was embedded in a CpG island, appeared open to transcription in all tissues by several criteria, including lack of DNA methylation, yet was used only in dividing tissues. The patterns of histone modifications over the two promoters were very different: ov

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O’Connor, Nolan J., Antoni E. Bordoy, and Anushree Chatterjee. "Engineering Transcriptional Interference through RNA Polymerase Processivity Control." ACS Synthetic Biology 10, no. 4 (March 12, 2021): 737–48. http://dx.doi.org/10.1021/acssynbio.0c00534.

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Hedtke, B., and B. Grimm. "Silencing of a plant gene by transcriptional interference." Nucleic Acids Research 37, no. 11 (April 17, 2009): 3739–46. http://dx.doi.org/10.1093/nar/gkp241.

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Ghosh, Soumendu, Tripti Bameta, Dipanwita Ghanti, and Debashish Chowdhury. "A multispecies exclusion model inspired by transcriptional interference." Journal of Statistical Mechanics: Theory and Experiment 2016, no. 12 (December 23, 2016): 123501. http://dx.doi.org/10.1088/1742-5468/aa50dd.

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Palvimo, Jorma J., Piia Reinikainen, Tarja Ikonen, Pekka J. Kallio, Anu Moilanen, and Olli A. Jänne. "Mutual Transcriptional Interference between RelA and Androgen Receptor." Journal of Biological Chemistry 271, no. 39 (September 27, 1996): 24151–56. http://dx.doi.org/10.1074/jbc.271.39.24151.

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Hoffmann, Stefan A., Nan Hao, Keith E. Shearwin, and Katja M. Arndt. "Characterizing Transcriptional Interference between Converging Genes in Bacteria." ACS Synthetic Biology 8, no. 3 (February 5, 2019): 466–73. http://dx.doi.org/10.1021/acssynbio.8b00477.

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Assis, Raquel. "Transcriptional Interference Promotes Rapid Expression Divergence ofDrosophilaNested Genes." Genome Biology and Evolution 8, no. 10 (September 23, 2016): 3149–58. http://dx.doi.org/10.1093/gbe/evw237.

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Binder, Stefan, and Axel Brennicke. "Gene expression in plant mitochondria: transcriptional and post–transcriptional control." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1429 (January 29, 2003): 181–89. http://dx.doi.org/10.1098/rstb.2002.1179.

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The informational content of the mitochondrial genome in plants is, although small, essential for each cell. Gene expression in these organelles involves a number of distinct transcriptional and post–transcriptional steps. The complex post–transcriptional processes of plant mitochondria such as 5′ and 3′ RNA processing, intron splicing, RNA editing and controlled RNA stability extensively modify individual steady–state RNA levels and influence the mRNA quantities available for translation. In this overview of the processes in mitochondrial gene expression, we focus on confirmed and potential s

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Martin, B. K., and J. H. Weis. "Functional identification of transcription control sequences of the mouse Crry gene." Journal of Immunology 151, no. 2 (July 15, 1993): 857–69. http://dx.doi.org/10.4049/jimmunol.151.2.857.

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Abstract The mouse C receptor-related gene Crry is expressed by a wide variety of cells. Those sequences required for the transcriptional control of this gene were identified by deletion analysis of regions 5' of the initiating ATG. Fusion of Crry promoter sequences to the reporter gene CAT identified a region approximately 1,500 bp upstream of the transcriptional start site that enhanced transcription of this gene construct. Gel shift and methylation interference assays were performed, and a specific protein-DNA complex was identified within this region. These assays defined a 16-bp sequence

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Wang, Kai, Feng Sun, and Hui Z. Sheng. "Regulated expression of TAF1 in 1-cell mouse embryos." Zygote 14, no. 3 (August 2006): 209–15. http://dx.doi.org/10.1017/s0967199406003704.

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SummaryTATA binding protein (TBP) associated factor 1 (TAF1) is a member of the general transcription machinery. Interference in the function of TAF1 causes a broad transcriptional defect in early development. To explore possible roles of TAF1 in embryonic transcriptional silence and zygotic genome activation, we examined the expression of TAF1 in 1-cell mouse embryos. Using an immunofluorescence assay, TAF1 was not detected in embryos in the first few hours after fertilization. TAF1 appeared in pronuclei 6 h post-fertilization and reached a relatively high level before zygotic genome activati

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Eszterhas, Susan K., Eric E. Bouhassira, David I. K. Martin, and Steven Fiering. "Transcriptional Interference by Independently Regulated Genes Occurs in Any Relative Arrangement of the Genes and Is Influenced by Chromosomal Integration Position." Molecular and Cellular Biology 22, no. 2 (January 15, 2002): 469–79. http://dx.doi.org/10.1128/mcb.22.2.469-479.2002.

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ABSTRACT Transcriptional interference is the influence, generally suppressive, of one active transcriptional unit on another unit linked in cis. Its wide occurrence in experimental systems suggests that it may also influence transcription in many loci, but little is known about its precise nature or underlying mechanisms. Here we report a study of the interaction of two nearly identical transcription units juxtaposed in various arrangements. Each reporter gene in the constructs has its own promoter and enhancer and a strong polyadenylation signal. We used recombinase-mediated cassette exchange

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Kannan, Perry, and Michael A. Tainsky. "Coactivator PC4 Mediates AP-2 Transcriptional Activity and Suppresses ras-Induced Transformation Dependent on AP-2 Transcriptional Interference." Molecular and Cellular Biology 19, no. 1 (January 1, 1999): 899–908. http://dx.doi.org/10.1128/mcb.19.1.899.

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ABSTRACT ras oncogene-transformed PA-1 human teratocarcinoma cells have abundant AP-2 mRNA but, paradoxically, little AP-2 transcriptional activity. We have previously shown that overexpression of AP-2 in nontumorigenic variants of PA-1 cells results in inhibition of AP-2 activity and induction of tumorigenicity similar to that caused by ras transformation of PA-1 cells. Evidence indicated the existence of a novel mechanism of inhibition of AP-2 activity involving sequestering of transcriptional coactivators. In this study, we found that PC4 is a positive coactivator of AP-2 and can restore AP

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Assis, Raquel. "No Expression Divergence despite Transcriptional Interference between Nested Protein-Coding Genes in Mammals." Genes 12, no. 9 (September 1, 2021): 1381. http://dx.doi.org/10.3390/genes12091381.

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Nested protein-coding genes accumulated throughout metazoan evolution, with early analyses of human and Drosophila microarray data indicating that this phenomenon was simply due to the presence of large introns. However, a recent study employing RNA-seq data uncovered evidence of transcriptional interference driving rapid expression divergence between Drosophila nested genes, illustrating that accurate expression estimation of overlapping genes can enhance detection of their relationships. Hence, here I apply an analogous approach to strand-specific RNA-seq data from human and mouse to revisit

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Soddu, S., G. Blandino, R. Scardigli, S. Coen, A. Marchetti, M. G. Rizzo, G. Bossi, L. Cimino, M. Crescenzi, and A. Sacchi. "Interference with p53 protein inhibits hematopoietic and muscle differentiation." Journal of Cell Biology 134, no. 1 (July 1, 1996): 193–204. http://dx.doi.org/10.1083/jcb.134.1.193.

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The involvement of p53 protein in cell differentiation has been recently suggested by some observations made with tumor cells and the correlation found between differentiation and increased levels of p53. However, the effect of p53 on differentiation is in apparent contrast with the normal development of p53-null mice. To test directly whether p53 has a function in cell differentiation, we interfered with the endogenous wt-p53 protein of nontransformed cells of two different murine histotypes: 32D myeloid progenitors, and C2C12 myoblasts. A drastic inhibition of terminal differentiation into g

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Sidahmed, Abubaker, Shaza Abdalla, Salahedin Mahmud, and Bruce Wilkie. "Antiviral innate immune response of RNA interference." Journal of Infection in Developing Countries 8, no. 07 (July 14, 2014): 804–10. http://dx.doi.org/10.3855/jidc.4187.

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RNA interference (RNAi) is an ancient, natural process conserved among species from different kingdoms. RNAi is a transcriptional and post-transcriptional gene silencing mechanism in which, double-stranded RNA or hairpin RNA is cleaved by an RNase III-type enzyme called Dicer into small interfering RNA duplex. This subsequently directs sequence-specific, homology dependent, Watson-Crick base-pairing post-transcriptional gene silencing by binding to its complementary RNA and initiating its elimination through degradation or by persuading translational inhibition. In plants, worms, and insects,

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Korde, Asawari, Jessica M. Rosselot, and David Donze. "Intergenic Transcriptional Interference Is Blocked by RNA Polymerase III Transcription Factor TFIIIB inSaccharomyces cerevisiae." Genetics 196, no. 2 (December 13, 2013): 427–38. http://dx.doi.org/10.1534/genetics.113.160093.

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Knutson, Bruce A., Jaewook Oh, and Steven S. Broyles. "Downregulation of vaccinia virus intermediate and late promoters by host transcription factor YY1." Journal of General Virology 90, no. 7 (July 1, 2009): 1592–99. http://dx.doi.org/10.1099/vir.0.006924-0.

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Approximately half of the intermediate and late gene transcriptional promoters of vaccinia virus have a binding site for the cellular transcription factor YY1 that overlaps the initiator elements. Depletion of YY1 using RNA interference enhanced the activity of these promoters, while overexpression of YY1 repressed their activity. Viral promoter nucleotide replacements that specifically impair the binding of YY1 mostly alleviated the transcriptional repression and correlated with the ability of YY1 to stably interact with the initiator DNAs in vitro. The transcriptional repression activity was

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Noma, Ken-ichi, Tomoyasu Sugiyama, Hugh Cam, Andre Verdel, Martin Zofall, Songtao Jia, Danesh Moazed, and Shiv I. S. Grewal. "RITS acts in cis to promote RNA interference–mediated transcriptional and post-transcriptional silencing." Nature Genetics 36, no. 11 (October 10, 2004): 1174–80. http://dx.doi.org/10.1038/ng1452.

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Baker, Christopher R., Victor Hanson-Smith, and Alexander D. Johnson. "Following Gene Duplication, Paralog Interference Constrains Transcriptional Circuit Evolution." Science 342, no. 6154 (October 3, 2013): 104–8. http://dx.doi.org/10.1126/science.1240810.

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Most models of gene duplication assume that the ancestral functions of the preduplication gene are independent and can therefore be neatly partitioned between descendant paralogs. However, many gene products, such as transcriptional regulators, are components within cooperative assemblies; here, we show that a natural consequence of duplication and divergence of such proteins can be competitive interference between the paralogs. Our example is based on the duplication of the essential MADS-box transcriptional regulator Mcm1, which is found in all fungi and regulates a large set of genes. We sh

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Pande, Amit, Jürgen Brosius, Izabela Makalowska, Wojciech Makalowski, and Carsten A. Raabe. "Transcriptional interference by small transcripts in proximal promoter regions." Nucleic Acids Research 46, no. 3 (January 4, 2018): 1069–88. http://dx.doi.org/10.1093/nar/gkx1242.

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Bordoy, Antoni E., Nolan J. O’Connor, and Anushree Chatterjee. "Construction of Two-Input Logic Gates Using Transcriptional Interference." ACS Synthetic Biology 8, no. 10 (September 18, 2019): 2428–41. http://dx.doi.org/10.1021/acssynbio.9b00321.

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44

Anhezini, Lucas, Ana P. Saita, Ricardo G. Ramos, and Claudio R. Simon. "Transcriptional silencing of jazigo using in vivo RNA interference." Developmental Biology 344, no. 1 (August 2010): 529. http://dx.doi.org/10.1016/j.ydbio.2010.05.388.

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Dodd, Ian B., Keith E. Shearwin, and Kim Sneppen. "Modelling Transcriptional Interference and DNA Looping in Gene Regulation." Journal of Molecular Biology 369, no. 5 (June 2007): 1200–1213. http://dx.doi.org/10.1016/j.jmb.2007.04.041.

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Karkare, Shantanu, Saurabha Daniel, and Deepak Bhatnagar. "RNA Interference Silencing the Transcriptional Message: Aspects and Applications." Applied Biochemistry and Biotechnology 119, no. 1 (2004): 01–12. http://dx.doi.org/10.1385/abab:119:1:01.

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Valerius, Oliver, Cornelia Brendel, Katrin Düvel, and Gerhard H. Braus. "Multiple Factors Prevent Transcriptional Interference at the YeastARO4-HIS7Locus." Journal of Biological Chemistry 277, no. 24 (April 5, 2002): 21440–45. http://dx.doi.org/10.1074/jbc.m201841200.

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Na, K. Y. "Silencing of TonEBP/NFAT5 Transcriptional Activator by RNA Interference." Journal of the American Society of Nephrology 14, no. 2 (February 1, 2003): 283–88. http://dx.doi.org/10.1097/01.asn.0000045050.19544.b2.

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Colgin, Mark A., and Jennifer K. Nyborg. "The Human T-Cell Leukemia Virus Type 1 Oncoprotein Tax Inhibits the Transcriptional Activity of c-Myb through Competition for the CREB Binding Protein." Journal of Virology 72, no. 11 (November 1, 1998): 9396–99. http://dx.doi.org/10.1128/jvi.72.11.9396-9399.1998.

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Abstract (sommario):

ABSTRACT Tax, the transforming protein of human T-cell leukemia virus type 1 (HTLV-1), is required for strong activation of HTLV-1 transcription. This activation is mediated through interaction with the KIX domain of the cellular coactivator CREB binding protein (CBP). In this study we examined the possibility that the Tax-KIX interaction may mediate effects on cellular gene transcription in vivo, as a growing number of cellular transcription factors have been shown to utilize CBP as a coactivator. We tested the ability of Tax to deregulate the activity of the cellular transcription factor, c-

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Castro Alvarez, Javier J., Maxime Revel, Judit Carrasco, Fabienne Cléard, Daniel Pauli, Valérie Hilgers, François Karch, and Robert K. Maeda. "Repression of the Hox gene abd-A by ELAV-mediated Transcriptional Interference." PLOS Genetics 17, no. 11 (November 15, 2021): e1009843. http://dx.doi.org/10.1371/journal.pgen.1009843.

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Abstract (sommario):

Intergenic transcription is a common feature of eukaryotic genomes and performs important and diverse cellular functions. Here, we investigate the iab-8 ncRNA from the Drosophila Bithorax Complex and show that this RNA is able to repress the transcription of genes located at its 3’ end by a sequence-independent, transcriptional interference mechanism. Although this RNA is expressed in the early epidermis and CNS, we find that its repressive activity is limited to the CNS, where, in wild-type embryos, it acts on the Hox gene, abd-A, located immediately downstream of it. The CNS specificity is a

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