Relevant bibliographies by topics / Transcriptional autoregulation

Academic literature on the topic 'Transcriptional autoregulation'

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Published: 6 September 2023

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Journal articles on the topic "Transcriptional autoregulation"

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De Siervi, Adriana, Paola De Luca, Jung S. Byun, Li Jun Di, Temesgen Fufa, Cynthia M. Haggerty, Elba Vazquez, Cristian Moiola, Dan L. Longo, and Kevin Gardner. "Transcriptional Autoregulation by BRCA1." Cancer Research 70, no. 2 (January 12, 2010): 532–42. http://dx.doi.org/10.1158/0008-5472.can-09-1477.

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Crews, Stephen T., and Joseph C. Pearson. "Transcriptional autoregulation in development." Current Biology 19, no. 6 (March 2009): R241—R246. http://dx.doi.org/10.1016/j.cub.2009.01.015.

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Hobert, Oliver. "Maintaining a memory by transcriptional autoregulation." Current Biology 21, no. 4 (February 2011): R146—R147. http://dx.doi.org/10.1016/j.cub.2011.01.005.

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Hearing, P., and T. Shenk. "Sequence-independent autoregulation of the adenovirus type 5 E1A transcription unit." Molecular and Cellular Biology 5, no. 11 (November 1985): 3214–21. http://dx.doi.org/10.1128/mcb.5.11.3214-3221.1985.

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The adenovirus E1A gene is known to be autoregulated at the level of transcription. Autoregulation was found to be mediated by products of the E1A 13S mRNA, which induced a fivefold increase in E1A transcription rate. Deletion analysis suggested that the autoregulation did not require any specific sequence in the E1A transcriptional control region. This conclusion was reinforced by the demonstration that a cellular alpha-globin gene substituted for the E1A gene on the adenovirus chromosome was also positively regulated by E1A gene products.
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Hearing, P., and T. Shenk. "Sequence-independent autoregulation of the adenovirus type 5 E1A transcription unit." Molecular and Cellular Biology 5, no. 11 (November 1985): 3214–21. http://dx.doi.org/10.1128/mcb.5.11.3214.

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The adenovirus E1A gene is known to be autoregulated at the level of transcription. Autoregulation was found to be mediated by products of the E1A 13S mRNA, which induced a fivefold increase in E1A transcription rate. Deletion analysis suggested that the autoregulation did not require any specific sequence in the E1A transcriptional control region. This conclusion was reinforced by the demonstration that a cellular alpha-globin gene substituted for the E1A gene on the adenovirus chromosome was also positively regulated by E1A gene products.
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Sassone-Corsi, Paolo, John C. Sisson, and Inder M. Verma. "Transcriptional autoregulation of the proto-oncogene fos." Nature 334, no. 6180 (July 1988): 314–19. http://dx.doi.org/10.1038/334314a0.

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MAGENHEIM, Judith, Rachel HERTZ, Ina BERMAN, Janna NOUSBECK, and Jacob BAR-TANA. "Negative autoregulation of HNF-4α gene expression by HNF-4α1." Biochemical Journal 388, no. 1 (May 10, 2005): 325–32. http://dx.doi.org/10.1042/bj20041802.

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HNF-4α (hepatocyte nuclear factor-4α) is required for tissue-specific expression of many of the hepatic, pancreatic, enteric and renal traits. Heterozygous HNF-4α mutants are inflicted by MODY-1 (maturity onset diabetes of the young type-1). HNF-4α expression is reported here to be negatively autoregulated by HNF-4α1 and to be activated by dominant-negative HNF-4α1. Deletion and chromatin immunoprecipitation analysis indicated that negative autoregulation by HNF-4α1 was mediated by its association with the TATA-less HNF-4α core promoter enriched in Sp1, but lacking DR-1 response elements. Also, negative autoregulation by HNF-4α1 was independent of its transactivation function, being similarly exerted by transcriptional-defective MODY-1 missense mutants of HNF-4α1, or under conditions of suppressing or enhancing HNF-4α activity by small heterodimer partner or by inhibiting histone deacetylase respectively. Negative autoregulation by HNF-4α1 was abrogated by overexpressed Sp1. Transcriptional suppression by HNF-4α1 independently of its transactivation function may extend the scope of its transcriptional activity to interference with docking of the pre-transcriptional initiation complex to TATA-less promoters.
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Delahodde, A., T. Delaveau, and C. Jacq. "Positive autoregulation of the yeast transcription factor Pdr3p, which is involved in control of drug resistance." Molecular and Cellular Biology 15, no. 8 (August 1995): 4043–51. http://dx.doi.org/10.1128/mcb.15.8.4043.

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Simultaneous resistance to an array of drugs with different cytotoxic activities is a property of Saccharomyces cerevisiae, in which the protein Pdr3p has recently been shown to play a role as a transcriptional regulator. We provide evidence that the yeast PDR3 gene, which encodes a zinc finger transcription factor implicated in certain drug resistance phenomena, is under positive autoregulation by Pdr3p. DNase I footprinting analyses using bacterially expressed Pdr3p showed specific recognition by this protein of at least two upstream activating sequences in the PDR3 promoter. The use of lacZ reporter constructs, a mutational analysis of the upstream activating sequences, as well as band shift experiments enabled the identification of two 5'TC CGCGGA3' sequence motifs in the PDR3 gene as consensus elements for the binding of Pdr3p. Several similar sequence motifs can be found in the promoter of PDR5, a gene encoding an ATP-dependent drug pump whose Pdr3p-induced overexpression is responsible for drug resistance phenomena. Recently one of these sequence elements was shown to be the target of Pdr3p to elevate the level of PDR5 transcription. Finally, we provide evidence in the absence of PDR1 for a PDR3-controlled transcriptional induction of the drug pump by cycloheximide and propose a model for the mechanism governing the transcriptional autoregulation of Pdr3p.
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Bell, Stephen D., and Stephen P. Jackson. "Mechanism of Autoregulation by an Archaeal Transcriptional Repressor." Journal of Biological Chemistry 275, no. 41 (July 18, 2000): 31624–29. http://dx.doi.org/10.1074/jbc.m005422200.

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Soncini, F. C., E. G. Véscovi, and E. A. Groisman. "Transcriptional autoregulation of the Salmonella typhimurium phoPQ operon." Journal of bacteriology 177, no. 15 (1995): 4364–71. http://dx.doi.org/10.1128/jb.177.15.4364-4371.1995.

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Dissertations / Theses on the topic "Transcriptional autoregulation"

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Zhu, Cong. "GENE REGULATORY NETWORKS OF AGL15 A PLANT MADS TRANSCRIPTION FACTOR." UKnowledge, 2005. http://uknowledge.uky.edu/gradschool_diss/446.

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Plant embryogenesis is an intriguing developmental process that is controlled by many genes. AGAMOUS Like 15 (AGL15) is a MADS-domain transcriptional regulator that accumulates preferentially during this stage. However, at the onset of this work it was unknown which genes are regulated by AGL15 or how AGL15 is regulated. This dissertation is part of the ongoing effort to understand the biological roles of AGL15. To decipher how AGL15 functions during plant development, a chromatin immunoprecipitation (ChIP) approach was adapted to obtain DNA fragments that are directly bound by AGL15 in vivo. Putative AGL15 targets were isolated, and binding and regulation was confirmed for one such target gene, ABF3. In addition, microarray experiments were performed to globally assess genes that are differentially expressed between wild type and agl15 young seeds. Among them, a gene, At5g23405, encoding an HMGB domain protein was identified and its response to AGL15 was confirmed. Preliminary results suggest that the loss-of-function of At5g23405 might have an effect on somatic embryogenesis, consistent with AGL15 repression of the expression of this gene. Lastly, to address the question about how the regulator is regulated, the cis elements controlling the expression of AGL15 must be identified. Deletion analysis of the AGL15 promoter indicated the presence of putative positive and negative cis elements contributing to the expression of AGL15. Further analysis suggested that AGL15 regulates the expression of its own gene and this regulation may partially be explained by the direct binding of the protein to the AGL15 promoter. The data presented in this dissertation demonstrate that ChIP can be used to identify previously unsuspected targets of AGL15. Based on ChIP, a ChIP-chip technique is being developed in the lab to allow a more global analysis of in vivo binding sites. The identification of target genes and cis elements in AGL15 promoter is a step towards characterization of the biological roles of AGL15.
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Unoarumhi, Yvette Ochuwa. "Evolution of a Bacterial Global Regulator- Lrp." University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1461859521.

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Vernié, Tatiana. "Analyse fonctionnelle d'EFD, un régulateur transcriptionnel de la nodulation au cours de l'interaction symbiotique entre Medicago truncatula et Sinorhizobium meliloti." Toulouse 3, 2008. http://thesesups.ups-tlse.fr/222/.

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Les Légumineuses sont capables d'établir une interaction symbiotique avec des bactéries de la rhizosphère, appelées Rhizobia. Cette interaction implique deux processus strictement contrôlés par la plante : une infection bactérienne et la formation d'un nouvel organe : le nodule, dans lequel l'azote atmosphérique est réduit. Les mécanismes de ces contrôles restent peu connus. A partir d'études transcriptomiques, nous avons sélectionné un régulateur potentiel, EFD (Ethylene response Factor required for nodule Differentiation), codant pour un facteur de transcription de type ERF. Le profil d'expression d'EFD a été caractérisé par des analyses de RT-PCR quantitatives, d'hybridation in situ et de fusions promoteur:GUS. Ces études ont révélé une expression spécifique d'EFD dans les primordia nodulaires et racinaires, ainsi que dans la zone d'infection des nodules, où les bactéries et tissus végétaux se différencient. Puis, grâce à des approches de surexpression et de RNAi sur des racines transformées, et à l'analyse d'un mutant de délétion, un rôle d'EFD lors de l'initiation et de la différenciation des nodules a été mis en évidence. Enfin, une cible principale, Mt RR4, a été identifiée par une approche transcriptomique. RR4 code pour un régulateur de la réponse aux cytokinines, dont le rôle lors de l'initiation des nodules a récemment été démontré. Nous proposons donc qu'en régulant l'expression de RR4, EFD modulerait la voie de réponse des cytokinines lors de la nodulation et coordonnerait ainsi l'initiation et le développement des nodules. .
Leguminous plants can establish symbiotic interaction with bacteria from the rhizosphere, called Rhizobia. During this interaction, plants control tightly two mechanisms: bacterial infection and formation of a new organ, the nodule in which nitrogen is fixed. But how plants control these mechanisms is still largely unknown. Starting from transcriptomic studies, we selected a potential regulator, EFD (Ethylene response Factor required for nodule Differentiation), coding for a transcription factor belonging to the ERF family. The expression profile of EFD has been characterized by quantitative RT-PCR, in situ hybridization and promoter:GUS fusion. These studies revealed a specific expression of EFD in nodule and root primordia, and in the infection zone of mature nodules, where bacteria and plant tissues differentiate. Using overexpression and RNAi approaches on transformed roots, and study of a deletion mutant, we then showed that EFD plays a role to control the number of nodules and their differentiation. Finally, we identified a major target of EFD by a transcriptomic approach. This target, Mt RR4, encodes a cytokinin response regulator. Cytokinins have recently been shown to be positive regulators of nodule initiation. Consequently, we propose that by regulating RR4 expression, EFD modulates the cytokinin pathway during nodulation to coordinate nodule initiation and development. .
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Wu, Tian-Yu, and 吳天宇. "Autoregulation of gbsR, identification of GbsR-binding sites, and transcriptional regulation of opuB and opuC operons in Bacillus subtilis." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/47042651578494871587.

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碩士
國立陽明大學
生化暨分子生物研究所
101
The soil bacterium Bacillus subtilis can use glycine betaine, which is one of the most important osmoprotectants in nature, to cope with the environmental osmotic stress. Choline oxidation by GbsB (choline dehydrogenase) and GbsA (glycine betaine aldehyde dehydrogenase) is the only known pathway for the synthesis of glycine betaine in B. subtilis. Choline cannot be synthesized by B. subtilis cells, but can be imported from the environment by osmoinducible ABC transporters OpuB and OpuC. GbsR is a choline-sensing regulator that negatively controls transcription of gbsAB and opuB operons. A previous study from our laboratory demonstrated that the opcR gene, which is located upstream of opuC, encodes a negative regulator for transcription of opuB and opuC operons. In this study, results from deletion and mutation analyses suggest the presence of putative GbsR operators in gbsA and opuB promoter regions, whose sequences and locations are somewhat different from the previously predicted ones. Electrophoretic mobility shift assays confirmed that these putative operators are required for the binding of GbsR. We also identified a previously unknown cis-acting element that negatively regulates opuB expression. In addition, we have found that gbsR expression is subject to negative autoregulation through the binding of GbsR to an operator in the gbsR promoter region. Moreover, we show that, in the absence of OpcR, choline exerts a suppressive effect on opuC expression during normal growth and under osmotic stress. In the absence of the choline-sensing repressor GbsR, opuB expression is also suppressed by choline.
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Dar, Roy David. "Adaptation and Stochasticity of Natural Complex Systems." 2011. http://trace.tennessee.edu/utk_graddiss/959.

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The methods that fueled the microscale revolution (top-down design/fabrication, combined with application of forces large enough to overpower stochasticity) constitute an approach that will not scale down to nanoscale systems. In contrast, in nanotechnology, we strive to embrace nature’s quite different paradigms to create functional systems, such as self-assembly to create structures, exploiting stochasticity, rather than overwhelming it, in order to create deterministic, yet highly adaptable, behavior. Nature’s approach, through billions of years of evolutionary development, has achieved self-assembling, self-duplicating, self-healing, adaptive systems. Compared to microprocessors, nature’s approach has achieved eight orders of magnitude higher memory density and three orders of magnitude higher computing capacity while utilizing eight orders of magnitude less power. Perhaps the most complex of functions, homeostatis by a biological cell – i.e., the regulation of its internal environment to maintain stability and function – in a fluctuating and unpredictable environment, emerges from the interactions between perhaps 50M molecules of a few thousand different types. Many of these molecules (e.g. proteins, RNA) are produced in the stochastic processes of gene expression, and the resulting populations of these molecules are distributed across a range of values. So although homeostasis is maintained at the system (i.e. cell) level, there are considerable and unavoidable fluctuations at the component (protein, RNA) level. While on at least some level, we understand the variability in individual components, we have no understanding of how to integrate these fluctuating components together to achieve complex function at the system level. This thesis will explore the regulation and control of stochasticity in cells. In particular, the focus will be on (1) how genetic circuits use noise to generate more function in less space; (2) how stochastic and deterministic responses are co-regulated to enhance function at a system level; and (3) the development of high-throughput analytical techniques that enable a comprehensive view of the structure and distribution of noise on a whole organism level.
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Chandra, Soumyanetra. "Probing Protein Sequence-Function Relationships using Deep Mutational Scanning." Thesis, 2021. https://etd.iisc.ac.in/handle/2005/5662.

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Deep Mutational Scanning (DMS) approaches help elucidate sequence-function-phenotype relationships in proteins, which ultimately improves our understanding of residue (or nucleotide)-specific contributions to protein function and organismal fitness. Such comprehensive knowledge finds use in reliable prediction of consequences of mutations, as well as in protein design and engineering. We have investigated the molecular mechanisms of how mutations at surface exposed sites, away from the active sites in a model protein, CcdB produce drastic defects on the protein’s activity and organismal phenotype. Subsequently, we have surveyed double mutant libraries of CcdB, using a DMS approach, to identify mutants that can suppress the inactive phenotypes of exposed non active-site mutants in CcdB. These studies provide insights into the generally overlooked mutations that alter the fraction of active protein expressed, without affecting the activity of the folded fraction. We next describe a facile DMS method to accurately estimate binding energetics of protein-protein interactions (PPIs) and have used this methodology to probe residue specific contributions to partner binding in an intrinsically disordered protein CcdA. We also developed a model based on the CcdA mutational landscape to predict mutational effects on binding affinities in other IDPs. Using the insights from the CcdA mutational study, we also describe how Aspartate Scanning can be used to predict interface residues and local secondary structures for the MazF6 interacting, intrinsically disordered domain of MazE6 protein. This rapid and inexpensive methodology is readily applicable to experimentally unexplored, protein-interacting, intrinsically disordered domains. Finally, we also investigate how mutations in the ccdA gene can affect the protein’s activity and phenotype of the bacterial cell harboring it, in its native operonic context, and found a surprisingly high sensitivity to mutations (including synonymous mutations) in a manner dependent on the codon usage in the genome.
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Books on the topic "Transcriptional autoregulation"

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Gill, Robert James Montgomery. Characterization of the human RB1 promoter and of elements involved in transcriptional autoregulation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Book chapters on the topic "Transcriptional autoregulation"

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Draper, David E. "Mechanisms of Ribosomal Protein Translational Autoregulation." In Post-Transcriptional Control of Gene Expression, 299–308. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75139-4_28.

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Oei, Shiao Li, Herbert Herzog, Monica Hirsch-Kauffmann, Rainer Schneider, Bernhard Auer, and Manfred Schweiger. "Transcriptional regulation and autoregulation of the human gene for ADP-ribosyltransferase." In ADP-Ribosylation: Metabolic Effects and Regulatory Functions, 99–104. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2614-8_13.

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Bateman, Erik. "Autoregulation of Eukaryotic Transcription Factors." In Progress in Nucleic Acid Research and Molecular Biology, 133–68. Elsevier, 1998. http://dx.doi.org/10.1016/s0079-6603(08)60892-2.

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Conference papers on the topic "Transcriptional autoregulation"

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Herlinger, Alice Laschuk, Min Gao, Ren-Chin Wu, Tian-Li Wang, Leticia B. A. Rangel, and Ie-Ming Shih. "Abstract A80: NAC1 attenuates BCL6 negative autoregulation and functions as a BCL6 coactivator of FOXQ1 transcription in ovarian cancer (OVCA)." In Abstracts: AACR Special Conference: Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; October 17-20, 2015; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.ovca15-a80.

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