Relevant bibliographies by topics / Transcriptional Regulatory Elements

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Transcriptional Regulatory Elements'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Transcriptional Regulatory Elements"

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Lee, Tsz Kin (Bernard), and J. M. Friedman. "Analysis ofNF1 transcriptional regulatory elements." American Journal of Medical Genetics Part A 137A, no. 2 (2005): 130–35. http://dx.doi.org/10.1002/ajmg.a.30699.

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Heo, Hyoung-Sam, S. June Oh, Ji Min Kim, Hyung Sik Kim, and Hae Young Chung. "TREP_DB: Transcriptional regulatory elements pattern database." Biochemical and Biophysical Research Communications 394, no. 2 (April 2010): 309–16. http://dx.doi.org/10.1016/j.bbrc.2010.02.169.

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Jones, L., H. Richardson, and R. Saint. "Tissue-specific regulation of cyclin E transcription during Drosophila melanogaster embryogenesis." Development 127, no. 21 (November 1, 2000): 4619–30. http://dx.doi.org/10.1242/dev.127.21.4619.

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Cyclin E is an essential regulator of S phase entry. We have previously shown that transcriptional regulation of the gene that encodes Drosophila cyclin E, DmcycE, plays an important role in the control of the G(1) to S phase transition during development. We report here the first comprehensive analysis of the transcriptional regulation of a G(1)phase cell cycle regulatory gene during embryogenesis. Analysis of deficiencies, a genomic transformant and reporter gene constructs revealed that DmcycE transcription is controlled by a large and complex cis-regulatory region containing tissue- and stage-specific components. Separate regulatory elements for transcription in epidermal cells during cell cycles 14–16, central nervous system cells and peripheral nervous system cells were found. An additional cis-regulatory element drives transcription in thoracic epidermal cells that undergo a 17th cell cycle when other epidermal cells have arrested in G(1)phase prior to terminal differentiation. The complexity of DmcycE transcriptional regulation argues against a model in which DmcycE transcription is regulated simply and solely by G(1) to S phase transcription regulators such as RB, E2F and DP. Rather, our study demonstrates that tissue-specific transcriptional regulatory mechanisms are important components of the control of cyclin E transcription and thus of cell proliferation in metazoans.
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Andersson, Robin, Albin Sandelin, and Charles G. Danko. "A unified architecture of transcriptional regulatory elements." Trends in Genetics 31, no. 8 (August 2015): 426–33. http://dx.doi.org/10.1016/j.tig.2015.05.007.

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Maston, Glenn A., Sara K. Evans, and Michael R. Green. "Transcriptional Regulatory Elements in the Human Genome." Annual Review of Genomics and Human Genetics 7, no. 1 (September 2006): 29–59. http://dx.doi.org/10.1146/annurev.genom.7.080505.115623.

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Yin, Wenbing, and Nancy P. Keller. "Transcriptional regulatory elements in fungal secondary metabolism." Journal of Microbiology 49, no. 3 (June 2011): 329–39. http://dx.doi.org/10.1007/s12275-011-1009-1.

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Rohrer, Jurg, and Mary Ellen Conley. "Transcriptional Regulatory Elements Within the First Intron of Bruton's Tyrosine Kinase." Blood 91, no. 1 (January 1, 1998): 214–21. http://dx.doi.org/10.1182/blood.v91.1.214.

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Abstract Defects in the gene for Bruton's tyrosine kinase (Btk) result in the disorder X-linked agammaglobulinemia (XLA). Whereas XLA is characterized by a profound defect in B-cell development, Btk is expressed in both the B lymphocyte and myeloid cell lineages. We evaluated a patient with XLA who had reduced amounts of Btk transcript but no abnormalities in his coding sequence. A single base-pair substitution in the first intron of Btk was identified in this patient, suggesting that this region may contain regulatory elements. Using reporter constructs we identified two transcriptional control elements in the first 500 bp of intron 1. A strong positive regulator, active in both pre-B cells and B cells, was identified within the first 43 bp of the intron. Gel-shift assays identified two Sp1 binding sites within this element. The patient's mutation results in an altered binding specificity of the proximal Sp1 binding site. A negative regulator, active in pre-B cells only, was located between base pairs 281 and 491 of the intron. These findings indicate that regulation of Btk transcription is complex and may involve several transcriptional regulatory factors at the different stages of B-cell differentiation.
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Rohrer, Jurg, and Mary Ellen Conley. "Transcriptional Regulatory Elements Within the First Intron of Bruton's Tyrosine Kinase." Blood 91, no. 1 (January 1, 1998): 214–21. http://dx.doi.org/10.1182/blood.v91.1.214.214_214_221.

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Defects in the gene for Bruton's tyrosine kinase (Btk) result in the disorder X-linked agammaglobulinemia (XLA). Whereas XLA is characterized by a profound defect in B-cell development, Btk is expressed in both the B lymphocyte and myeloid cell lineages. We evaluated a patient with XLA who had reduced amounts of Btk transcript but no abnormalities in his coding sequence. A single base-pair substitution in the first intron of Btk was identified in this patient, suggesting that this region may contain regulatory elements. Using reporter constructs we identified two transcriptional control elements in the first 500 bp of intron 1. A strong positive regulator, active in both pre-B cells and B cells, was identified within the first 43 bp of the intron. Gel-shift assays identified two Sp1 binding sites within this element. The patient's mutation results in an altered binding specificity of the proximal Sp1 binding site. A negative regulator, active in pre-B cells only, was located between base pairs 281 and 491 of the intron. These findings indicate that regulation of Btk transcription is complex and may involve several transcriptional regulatory factors at the different stages of B-cell differentiation.
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Chávez, Joselyn, Damien P. Devos, and Enrique Merino. "Complementary Tendencies in the Use of Regulatory Elements (Transcription Factors, Sigma Factors, and Riboswitches) in Bacteria and Archaea." Journal of Bacteriology 203, no. 2 (October 19, 2020): e00413-20. http://dx.doi.org/10.1128/jb.00413-20.

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ABSTRACTIn prokaryotes, the key players in transcription initiation are sigma factors and transcription factors that bind to DNA to modulate the process, while premature transcription termination at the 5′ end of the genes is regulated by attenuation and, in particular, by attenuation associated with riboswitches. In this study, we describe the distribution of these regulators across phylogenetic groups of bacteria and archaea and find that their abundance not only depends on the genome size, as previously described, but also varies according to the phylogeny of the organism. Furthermore, we observed a tendency for organisms to compensate for the low frequencies of a particular type of regulatory element (i.e., transcription factors) with a high frequency of other types of regulatory elements (i.e., sigma factors). This study provides a comprehensive description of the more abundant COG, KEGG, and Rfam families of transcriptional regulators present in prokaryotic genomes.IMPORTANCE In this study, we analyzed the relationship between the relative frequencies of the primary regulatory elements in bacteria and archaea, namely, transcription factors, sigma factors, and riboswitches. In bacteria, we reveal a compensatory behavior for transcription factors and sigma factors, meaning that in phylogenetic groups in which the relative number of transcription factors was low, we found a tendency for the number of sigma factors to be high and vice versa. For most of the phylogenetic groups analyzed here, except for Firmicutes and Tenericutes, a clear relationship with other mechanisms was not detected for transcriptional riboswitches, suggesting that their low frequency in most genomes does not constitute a significant impact on the global variety of transcriptional regulatory elements in prokaryotic organisms.
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Iñiguez-Lluhí, Jorge A., and David Pearce. "A Common Motif within the Negative Regulatory Regions of Multiple Factors Inhibits Their Transcriptional Synergy." Molecular and Cellular Biology 20, no. 16 (August 15, 2000): 6040–50. http://dx.doi.org/10.1128/mcb.20.16.6040-6050.2000.

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ABSTRACT DNA regulatory elements frequently harbor multiple recognition sites for several transcriptional activators. The response mounted from such compound response elements is often more pronounced than the simple sum of effects observed at single binding sites. The determinants of such transcriptional synergy and its control, however, are poorly understood. Through a genetic approach, we have uncovered a novel protein motif that limits the transcriptional synergy of multiple DNA-binding regulators. Disruption of these conserved synergy control motifs (SC motifs) selectively increases activity at compound, but not single, response elements. Although isolated SC motifs do not regulate transcription when tethered to DNA, their transfer to an activator lacking them is sufficient to impose limits on synergy. Mechanistic analysis of the two SC motifs found in the glucocorticoid receptor N-terminal region reveals that they function irrespective of the arrangement of the receptor binding sites or their distance from the transcription start site. Proper function, however, requires the receptor's ligand-binding domain and an engaged dimer interface. Notably, the motifs are not functional in yeast and do not alter the effect of p160 coactivators, suggesting that they require other nonconserved components to operate. Many activators across multiple classes harbor seemingly unrelated negative regulatory regions. The presence of SC motifs within them, however, suggests a common function and identifies SC motifs as critical elements of a general mechanism to modulate higher-order interactions among transcriptional regulators.
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Dissertations / Theses on the topic "Transcriptional Regulatory Elements"

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Otto, Wolfgang. "Transcriptional Regulatory Elements." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-78960.

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A major challenge in life sciences is the understanding of mechanisms that regulate the expression of genes. An important step towards this goal is the ability to identify transcriptional regulatory elements like binding sites for transcription factors. In computational biology, a popular approach for this task is comparative sequence analysis using both distantly as well as closely related species. Although this method has successfully identified conserved regulatory regions, the majority of binding sites can change rapidly even between closely related species. This makes it difficult to detect them using DNA sequences alone. In this thesis, we introduce two new approaches for the detection and evolutionary analysis of transcriptional elements that consider the challenges of binding site turnover. In the first part, we develop a method for detecting homologous motifs in a given set of sequences in order to obtain evidence for evolutionary events and turnover. Based on a detailed theoretical scaffold, we develop a simple, but effective and efficient heuristic for assembling local pairwise sequence alignments into a local multiple sequence alignment. This kind of multiple alignment only contains conserved motifs represented in columns which satisfy the order implied by the underlying sequences. By favoring motifs that are contained in a great range of sequences, our method is additionally able to detect even small conserved motifs. Furthermore, the calculation of the initial local pairwise alignments is generic. This allows the use of fast heuristic methods in case of large data sets while exact alignment programs can be used for small data sets where detailed information is needed. Application to artificial as well as biological data sets demonstrate the capabilities of our algorithm. In the second part, we propose a conceptually simple, but mathematically non-trivial, phenomenological model for the binding site turnover at a genomic locus. The model is based on the assumption that binding sites have a constant rate of origination and a constant decay rate per binding site. The elementary derivation of the transient probability distribution is affirmed by simulations of sequence evolution as well as biological data. Based on the derived distribution, we develop a phenomenological model of binding site number dynamics in order to detect changes in selective constraints acting on transcription factor binding sites. Using a maximum likelihood implementation as well as exploratory data analysis, we show the functionality of the model by identifying functionally important changes in the evolutionary turnover rates on biological data. Each part of this thesis leads to the development of a new program. While Tracker allows the computation of conserved homologous motifs and their representation in a local multiple alignment, Creto determines the evolutionary turnover rates for arbitrary clades of a phylogenetic tree with given binding site numbers at the final taxa. Both software tools are freely available to the scientific community for further research in this important and exciting field.
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Romanish, Mark Taras. "Regulatory elements within repeated elements : a case study of NAIP transcriptional innovation." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/12271.

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Neuronal Apoptosis Inhibitory Protein (NAIP, also known as BIRC1) is a member of the conserved Inhibitor of Apoptosis Protein (IAP) family. However, it is no longer principally considered an apoptosis inhibitor since its domain structure and functions in innate immunity also warrant inclusion in the Nod-Like Receptor (NLR) superfamily. Lineage-specific rearrangement and expansion of this locus have yielded different copy numbers among primates and rodents, providing an interesting case study in which to study transcriptional regulatory changes by a rapidly evolving gene. In the first stage of my thesis, I show that NAIP has multiple promoters sharing no similarity between human and rodents. Moreover, I demonstrate that multiple, domesticated long terminal repeats (LTRs) of endogenous retroviral (ERV) elements provide NAIP promoter function in human, mouse and rat. In human, an LTR serves as a tissue-specific promoter active primarily in testis. However, in rodents, our evidence indicates that an ancestral LTR common to all rodent genes is the major, constitutive promoter for these genes and that a second LTR found in two of the mouse genes is a minor promoter. Thus, independently acquired LTRs have assumed regulatory roles for orthologous genes, a remarkable evolutionary scenario. It is also demonstrated that 5’ flanking regions of IAP family genes as a group, in both human and mouse, are enriched for LTR insertions compared to average genes. In the second stage of my thesis, I demonstrate that several of the human NAIP paralogues are expressed, and that novel transcripts arise from both internal and upstream transcription start sites. Remarkably, two internal start sites initiate within Alu short interspersed element (SINE) retrotransposons, and a third novel transcription start site exists within the final intron of the GUSBP1 gene, upstream of only two NAIP copies. One Alu functions alone as a promoter in transient assays, while the other likely combines with upstream L1 sequences to form a composite promoter. The novel transcripts encode shortened open reading frames and I show that corresponding proteins are translated in a number of cell lines and primary tissues, in some cases above the level of full length NAIP. Interestingly, some NAIP isoforms lack their caspase-sequestering motifs, indicating that they have novel functions. My results support an important role for transposable elements in NAIP evolution, particularly as transcriptional regulatory modules, and illustrate a fascinating example of regulatory innovations adopted by a rapidly evolving gene.
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Schoenborn, Jamie R. "Comprehensive epigenetic profiling identifies multiple distal regulatory elements directing Ifng transcription /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5098.

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Leblanc, Jean-François. "Functional analysis of human interferon-beta gene transcriptional regulatory elements." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59923.

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One of the main goals of this project was to systematically evaluate the virus-inducible properties of the individual human interferon-beta (IFN-$ beta$) enhansons. Synthetic oligonucleotides representing the different enhansons were subcloned into an enhancerless SV$ sb1$CAT vector; the hybrid plasmids obtained were tested in different human cell lines by transient expression assay. The P2 motif, which is 80% homologous to the NF-$ kappa$B recognition sequence, was inducible by Sendai virus. In contrast, the P1 enhanson was transcriptionally silent. Unexpectedly, a multimer of the P5 motif conferred significant virus inducibility to a heterologous transcription unit. A DNA fragment encompassing P5, P1, and P2 mimicked the transcriptional activity of the whole IFN-$ beta$ promoter, indicating that the three enhansons act synergistically to confer a virus-inducible expression pattern. The effect of certain trans-acting factors on the individual IFN-$ beta$ enhansons was also assessed. Together, these experiments indicate that the synergism between the P5, P1, and P2 enhansons is mediated by at least two distinct transcription factors, NF-$ kappa$B and IRF-1.
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Ewart, Marie-Ann. "Analysis of transcriptional regulatory elements of the human CD23 gene." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343975.

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Yao, Ya-Li. "Regulation of yy1, a multifunctional transciption [sic] factor /." [Tampa, Fla.] : University of South Florida, 2001. http://purl.fcla.edu/fcla/etd/SFE0000626.

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Vangala, Pranitha. "Role of Cis-regulatory Elements in Transcriptional Regulation: From Evolution to 4D Interactions." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1082.

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Transcriptional regulation is the principal mechanism in establishing cell-type specific gene activity by exploring an almost infinite space of different combinations of regulatory elements, transcription factors with high precision. Recent efforts have mapped thousands of candidate regulatory elements, of which a great portion is cell-type specific yet it is still unclear as to what fraction of these elements is functional, what genes these elements regulate, or how they are established in a cell-type specific manner. In this dissertation, I will discuss methods and approaches I developed to better understand the role of regulatory elements and transcription factors in gene expression regulation. First, by comparing the transcriptome and chromatin landscape between mouse and human innate immune cells I showed specific gene expression programs are regulated by highly conserved regulatory elements that contain a set of constrained sequence motifs, which can successfully classify gene-induction in both species. Next, using chromatin interactions I accurately defined functional enhancers and their target genes. This fine mapping dramatically improved the prediction of transcriptional changes. Finally, we built a supervised learning approach to detect the short DNA sequences motifs that regulate the activation of regulatory elements following LPS stimulation. This approach detected several transcription factors to be critical in remodeling the epigenetic landscape both across time and individuals. Overall this thesis addresses several important aspects of cis-regulatory elements in transcriptional regulation and started to derive principles and models of gene-expression regulation that address the fundamental question: “How do cis-regulatory elements drive cell-type-specific transcription?”
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Hilbert, Brendan J. "Structure-based Targeting of Transcriptional Regulatory Complexes Implicated in Human Disease: A Dissertation." eScholarship@UMMS, 2007. http://escholarship.umassmed.edu/gsbs_diss/681.

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Transcriptional regulatory complexes control gene expression patterns and permit cellular responses to stimuli. Deregulation of complex components upsets target gene expression and can lead to disease. This dissertation examines proteins involved in two distinct regulatory complexes: C-terminal binding protein (CtBP) 1 and 2, and Interferon Regulatory Factors (IRF) 3 and 5. Although critical in developmental processes and injury response, CtBP transcriptional repression of cell adhesion proteins, pro-apoptotic factors, and tumor suppressors has been linked to the pathogenesis of multiple forms of cancer. IRFs function in the immune system and have been implicated in autoimmune disorders. Understanding IRF activation is critical to treating pathogens that target IRF function or for future autoimmune disease therapies. We attempted to determine crystal structures that would provide the details of IRF activation, allowing insight into mechanisms of pathogen immune evasion and autoimmune disorders. Although no new structures were solved, we have optimized expression of C-terminal IRF-3 / co-activator complexes, as well as full-length IRF3 and IRF5 constructs. Modifying the constructs coupled with new crystal screening will soon result in structures which detail IRF activation, advancing understanding of the roles of IRF family members in disease. Through structural and biochemical characterization we sought to identify and develop inhibitors of CtBP transcriptional regulatory functions. High concentrations of CtBP substrate, 4-Methylthio 2-oxobutyric acid (MTOB), have been shown in different cancer models to interfere with CtBP transcriptional regulation. We began the process of structure based drug design by solving crystal structures of both CtBP family members bound to MTOB. The resulting models identified critical ligand contacts and unique active site features, which were utilized in inhibitor design. Potential CtBP inhibitors were identified and co-crystallized with CtBP1. One such compound binds to CtBP more than 1000 times more tightly than does MTOB, as a result of our structure-based inclusion of a phenyl ring and a novel pattern of hydrogen bonding. This molecule provides a starting point for the development of compounds that will both bind more tightly and interfere with transcriptional signaling as we progress towards pharmacologically targeting CtBP as a therapy for specific cancers.
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Hilbert, Brendan J. "Structure-based Targeting of Transcriptional Regulatory Complexes Implicated in Human Disease: A Dissertation." eScholarship@UMMS, 2013. https://escholarship.umassmed.edu/gsbs_diss/681.

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Transcriptional regulatory complexes control gene expression patterns and permit cellular responses to stimuli. Deregulation of complex components upsets target gene expression and can lead to disease. This dissertation examines proteins involved in two distinct regulatory complexes: C-terminal binding protein (CtBP) 1 and 2, and Interferon Regulatory Factors (IRF) 3 and 5. Although critical in developmental processes and injury response, CtBP transcriptional repression of cell adhesion proteins, pro-apoptotic factors, and tumor suppressors has been linked to the pathogenesis of multiple forms of cancer. IRFs function in the immune system and have been implicated in autoimmune disorders. Understanding IRF activation is critical to treating pathogens that target IRF function or for future autoimmune disease therapies. We attempted to determine crystal structures that would provide the details of IRF activation, allowing insight into mechanisms of pathogen immune evasion and autoimmune disorders. Although no new structures were solved, we have optimized expression of C-terminal IRF-3 / co-activator complexes, as well as full-length IRF3 and IRF5 constructs. Modifying the constructs coupled with new crystal screening will soon result in structures which detail IRF activation, advancing understanding of the roles of IRF family members in disease. Through structural and biochemical characterization we sought to identify and develop inhibitors of CtBP transcriptional regulatory functions. High concentrations of CtBP substrate, 4-Methylthio 2-oxobutyric acid (MTOB), have been shown in different cancer models to interfere with CtBP transcriptional regulation. We began the process of structure based drug design by solving crystal structures of both CtBP family members bound to MTOB. The resulting models identified critical ligand contacts and unique active site features, which were utilized in inhibitor design. Potential CtBP inhibitors were identified and co-crystallized with CtBP1. One such compound binds to CtBP more than 1000 times more tightly than does MTOB, as a result of our structure-based inclusion of a phenyl ring and a novel pattern of hydrogen bonding. This molecule provides a starting point for the development of compounds that will both bind more tightly and interfere with transcriptional signaling as we progress towards pharmacologically targeting CtBP as a therapy for specific cancers.
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Christjanson, Lisa J. "Transcriptional regulatory elements in the interleukin-8 receptor type B (IL-8RB) proximal promoter." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq21038.pdf.

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Books on the topic "Transcriptional Regulatory Elements"

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Fulcoli, F. Gabriella, and Antonio Baldini. Transcriptional regulation of early cardiovascular development. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0006.

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The two major cardiac cell lineages of the vertebrate heart, the first and second cardiac fields (FHF and SHF), have different developmental ontogeny and thus different transcription programs. Most remarkably, the fate of cardiac progenitors (CPs) of the FHF is restricted to cardiomyocyte differentiation. In contrast, SHF CPs, which are specified independently, are maintained in a multipotent state for a relatively longer developmental time and can differentiate into multiple cell types. The identity of the transcription factors and regulatory elements involved in progenitor cell programming and fate are only now beginning to emerge. Apparent inconsistencies between studies based on tissue culture and in vivo embryonic studies confirm that the ontogeny of cardiac progenitors is strongly driven or affected by regionalization, and thus by the signals that they receive in different regions. This chapter summarizes current knowledge about transcription factors and mechanisms driving CP ontogeny, with special focus on SHF development.
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Microarrays And Transcription Networks. Landes Bioscience, 2005.

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Book chapters on the topic "Transcriptional Regulatory Elements"

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Guo, Zong-Sheng, Maria Wiekowski, Sadhan Majumder, Miriam Miranda, and Melvin L. DePamphilis. "Role of Transcriptional Elements in Activating Origins of Replication." In DNA Replication: The Regulatory Mechanisms, 129–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76988-7_12.

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Agnew, Daniel E., and Brian F. Pfleger. "Optimization of Synthetic Operons Using Libraries of Post-Transcriptional Regulatory Elements." In Methods in Molecular Biology, 99–111. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-197-0_7.

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Mariati, Steven C. L. Ho, Miranda G. S. Yap, and Yuansheng Yang. "Post-transcriptional Regulatory Elements for Enhancing Transient Gene Expression Levels in Mammalian Cells." In Methods in Molecular Biology, 125–35. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-352-3_9.

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Collins, Patricia E., Christine O’Carroll, and Ruaidhrí J. Carmody. "Measurement of NF-κB Transcriptional Activity and Identification of NF-κB cis-Regulatory Elements Using Luciferase Assays." In Methods in Molecular Biology, 25–43. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2422-6_3.

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Lin, Jim Jung-Ching, Shaun E. Grosskurth, Shannon M. Harlan, Elisabeth A. Gustafson-Wagner, and Qin Wang. "Characterization of cis-Regulatory Elements and Transcription Factor Binding." In Methods in Molecular Biology, 183–201. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-030-0_10.

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Naeve, Gregory S., Li-jing Li, Lin Guo, Ajay Sharma, and Amy S. Lee. "G1-S Regulatory Promoter Elements and their Interacting Transcription Factors." In The Cell Cycle, 127–39. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_14.

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Contreras-Moreira, Bruno, and Alvaro Sebastian. "FootprintDB: Analysis of Plant Cis-Regulatory Elements, Transcription Factors, and Binding Interfaces." In Methods in Molecular Biology, 259–77. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6396-6_17.

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Fang, Wei, Yi Wen, and Xiangyun Wei. "Identification and Characterization of Cis-Regulatory Elements for Photoreceptor-Type-Specific Transcription in ZebraFish." In Retinal Development, 123–45. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0175-4_10.

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Banerjee, Nilanjana, and Andrea Califano. "Transcription Factor Centric Discovery of Regulatory Elements in Mammalian Genomes Using Alignment-Independent Conservation Maps." In Comparative Genomics, 200–214. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11864127_16.

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Pay, A., E. Fejes, M. Szell, E. Adam, and F. Nagy. "CIS-Regulatory Elements for the Circadian Clock Regulated Transcription of the Wheat CAB-1 Gene." In Plant Molecular Biology 2, 519–25. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3304-7_50.

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Conference papers on the topic "Transcriptional Regulatory Elements"

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Xiong, Yun, Guangyong Zheng, Qing Yang, and Yangyong Zhu. "An Agent-Based Approach to Mine Transcriptional Regulatory Elements." In 2008 IEEE/WIC/ACM International Conference on Web Intelligence and Intelligent Agent Technology. IEEE, 2008. http://dx.doi.org/10.1109/wiiat.2008.224.

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Jiang, Xin, Patricia Reynaud-Bouret, Vincent Rivoirard, Laure Sansonnet, and Rebecca Willett. "Genomic transcription regulatory element location analysis via poisson weighted lasso." In 2016 IEEE Statistical Signal Processing Workshop (SSP). IEEE, 2016. http://dx.doi.org/10.1109/ssp.2016.7551831.

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Yao, Lijing, Hui Shen, Peter Laird, Peggy Farnham, and Berman Benjamin. "Abstract 22: Inferring regulatory element landscapes and transcription factor networks from cancer methylomes." In Abstracts: AACR Precision Medicine Series: Integrating Clinical Genomics and Cancer Therapy; June 13-16, 2015; Salt Lake City, UT. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.pmsclingen15-22.

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Lamas-Maceiras, M., and M. A. Freire-Picos. "A YARE-like element as the binding site for specific KlHIS4 transcriptional regulators and its implication in cadmium toxicity." In Proceedings of the III International Conference on Environmental, Industrial and Applied Microbiology (BioMicroWorld2009). WORLD SCIENTIFIC, 2010. http://dx.doi.org/10.1142/9789814322119_0133.

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Bosma, P. J., E. A. van den Berg, and T. Kooistra. "ISOLATION OF THE GENE CODING FOR HUMAN PLASMINOGEN ACTIVATOR INHIBITOR TYPE 1 (PAI-1)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644440.

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Abstract:
A human placenta genomic DNA cosmid library was screened for the presence of the PAI-1 gene using a cDNA probe coding for PAI-1. Two overlapping recombinant cosmids were obtained that contain human DNA spanning 55 kb. The cosmids were mapped using 3' and 5' end probes isolated from an almost full-length cDNA clone of 2.5 kb. The two cosmids were found to contain the entire structural PAI-1 gene (approximately 15 kb) and also included 25 kb 5' flanking sequences. The transcription initiation site was identified by SI nuclease protection experiments and the promotor region was sequenced. Further experiments will be directed at characterizing the regulatory elements of the PAI-1 gene.In order to determine the chromosomal localization of the PAI-1 gene we have hybridized our genomic clones in situ to metaphase chromosomes of a human blood cell culture. Preliminary experiments show a specific hybridization signal which will enable us to sublocalize the chromosomal position of the PAI-1 gene.
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Guan, Min, Chunling Jiang, Kristen N. Fousek, Song Guo, and Warren Chow. "Abstract 2609: Nelfinavir induces liposarcoma apoptosis through inhibition of regulated intramembrane proteolysis of sterol regulatory element binding protein-1 and activating transcription factor 6." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2609.

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