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Journal articles on the topic 'Transcriptional enhancer'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Su, Guangsong, Wenbin Wang, Xueyuan Zhao, et al. "Enhancer architecture-dependent multilayered transcriptional regulation orchestrates RA signaling-induced early lineage differentiation of ESCs." Nucleic Acids Research 49, no. 20 (2021): 11575–95. http://dx.doi.org/10.1093/nar/gkab1001.

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Abstract Signaling pathway-driven target gene transcription is critical for fate determination of embryonic stem cells (ESCs), but enhancer-dependent transcriptional regulation in these processes remains poorly understood. Here, we report enhancer architecture-dependent multilayered transcriptional regulation at the Halr1–Hoxa1 locus that orchestrates retinoic acid (RA) signaling-induced early lineage differentiation of ESCs. We show that both homeobox A1 (Hoxa1) and Hoxa adjacent long non-coding RNA 1 (Halr1) are identified as direct downstream targets of RA signaling and regulated by RARA/RX

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2

Liu, Jing, Sharon Ochs та Courtney Sulentic. "Transcriptional regulation by 2,3,7,8-tetrachlorodibenzo-ρ-dioxin within the human polymorphic hs1,2 enhancer (42.7)". Journal of Immunology 188, № 1_Supplement (2012): 42.7. http://dx.doi.org/10.4049/jimmunol.188.supp.42.7.

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Abstract The environmental contaminant 2,3,7,8-tetrachlorodibenzo-ρ-dioxin (TCDD) inhibits Ig expression and secretion. Within the IgH gene, the 3’IgH regulatory region (3’IgHRR) has been identified as a transcriptional target of TCDD. TCDD inhibits mouse 3’IgHRR and induces aryl hydrocarbon receptor (AhR) binding to dioxin response elements (DREs) within the hs1,2 and hs4 enhancers. The human hs1,2 enhancer is polymorphic due to the presence of one to four invariant sequences (IS) which have been correlated with several autoimmune disorders. Interestingly, TCDD inhibits the transcriptional ac

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Yi, Mei, Yixin Tan, Li Wang, et al. "TP63 links chromatin remodeling and enhancer reprogramming to epidermal differentiation and squamous cell carcinoma development." Cellular and Molecular Life Sciences 77, no. 21 (2020): 4325–46. http://dx.doi.org/10.1007/s00018-020-03539-2.

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Abstract Squamous cell carcinoma (SCC) is an aggressive malignancy that can originate from various organs. TP63 is a master regulator that plays an essential role in epidermal differentiation. It is also a lineage-dependent oncogene in SCC. ΔNp63α is the prominent isoform of TP63 expressed in epidermal cells and SCC, and overexpression promotes SCC development through a variety of mechanisms. Recently, ΔNp63α was highlighted to act as an epidermal-specific pioneer factor that binds closed chromatin and enhances chromatin accessibility at epidermal enhancers. ΔNp63α coordinates chromatin-remode

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4

Zuin, Jessica, Gregory Roth, Yinxiu Zhan, et al. "Nonlinear control of transcription through enhancer–promoter interactions." Nature 604, no. 7906 (2022): 571–77. http://dx.doi.org/10.1038/s41586-022-04570-y.

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AbstractChromosome structure in mammals is thought to regulate transcription by modulating three-dimensional interactions between enhancers and promoters, notably through CTCF-mediated loops and topologically associating domains (TADs)1–4. However, how chromosome interactions are actually translated into transcriptional outputs remains unclear. Here, to address this question, we use an assay to position an enhancer at large numbers of densely spaced chromosomal locations relative to a fixed promoter, and measure promoter output and interactions within a genomic region with minimal regulatory a

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5

Carullo, Nancy V. N., Robert A. Phillips III, Rhiana C. Simon, et al. "Enhancer RNAs predict enhancer–gene regulatory links and are critical for enhancer function in neuronal systems." Nucleic Acids Research 48, no. 17 (2020): 9550–70. http://dx.doi.org/10.1093/nar/gkaa671.

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Abstract Genomic enhancer elements regulate gene expression programs important for neuronal fate and function and are implicated in brain disease states. Enhancers undergo bidirectional transcription to generate non-coding enhancer RNAs (eRNAs). However, eRNA function remains controversial. Here, we combined Assay for Transposase-Accessible Chromatin using Sequencing (ATAC-Seq) and RNA-Seq datasets from three distinct neuronal culture systems in two activity states, enabling genome-wide enhancer identification and prediction of putative enhancer–gene pairs based on correlation of transcription

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Fletcher, Alvaro, Zeba Wunderlich, and German Enciso. "Shadow enhancers mediate trade-offs between transcriptional noise and fidelity." PLOS Computational Biology 19, no. 5 (2023): e1011071. http://dx.doi.org/10.1371/journal.pcbi.1011071.

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Enhancers are stretches of regulatory DNA that bind transcription factors (TFs) and regulate the expression of a target gene. Shadow enhancers are two or more enhancers that regulate the same target gene in space and time and are associated with most animal developmental genes. These multi-enhancer systems can drive more consistent transcription than single enhancer systems. Nevertheless, it remains unclear why shadow enhancer TF binding sites are distributed across multiple enhancers rather than within a single large enhancer. Here, we use a computational approach to study systems with varyin

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7

Pauli, Sandra, Helen M. Rothnie, Gang Chen, Xiaoyuan He, and Thomas Hohn. "The Cauliflower Mosaic Virus 35S Promoter Extends into the Transcribed Region." Journal of Virology 78, no. 22 (2004): 12120–28. http://dx.doi.org/10.1128/jvi.78.22.12120-12128.2004.

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ABSTRACT A 60-nucleotide region (S1) downstream of the transcription start site of the cauliflower mosaic virus 35S RNA can enhance gene expression. By using transient expression assays with plant protoplasts, this activity was shown to be at least partially due to the effect of transcriptional enhancers within this region. We identify sequence motifs with enhancer function, which are normally masked by the powerful upstream enhancers of the 35S promoter. A repeated CT-rich motif is involved both in enhancer function and in interaction with plant nuclear proteins. The S1 region can also enhanc

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8

Li, Guowang, Yuxiang Kang, Xiangling Feng, et al. "Dynamic changes of enhancer and super enhancer landscape in degenerated nucleus pulposus cells." Life Science Alliance 6, no. 6 (2023): e202201854. http://dx.doi.org/10.26508/lsa.202201854.

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Inflammatory cascade and extracellular matrix remodeling have been identified as pivotal pathological factors in the progression of intervertebral disc degeneration (IDD), but the mechanisms underlying the aberrant activation of transcription during nucleus pulposus (NP) cell degeneration remain elusive. Super-enhancers (SEs) are large clusters of adjacent lone enhancers, which control expression modes of cellular fate and pathogenic genes. Here, we showed that SEs underwent tremendous remodeling during NP cell degeneration and that SE-related transcripts were most abundant in inflammatory cas

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9

Ibragimov, Airat N., Oleg V. Bylino, and Yulii V. Shidlovskii. "Molecular Basis of the Function of Transcriptional Enhancers." Cells 9, no. 7 (2020): 1620. http://dx.doi.org/10.3390/cells9071620.

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Transcriptional enhancers are major genomic elements that control gene activity in eukaryotes. Recent studies provided deeper insight into the temporal and spatial organization of transcription in the nucleus, the role of non-coding RNAs in the process, and the epigenetic control of gene expression. Thus, multiple molecular details of enhancer functioning were revealed. Here, we describe the recent data and models of molecular organization of enhancer-driven transcription.

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10

Banditt, Michael, Theo Koller, and José M. Sogo. "Transcriptional Activity and Chromatin Structure of Enhancer-Deleted rRNA Genes in Saccharomyces cerevisiae." Molecular and Cellular Biology 19, no. 7 (1999): 4953–60. http://dx.doi.org/10.1128/mcb.19.7.4953.

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ABSTRACT We used the psoralen gel retardation assay and Northern blot analysis in an in vivo yeast system to analyze effects of rDNA enhancer deletions on the chromatin structure and the transcription of tagged rDNA units. We found that upon deletion of a single enhancer element, transcription of the upstream and downstream rRNA gene was reduced by about 50%. Although removing both flanking enhancers of an rRNA gene led to a further reduction in transcription levels, a significant amount of transcriptional activity remained, either resulting from the influence of more distantly located enhance

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11

Dickel, D. E., A. Visel, and L. A. Pennacchio. "Functional anatomy of distant-acting mammalian enhancers." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1620 (2013): 20120359. http://dx.doi.org/10.1098/rstb.2012.0359.

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Transcriptional enhancers are a major class of functional element embedded in the vast non-coding portion of the human genome. Acting over large genomic distances, enhancers play critical roles in the tissue and cell type-specific regulation of genes, and there is mounting evidence that they contribute to the aetiology of many human diseases. Methods for genome-wide mapping of enhancer regions are now available, but the functional architecture contained within human enhancer elements remains unclear. Here, we review recent approaches aimed at understanding the functional anatomy of individual

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12

Lewis, Michael W., Shen Li, and Hector L. Franco. "Transcriptional control by enhancers and enhancer RNAs." Transcription 10, no. 4-5 (2019): 171–86. http://dx.doi.org/10.1080/21541264.2019.1695492.

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13

Kustu, Sydney, Anne K. North, and David S. Weiss. "Prokaryotic transcriptional enhancers and enhancer-binding proteins." Trends in Biochemical Sciences 16 (January 1991): 397–402. http://dx.doi.org/10.1016/0968-0004(91)90163-p.

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14

Neri, Paola. "Enhancer Deregulation in Myeloma." Blood 132, Supplement 1 (2018): SCI—38—SCI—38. http://dx.doi.org/10.1182/blood-2018-99-109523.

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Abstract The complexity of gene expression regulation is the result of a composite interplay between promoters, enhancers and other cis-acting regulatory elements bound by transcription factors (TFs) that controls the transcriptional activity of genes. Primary tumor cells, in comparison to their healthy counterparts, are known to display altered enhancer repertoires that are associated with tumor-specific transcription. Large groups of transcriptional enhancers cluster together to form super-enhancers (SEs). These elements have been shown to control genes that are important for maintaining cel

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Xu, Jian. "In Situ Capture of the Molecular Composition of Erythroid Transcriptional Enhancers." Blood 130, Suppl_1 (2017): SCI—17—SCI—17. http://dx.doi.org/10.1182/blood.v130.suppl_1.sci-17.sci-17.

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Elucidating mechanisms that regulate gene transcription during erythropoiesis is critical for identifying fundamental principles of cellular differentiation, and for developing new therapies for blood disorders. Transcriptional enhancers determine cell identity by directing spatiotemporal gene expression, yet the molecular processes controlling enhancer activation and deactivation during lineage differentiation remain largely unknown. Recently, we and others have identified human erythroid cell-specific enhancers by mapping histone modifications, transcription factor binding and transcriptomic

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16

Kelley, D. E., B. A. Pollok, M. L. Atchison, and R. P. Perry. "The coupling between enhancer activity and hypomethylation of kappa immunoglobulin genes is developmentally regulated." Molecular and Cellular Biology 8, no. 2 (1988): 930–37. http://dx.doi.org/10.1128/mcb.8.2.930-937.1988.

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Previous studies have indicated that immunoglobulin enhancers are essential for establishing transcriptional competence but not for maintaining the activity of constitutively transcribed genes. To understand the basis for this developmental shift away from dependence on enhancer function, we have investigated the relationship between transcriptional activity and methylation status of the immunoglobulin kappa light-chain genes (kappa genes) in mouse cell lines representing different stages of B-cell maturation. Using pre-B-cell lines in which the level of a critical kappa enhancer-binding facto

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Kelley, D. E., B. A. Pollok, M. L. Atchison, and R. P. Perry. "The coupling between enhancer activity and hypomethylation of kappa immunoglobulin genes is developmentally regulated." Molecular and Cellular Biology 8, no. 2 (1988): 930–37. http://dx.doi.org/10.1128/mcb.8.2.930.

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Previous studies have indicated that immunoglobulin enhancers are essential for establishing transcriptional competence but not for maintaining the activity of constitutively transcribed genes. To understand the basis for this developmental shift away from dependence on enhancer function, we have investigated the relationship between transcriptional activity and methylation status of the immunoglobulin kappa light-chain genes (kappa genes) in mouse cell lines representing different stages of B-cell maturation. Using pre-B-cell lines in which the level of a critical kappa enhancer-binding facto

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18

Keller, Samuel H., Siddhartha G. Jena, Yuji Yamazaki, and Bomyi Lim. "Regulation of spatiotemporal limits of developmental gene expression via enhancer grammar." Proceedings of the National Academy of Sciences 117, no. 26 (2020): 15096–103. http://dx.doi.org/10.1073/pnas.1917040117.

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The regulatory specificity of a gene is determined by the structure of its enhancers, which contain multiple transcription factor binding sites. A unique combination of transcription factor binding sites in an enhancer determines the boundary of target gene expression, and their disruption often leads to developmental defects. Despite extensive characterization of binding motifs in an enhancer, it is still unclear how each binding site contributes to overall transcriptional activity. Using live imaging, quantitative analysis, and mathematical modeling, we measured the contribution of individua

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19

Zhang, Tianjiao, Rongjie Wang, Qinghua Jiang, and Yadong Wang. "An Information Gain-based Method for Evaluating the Classification Power of Features Towards Identifying Enhancers." Current Bioinformatics 15, no. 6 (2020): 574–80. http://dx.doi.org/10.2174/1574893614666191120141032.

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Background: Enhancers are cis-regulatory elements that enhance gene expression on DNA sequences. Since most of enhancers are located far from transcription start sites, it is difficult to identify them. As other regulatory elements, the regions around enhancers contain a variety of features, which can help in enhancer recognition. Objective: The classification power of features differs significantly, the performances of existing methods that use one or a few features for identifying enhancer vary greatly. Therefore, evaluating the classification power of each feature can improve the predictive

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20

Fernex, C., M. Capone, and P. Ferrier. "The V(D)J recombinational and transcriptional activities of the immunoglobulin heavy-chain intronic enhancer can be mediated through distinct protein-binding sites in a transgenic substrate." Molecular and Cellular Biology 15, no. 6 (1995): 3217–26. http://dx.doi.org/10.1128/mcb.15.6.3217.

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Immunoglobulin and T-cell receptor gene transcriptional enhancers encompass sequences which stimulate V(D)J recombination of associated variable gene segments. To address the question of whether enhancer-mediated transcriptional activation and recombinational activation depend on the same cis-regulatory sequences, we have produced transgenic mice by using recombination substrates containing various mutations in the immunoglobulin heavy-chain intronic enhancer (E mu). Analysis of substrate rearrangements indicated that specific compound elements including E-box transcriptional motifs are crucia

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21

Borczyk, Malgorzata, Mateusz Zieba, Michał Korostyński, and Marcin Piechota. "Role of Non-Coding Regulatory Elements in the Control of GR-Dependent Gene Expression." International Journal of Molecular Sciences 22, no. 8 (2021): 4258. http://dx.doi.org/10.3390/ijms22084258.

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The glucocorticoid receptor (GR, also known as NR3C1) coordinates molecular responses to stress. It is a potent transcription activator and repressor that influences hundreds of genes. Enhancers are non-coding DNA regions outside of the core promoters that increase transcriptional activity via long-distance interactions. Active GR binds to pre-existing enhancer sites and recruits further factors, including EP300, a known transcriptional coactivator. However, it is not known how the timing of GR-binding-induced enhancer remodeling relates to transcriptional changes. Here we analyze data from th

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22

Mulet-Lazaro, Roger, and Ruud Delwel. "From Genotype to Phenotype: How Enhancers Control Gene Expression and Cell Identity in Hematopoiesis." HemaSphere 7, no. 11 (2023): e969. http://dx.doi.org/10.1097/hs9.0000000000000969.

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Blood comprises a wide array of specialized cells, all of which share the same genetic information and ultimately derive from the same precursor, the hematopoietic stem cell (HSC). This diversity of phenotypes is underpinned by unique transcriptional programs gradually acquired in the process known as hematopoiesis. Spatiotemporal regulation of gene expression depends on many factors, but critical among them are enhancers—sequences of DNA that bind transcription factors and increase transcription of genes under their control. Thus, hematopoiesis involves the activation of specific enhancer rep

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Fenelon, Kelli D., Priyanshi Borad, Biraaj Rout, et al. "Su(H) Modulates Enhancer Transcriptional Bursting in Prelude to Gastrulation." Cells 13, no. 21 (2024): 1759. http://dx.doi.org/10.3390/cells13211759.

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Transcriptional regulation, orchestrated by the interplay between transcription factors (TFs) and enhancers, governs gene expression dynamics crucial for cellular processes. While gross qualitative fluctuations in transcription factor-dependent gene expression patterning have a long history of characterization, the roles of these factors in the nuclei retaining expression in the presence or absence of these factors are now observable using modern techniques. Our study investigates the impact of Suppressor of Hairless (Su(H)), a broadly expressed transcription factor, on enhancer-driven transcr

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Barshad, Gilad, and Charles G. Danko. "Revisiting models of enhancer–promoter communication in gene regulation." Genome Research 35, no. 6 (2025): 1277–86. https://doi.org/10.1101/gr.278389.123.

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Enhancer–promoter communication is fundamental to gene regulation in metazoans, yet the mechanisms underlying these interactions remain debated. Two primary models have been proposed: the structural bridge model, in which enhancers and promoters come into close proximity through stable, protein-mediated interactions, and the hub model, in which dynamic clusters of transcription-associated proteins facilitate communication over variable distances. Emerging evidence suggests that although enhancer–promoter pairs do come into close proximity during transcriptional activation, these interactions a

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Matthias, P., and D. Baltimore. "The immunoglobulin heavy chain locus contains another B-cell-specific 3' enhancer close to the alpha constant region." Molecular and Cellular Biology 13, no. 3 (1993): 1547–53. http://dx.doi.org/10.1128/mcb.13.3.1547-1553.1993.

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The transcription of immunoglobulin genes is controlled by variable region promoters and by enhancers, both of which are lymphoid specific. Because immunoglobulin genes are subject to an extremely complex regulation, we anticipated that there might be additional control elements for these genes. We therefore sought additional enhancers and demonstrate here that there is indeed another weak transcriptional enhancer just 3' to the mouse alpha constant region. This novel immunoglobulin enhancer is lymphoid specific and at two positions can bind members of the Oct family of transcription factors.

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Matthias, P., and D. Baltimore. "The immunoglobulin heavy chain locus contains another B-cell-specific 3' enhancer close to the alpha constant region." Molecular and Cellular Biology 13, no. 3 (1993): 1547–53. http://dx.doi.org/10.1128/mcb.13.3.1547.

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The transcription of immunoglobulin genes is controlled by variable region promoters and by enhancers, both of which are lymphoid specific. Because immunoglobulin genes are subject to an extremely complex regulation, we anticipated that there might be additional control elements for these genes. We therefore sought additional enhancers and demonstrate here that there is indeed another weak transcriptional enhancer just 3' to the mouse alpha constant region. This novel immunoglobulin enhancer is lymphoid specific and at two positions can bind members of the Oct family of transcription factors.

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Kim, Hee-Dae, Han Kyoung Choe, Sooyoung Chung, et al. "Class-C SOX Transcription Factors Control GnRH Gene Expression via the Intronic Transcriptional Enhancer." Molecular Endocrinology 25, no. 7 (2011): 1184–96. http://dx.doi.org/10.1210/me.2010-0332.

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Abstract GnRH is a pivotal hypothalamic neurohormone governing reproduction and sexual development. Because transcriptional regulation is crucial for the spatial and temporal expression of the GnRH gene, a region approximately 3.0 kb upstream of the mammalian GnRH promoter has been extensive studied. In the present study, we demonstrate a transcription-enhancer located in the first intron (intron A) region of the GnRH gene. This transcriptional enhancer harbors putative sex-determining region Y-related high-mobility-group box (SOX) family transcription factor-binding sites, which are well cons

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Quintero-Cadena, Porfirio, and Paul W. Sternberg. "Enhancer Sharing Promotes Neighborhoods of Transcriptional Regulation Across Eukaryotes." G3 Genes|Genomes|Genetics 6, no. 12 (2016): 4167–74. http://dx.doi.org/10.1534/g3.116.036228.

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Abstract Enhancers physically interact with transcriptional promoters, looping over distances that can span multiple regulatory elements. Given that enhancer–promoter (EP) interactions generally occur via common protein complexes, it is unclear whether EP pairing is predominantly deterministic or proximity guided. Here, we present cross-organismic evidence suggesting that most EP pairs are compatible, largely determined by physical proximity rather than specific interactions. By reanalyzing transcriptome datasets, we find that the transcription of gene neighbors is correlated over distances th

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Heist, Tyler, Takashi Fukaya, and Michael Levine. "Large distances separate coregulated genes in living Drosophila embryos." Proceedings of the National Academy of Sciences 116, no. 30 (2019): 15062–67. http://dx.doi.org/10.1073/pnas.1908962116.

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Transcriptional enhancers are short segments of DNA that switch genes on and off in response to a variety of cellular signals. Many enhancers map quite far from their target genes, on the order of tens or even hundreds of kilobases. There is extensive evidence that remote enhancers are brought into proximity with their target promoters via long-range looping interactions. However, the exact physical distances of these enhancer–promoter interactions remain uncertain. Here, we employ high-resolution imaging of living Drosophila embryos to visualize the distances separating linked genes that are

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Tan, Jennifer Y., Adriano Biasini, Robert S. Young, and Ana C. Marques. "Splicing of enhancer-associated lincRNAs contributes to enhancer activity." Life Science Alliance 3, no. 4 (2020): e202000663. http://dx.doi.org/10.26508/lsa.202000663.

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Transcription is common at active mammalian enhancers sometimes giving rise to stable enhancer-associated long intergenic noncoding RNAs (elincRNAs). Expression of elincRNA is associated with changes in neighboring gene product abundance and local chromosomal topology, suggesting that transcription at these loci contributes to gene expression regulation in cis. Despite the lack of evidence supporting sequence-dependent functions for most elincRNAs, splicing of these transcripts is unexpectedly common. Whether elincRNA splicing is a mere consequence of cognate enhancer activity or if it directl

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de Lara, Josué Cortés-Fernández, Rodrigo G. Arzate-Mejía, and Félix Recillas-Targa. "Enhancer RNAs: Insights Into Their Biological Role." Epigenetics Insights 12 (January 2019): 251686571984609. http://dx.doi.org/10.1177/2516865719846093.

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Enhancers play a central role in the transcriptional regulation of metazoans. Almost a decade ago, the discovery of their pervasive transcription into noncoding RNAs, termed enhancer RNAs (eRNAs), opened a whole new field of study. The presence of eRNAs correlates with enhancer activity; however, whether they act as functional molecules remains controversial. Here we review direct experimental evidence supporting a functional role of eRNAs in transcription and provide a general pipeline that could help in the design of experimental approaches to investigate the function of eRNAs. We propose th

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Göttgens, Berthold, Ian J. Donaldson, Michael Chapman, et al. "Genome-Wide Identification of Cis-Regulatory Sequences Controlling Blood and Endothelial Development." Blood 104, no. 11 (2004): 1616. http://dx.doi.org/10.1182/blood.v104.11.1616.1616.

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Abstract Haematopoiesis has long served as a paradigm for adult stem cell systems and studies over the last 20 years have established that transcriptional control is central to the specification and subsequent differentiation of haematopoietic stem cells (HSCs). With many of the key transcription factors known, haematopoiesis provides a powerful cellular system for the analysis of mammalian gene regulatory networks. The key missing ingredient, particularly for the stem and progenitor cell stages, is a set of experimentally validated gene regulatory regions together with a molecular understandi

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Hamdan, Feda H., and Steven A. Johnsen. "Perturbing Enhancer Activity in Cancer Therapy." Cancers 11, no. 5 (2019): 634. http://dx.doi.org/10.3390/cancers11050634.

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Tight regulation of gene transcription is essential for normal development, tissue homeostasis, and disease-free survival. Enhancers are distal regulatory elements in the genome that provide specificity to gene expression programs and are frequently misregulated in cancer. Recent studies examined various enhancer-driven malignant dependencies and identified different approaches to specifically target these programs. In this review, we describe numerous features that make enhancers good transcriptional targets in cancer therapy and discuss different approaches to overcome enhancer perturbation.

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Hah, Nasun, Chris Benner, Ling-Wa Chong, Ruth T. Yu, Michael Downes, and Ronald M. Evans. "Inflammation-sensitive super enhancers form domains of coordinately regulated enhancer RNAs." Proceedings of the National Academy of Sciences 112, no. 3 (2015): E297—E302. http://dx.doi.org/10.1073/pnas.1424028112.

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Enhancers are critical genomic elements that define cellular and functional identity through the spatial and temporal regulation of gene expression. Recent studies suggest that key genes regulating cell type-specific functions reside in enhancer-dense genomic regions (i.e., super enhancers, stretch enhancers). Here we report that enhancer RNAs (eRNAs) identified by global nuclear run-on sequencing are extensively transcribed within super enhancers and are dynamically regulated in response to cellular signaling. Using Toll-like receptor 4 (TLR4) signaling in macrophages as a model system, we fi

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Oltz, E. M., F. W. Alt, W. C. Lin, et al. "A V(D)J recombinase-inducible B-cell line: role of transcriptional enhancer elements in directing V(D)J recombination." Molecular and Cellular Biology 13, no. 10 (1993): 6223–30. http://dx.doi.org/10.1128/mcb.13.10.6223-6230.1993.

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Rapid analysis of mechanisms that regulate V(D)J recombination has been hampered by the lack of appropriate cell systems that reproduce aspects of normal prelymphocyte physiology in which the recombinase is activated, accessible antigen receptor loci are rearranged, and rearrangement status is fixed by termination of recombinase expression. To generate such a system, we introduced heat shock-inducible V(D)J recombination-activating genes (RAG) 1 and 2 into a recombinationally inert B-cell line. Heat shock treatment of these cells rapidly induced high levels of RAG transcripts and RAG proteins

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Oltz, E. M., F. W. Alt, W. C. Lin, et al. "A V(D)J recombinase-inducible B-cell line: role of transcriptional enhancer elements in directing V(D)J recombination." Molecular and Cellular Biology 13, no. 10 (1993): 6223–30. http://dx.doi.org/10.1128/mcb.13.10.6223.

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Rapid analysis of mechanisms that regulate V(D)J recombination has been hampered by the lack of appropriate cell systems that reproduce aspects of normal prelymphocyte physiology in which the recombinase is activated, accessible antigen receptor loci are rearranged, and rearrangement status is fixed by termination of recombinase expression. To generate such a system, we introduced heat shock-inducible V(D)J recombination-activating genes (RAG) 1 and 2 into a recombinationally inert B-cell line. Heat shock treatment of these cells rapidly induced high levels of RAG transcripts and RAG proteins

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Santiago-Algarra, David, Lan T. M. Dao, Lydie Pradel, Alexandre España, and Salvatore Spicuglia. "Recent advances in high-throughput approaches to dissect enhancer function." F1000Research 6 (June 19, 2017): 939. http://dx.doi.org/10.12688/f1000research.11581.1.

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The regulation of gene transcription in higher eukaryotes is accomplished through the involvement of transcription start site (TSS)-proximal (promoters) and -distal (enhancers) regulatory elements. It is now well acknowledged that enhancer elements play an essential role during development and cell differentiation, while genetic alterations in these elements are a major cause of human disease. Many strategies have been developed to identify and characterize enhancers. Here, we discuss recent advances in high-throughput approaches to assess enhancer activity, from the well-established massively

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Carullo, Nancy V. N., and Jeremy J. Day. "Genomic Enhancers in Brain Health and Disease." Genes 10, no. 1 (2019): 43. http://dx.doi.org/10.3390/genes10010043.

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Enhancers are non-coding DNA elements that function in cis to regulate transcription from nearby genes. Through direct interactions with gene promoters, enhancers give rise to spatially and temporally precise gene expression profiles in distinct cell or tissue types. In the brain, the accurate regulation of these intricate expression programs across different neuronal classes gives rise to an incredible cellular and functional diversity. Newly developed technologies have recently allowed more accurate enhancer mapping and more sophisticated enhancer manipulation, producing rapid progress in ou

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Wysocka, Joanna. "Enhancers and Transcriptional Regulation." Blood 128, no. 22 (2016): SCI—14—SCI—14. http://dx.doi.org/10.1182/blood.v128.22.sci-14.sci-14.

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Abstract Interactions between the genome and its cellular and signaling environments, which ultimately occur at the level of chromatin, are the key to comprehending how cell-type-specific gene expression patterns arise and are maintained during development or are misregulated in disease. Central to the cell type-specific transcriptional regulation are distal cis-regulatory elements called enhancers, which function in a modular way to provide exquisite spatiotemporal control of gene expression during development. We are using a combination of genomic, genetic, biochemical, and single-cell appro

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Smith, Alastair L., Nicholas Denny, Catherine M. Chahrour, et al. "Differential Gene Expression in KMT2A::AFF1 Leukemia Is Driven By Enhancer Heterogeneity." Blood 144, Supplement 1 (2024): 201. https://doi.org/10.1182/blood-2024-208035.

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Although genetic alterations drive carcinogenesis (PMID: 29439951), they alone cannot account for the diverse phenotypes of cancer cells. Even cancers with the same driver mutation show significant transcriptional heterogeneity and varied responses to therapy (PMID: 32807900). However, the mechanisms underpinning this heterogeneity remain under-explored. Aberrant enhancer activity is a hallmark of many cancers, including KMT2A::AFF1 acute lymphoblastic leukemia (ALL; PMID: 37626123), an aggressive leukemia subtype with a poor prognosis (PMID: 32376390) and a nearly mutationally silent genetic

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Kamps-Hughes, Nick, Jessica L. Preston, Melissa A. Randel, and Eric A. Johnson. "Genome-wide identification of hypoxia-induced enhancer regions." PeerJ 3 (December 21, 2015): e1527. http://dx.doi.org/10.7717/peerj.1527.

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Here we present a genome-wide method forde novoidentification of enhancer regions. This approach enables massively parallel empirical investigation of DNA sequences that mediate transcriptional activation and provides a platform for discovery of regulatory modules capable of driving context-specific gene expression. The method links fragmented genomic DNA to the transcription of randomer molecule identifiers and measures the functional enhancer activity of the library by massively parallel sequencing. We transfected aDrosophila melanogasterlibrary into S2 cells in normoxia and hypoxia, and ass

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Kropp, Kai A., Christian O. Simon, Annette Fink, et al. "Synergism between the components of the bipartite major immediate-early transcriptional enhancer of murine cytomegalovirus does not accelerate virus replication in cell culture and host tissues." Journal of General Virology 90, no. 10 (2009): 2395–401. http://dx.doi.org/10.1099/vir.0.012245-0.

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Major immediate-early (MIE) transcriptional enhancers of cytomegaloviruses are key regulators that are regarded as determinants of virus replicative fitness and pathogenicity. The MIE locus of murine cytomegalovirus (mCMV) shows bidirectional gene-pair architecture, with a bipartite enhancer flanked by divergent core promoters. Here, we have constructed recombinant viruses mCMV-ΔEnh1 and mCMV-ΔEnh2 to study the impact of either enhancer component on bidirectional MIE gene transcription and on virus replication in cell culture and various host tissues that are relevant to CMV disease. The data

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Xu, Liang, Ye Chen, Yulun Huang, et al. "Topography of transcriptionally active chromatin in glioblastoma." Science Advances 7, no. 18 (2021): eabd4676. http://dx.doi.org/10.1126/sciadv.abd4676.

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Molecular profiling of the most aggressive brain tumor glioblastoma (GBM) on the basis of gene expression, DNA methylation, and genomic variations advances both cancer research and clinical diagnosis. The enhancer architectures and regulatory circuitries governing tumor-intrinsic transcriptional diversity and subtype identity are still elusive. Here, by mapping H3K27ac deposition, we analyze the active regulatory landscapes across 95 GBM biopsies, 12 normal brain tissues, and 38 cell line counterparts. Analyses of differentially regulated enhancers and super-enhancers uncovered previously unre

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Ruby Dhar, Arun Kumar, and Subhradip Karmakar. "Enhancer hijacking: Innovative ways of carcinogenesis." Asian Journal of Medical Sciences 15, no. 9 (2024): 1–2. https://doi.org/10.71152/ajms.v15i9.4197.

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Enhancer elements are specific DNA sequences that play a crucial role in regulating gene expression. Located upstream or downstream in the genomic context, enhancers enhance the transcription of linked genes. This is achieved by providing binding sites for transcription factors and other proteins, acting as a nucleation point that promotes the assembly of the transcriptional machinery. What makes enhancers unique is that located even thousands of base pairs away, they can exert their function. They can act over long distances, looping to interact with the promoter region of their target genes.

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Ruby Dhar, Arun Kumar, and Subhradip Karmakar. "Enhancer hijacking: Innovative ways of carcinogenesis." Asian Journal of Medical Sciences 15, no. 9 (2024): 1–2. http://dx.doi.org/10.3126/ajms.v15i9.68519.

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Abstract:

Enhancer elements are specific DNA sequences that play a crucial role in regulating gene expression. Located upstream or downstream in the genomic context, enhancers enhance the transcription of linked genes. This is achieved by providing binding sites for transcription factors and other proteins, acting as a nucleation point that promotes the assembly of the transcriptional machinery. What makes enhancers unique is that located even thousands of base pairs away, they can exert their function. They can act over long distances, looping to interact with the promoter region of their target genes.

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Parmacek, M. S., H. S. Ip, F. Jung, et al. "A novel myogenic regulatory circuit controls slow/cardiac troponin C gene transcription in skeletal muscle." Molecular and Cellular Biology 14, no. 3 (1994): 1870–85. http://dx.doi.org/10.1128/mcb.14.3.1870-1885.1994.

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The slow/cardiac troponin C (cTnC) gene is expressed in three distinct striated muscle lineages: cardiac myocytes, embryonic fast skeletal myotubes, and adult slow skeletal myocytes. We have reported previously that cTnC gene expression in cardiac muscle is regulated by a cardiac-specific promoter/enhancer located in the 5' flanking region of the gene (bp -124 to +1). In this report, we demonstrate that the cTnC gene contains a second distinct and independent transcriptional enhancer which is located in the first intron. This second enhancer is skeletal myotube specific and is developmentally

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47

Parmacek, M. S., H. S. Ip, F. Jung, et al. "A novel myogenic regulatory circuit controls slow/cardiac troponin C gene transcription in skeletal muscle." Molecular and Cellular Biology 14, no. 3 (1994): 1870–85. http://dx.doi.org/10.1128/mcb.14.3.1870.

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The slow/cardiac troponin C (cTnC) gene is expressed in three distinct striated muscle lineages: cardiac myocytes, embryonic fast skeletal myotubes, and adult slow skeletal myocytes. We have reported previously that cTnC gene expression in cardiac muscle is regulated by a cardiac-specific promoter/enhancer located in the 5' flanking region of the gene (bp -124 to +1). In this report, we demonstrate that the cTnC gene contains a second distinct and independent transcriptional enhancer which is located in the first intron. This second enhancer is skeletal myotube specific and is developmentally

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Halfon, Marc S. "(Re)modeling the transcriptional enhancer." Nature Genetics 38, no. 10 (2006): 1102–3. http://dx.doi.org/10.1038/ng1006-1102.

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Fukaya, Takashi, Bomyi Lim, and Michael Levine. "Enhancer Control of Transcriptional Bursting." Cell 166, no. 2 (2016): 358–68. http://dx.doi.org/10.1016/j.cell.2016.05.025.

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Arthur, Robert K., Ningfei An, Saira Kahn, and Megan E. McNerney. "Enhancer-Promoter Looping Deciphers Dosage of the Haploinsufficient Transcription Factor, CUX1." Blood 128, no. 22 (2016): 2700. http://dx.doi.org/10.1182/blood.v128.22.2700.2700.

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Abstract One third of tumor suppressor genes encode haploinsufficient transcriptional regulators, including transcription factors and chromatin remodelers. This presents a major barrier in oncology, as tumor suppressor genes and transcription factors are inherently difficult to target therapeutically. It remains unknown how a 50% reduction of a transcriptional regulator translates at the cis-regulatory level into a malignant transcriptional program. It is imperative to address this question, in order to predict and target aberrant downstream pathways. CUX1 encodes a quintessential haploinsuffi

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