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Journal articles on the topic 'Transcription regulation model'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Geng, Yuncong, Christopher Herrick Bohrer, Nicolás Yehya, et al. "A spatially resolved stochastic model reveals the role of supercoiling in transcription regulation." PLOS Computational Biology 18, no. 9 (2022): e1009788. http://dx.doi.org/10.1371/journal.pcbi.1009788.

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In Escherichia coli, translocation of RNA polymerase (RNAP) during transcription introduces supercoiling to DNA, which influences the initiation and elongation behaviors of RNAP. To quantify the role of supercoiling in transcription regulation, we developed a spatially resolved supercoiling model of transcription. The integrated model describes how RNAP activity feeds back with the local DNA supercoiling and how this mechanochemical feedback controls transcription, subject to topoisomerase activities and stochastic topological domain formation. This model establishes that transcription-induced

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Asada, Ryuta, and Kouji Hirota. "Multi-Layered Regulations on the Chromatin Architectures: Establishing the Tight and Specific Responses of Fission Yeast fbp1 Gene Transcription." Biomolecules 12, no. 11 (2022): 1642. http://dx.doi.org/10.3390/biom12111642.

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Transcriptional regulation is pivotal for all living organisms and is required for adequate response to environmental fluctuations and intercellular signaling molecules. For precise regulation of transcription, cells have evolved regulatory systems on the genome architecture, including the chromosome higher-order structure (e.g., chromatin loops), location of transcription factor (TF)-binding sequences, non-coding RNA (ncRNA) transcription, chromatin configuration (e.g., nucleosome positioning and histone modifications), and the topological state of the DNA double helix. To understand how thes

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Carrera, Javier, Guillermo Rodrigo, and Alfonso Jaramillo. "Model-based redesign of global transcription regulation." Nucleic Acids Research 37, no. 5 (2009): e38-e38. http://dx.doi.org/10.1093/nar/gkp022.

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MJOLSNESS, ERIC. "ON COOPERATIVE QUASI-EQUILIBRIUM MODELS OF TRANSCRIPTIONAL REGULATION." Journal of Bioinformatics and Computational Biology 05, no. 02b (2007): 467–90. http://dx.doi.org/10.1142/s0219720007002874.

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Mechanistic models for transcriptional regulation are derived using the methods of equilibrium statistical mechanics, to model equilibrating processes that occur at a fast time scale. These processes regulate slower changes in the synthesis and expression of transcription factors that feed back and cooperatively regulate transcription, forming a gene regulation network (GRN). We rederive and extend two previous quasi-equilibrium models of transcriptional regulation, and demonstrate circumstances under which they can be approximated at each transcription complex by feed-forward artificial neura

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Akberdin, I. R., A. Yu Vertyshev, S. S. Pintus, D. V. Popov, and F. A. Kolpakov. "A Mathematical Model Linking Ca2+-Dependent Signaling Pathway and Gene Expression Regulation in Human Skeletal Muscle." Mathematical Biology and Bioinformatics 15, no. 1 (2020): 20–39. http://dx.doi.org/10.17537/2020.15.20.

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The physiological adaptation to aerobic endurance exercises is provided by activation of signaling pathways in skeletal muscle cells. Training-induced activation of specific signaling pathways results in significant transcriptional responses. Despite the ongoing endeavours to experimentally investigate regulatory mechanisms and signal transduction pathways involved in the contraction-induced adaptation, quantitative contribution of certain signal molecules in expression regulation of genes responsible for intracellular response has not been studied comprehensively yet. The paper presents novel

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Jackson, Kelly A., Ruth A. Valentine, Lisa J. Coneyworth, John C. Mathers, and Dianne Ford. "Mechanisms of mammalian zinc-regulated gene expression." Biochemical Society Transactions 36, no. 6 (2008): 1262–66. http://dx.doi.org/10.1042/bst0361262.

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Mechanisms through which gene expression is regulated by zinc are central to cellular zinc homoeostasis. In this context, evidence for the involvement of zinc dyshomoeostasis in the aetiology of diseases, including Type 2 diabetes, Alzheimer's disease and cancer, highlights the importance of zinc-regulated gene expression. Mechanisms elucidated in bacteria and yeast provide examples of different possible modes of zinc-sensitive gene regulation, involving the zinc-regulated binding of transcriptional activators and repressors to gene promoter regions. A mammalian transcriptional regulatory mech

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Murray, Philip J., Eleonore Ocana, Hedda A. Meijer, and Jacqueline Kim Dale. "Auto-Regulation of Transcription and Translation: Oscillations, Excitability and Intermittency." Biomolecules 11, no. 11 (2021): 1566. http://dx.doi.org/10.3390/biom11111566.

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Several members of the Hes/Her family, conserved targets of the Notch signalling pathway, encode transcriptional repressors that dimerise, bind DNA and self-repress. Such autoinhibition of transcription can yield homeostasis and, in the presence of delays that account for processes such as transcription, splicing and transport, oscillations. Whilst previous models of autoinhibition of transcription have tended to treat processes such as translation as being unregulated (and hence linear), here we develop and explore a mathematical model that considers autoinhibition of transcription together w

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TUĞRUL, MURAT, and ALKAN KABAKÇIOĞLU. "ROBUSTNESS OF TRANSCRIPTIONAL REGULATION IN YEAST-LIKE MODEL BOOLEAN NETWORKS." International Journal of Bifurcation and Chaos 20, no. 03 (2010): 929–35. http://dx.doi.org/10.1142/s0218127410026228.

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We investigate the dynamical properties of the transcriptional regulation of gene expression in the yeast Saccharomyces Cerevisiae within the framework of a synchronously and deterministically updated Boolean network model. With a dynamically determinant subnetwork, we explore the robustness of transcriptional regulation as a function of the type of Boolean functions used in the model that mimic the influence of regulating agents on the transcription level of a gene. We compare the results obtained for the actual yeast network with those from two different model networks, one with similar in-d

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Huang, Gang, Shannon Elf, Xiaomei Yan, et al. "Previously Unknown Interactions Between AML1 and MLL Provide Epigenetic Regulation of Gene Expression in Normal Hematopoiesis and in Leukemia." Blood 112, no. 11 (2008): 282. http://dx.doi.org/10.1182/blood.v112.11.282.282.

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Abstract In all organisms, the fundamental process of transcriptional regulation requires transcription factors, which bind to DNA in response to extra-cellular signals and regulate transcription of target genes. In eukaryotes, this process also involves epigenetic regulation, which includes DNA and histone modifications. Hematopoiesis and leukemia are excellent model systems for studying the higher eukaryotic regulations of gene expression and for identifying important molecules involved in genetic and epigenetic transcriptional regulation. The Mixed-Lineage Leukemia (MLL) protein, a Set1-lik

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Ahmed, Mahmoud, Trang Huyen Lai, Trang Minh Pham, et al. "Hierarchical regulation of autophagy during adipocyte differentiation." PLOS ONE 17, no. 1 (2022): e0250865. http://dx.doi.org/10.1371/journal.pone.0250865.

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We previously showed that some adipogenic transcription factors such as CEBPB and PPARG directly and indirectly regulate autophagy gene expression in adipogenesis. The order and effect of these events are undetermined. In this study, we modeled the gene expression, DNA-binding of transcriptional regulators, and histone modifications during adipocyte differentiation and evaluated the effect of the regulators on gene expression in terms of direction and magnitude. Then, we identified the overlap of the transcription factors and co-factors binding sites and targets. Finally, we built a chromatin

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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 (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 st

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12

Wang, Guohua, Fang Wang, Qian Huang, Yu Li, Yunlong Liu, and Yadong Wang. "Understanding Transcription Factor Regulation by Integrating Gene Expression and DNase I Hypersensitive Sites." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/757530.

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Transcription factors are proteins that bind to DNA sequences to regulate gene transcription. The transcription factor binding sites are short DNA sequences (5–20 bp long) specifically bound by one or more transcription factors. The identification of transcription factor binding sites and prediction of their function continue to be challenging problems in computational biology. In this study, by integrating the DNase I hypersensitive sites with known position weight matrices in the TRANSFAC database, the transcription factor binding sites in gene regulatory region are identified. Based on the

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Choi, Seung H., Leslie Lupien, Adam N. Boynton, Pratiti Bandopadhayay, and John R. Prensner. "MDB-38. AN INTEGRATED MODEL FOR RESISTANCE TO BROMODOMAIN INHIBITORS IN CHILDHOOD MEDULLOBLASTOMA." Neuro-Oncology 26, Supplement_4 (2024): 0. http://dx.doi.org/10.1093/neuonc/noae064.487.

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Abstract BACKGROUND Bromodomain inhibitors (BETi) have emerged as a potential treatment option for children with medulloblastoma, where hyperactivation of gene transcription by the MYC and MYCN transcription factors may lead to a transcriptional dependency. Yet, drug resistance limits the utility of these agents when employed as a monotherapy. We therefore sought to identify mechanisms of BETi resistance that inform rational development of multimodal therapy options. METHODS We used CRISPR screening of D458 medulloblastoma cells that have acquired resistance to the JQ1 inhibitor. We subsequent

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Valin, A., and G. Gill. "Regulation of the dual-function transcription factor Sp3 by SUMO." Biochemical Society Transactions 35, no. 6 (2007): 1393–96. http://dx.doi.org/10.1042/bst0351393.

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In eukaryotes, gene expression is controlled by a relatively small number of regulators. Post-translational modifications dramatically increase the functional possibilities of those regulators. Modification of many transcription factors and cofactors by SUMO (small ubiquitin-related modifier) correlates, in most cases, with inhibition of transcription. Recent studies suggest a model whereby SUMO conjugation to transcription factors promotes the recruitment of co-repressors through direct protein–protein interaction with the SUMO protein. HDACs (histone deacetylases) are important, but not excl

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Chen, Cai, and Ralf Bundschuh. "Quantitative models for accelerated protein dissociation from nucleosomal DNA." Nucleic Acids Research 42, no. 15 (2014): 9753–60. http://dx.doi.org/10.1093/nar/gku719.

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Abstract Binding of transcription factors to their binding sites in promoter regions is the fundamental event in transcriptional gene regulation. When a transcription factor binding site is located within a nucleosome, the DNA has to partially unwrap from the nucleosome to allow transcription factor binding. This reduces the rate of transcription factor binding and is a known mechanism for regulation of gene expression via chromatin structure. Recently a second mechanism has been reported where transcription factor off-rates are dramatically increased when binding to target sites within the nu

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Almawi, WY, and OK Melemedjian. "Negative regulation of nuclear factor-kappaB activation and function by glucocorticoids." Journal of Molecular Endocrinology 28, no. 2 (2002): 69–78. http://dx.doi.org/10.1677/jme.0.0280069.

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Glucocorticoids (GCs) exert their anti-inflammatory and antiproliferative effects principally by inhibiting the expression of cytokines and adhesion molecules. Mechanistically, GCs diffuse through the cell membrane, and bind to their inactive cytosolic receptors (GRs), which then undergo conformational modifications that allow for their nuclear translocation. In the nucleus, activated GRs modulate transcriptional events by directly associating with DNA elements, compatible with the GCs response elements (GRE) motif, and located in variable copy numbers and at variable distances from the TATA b

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Yu, Helen, Nazar Mashtalir, Salima Daou, et al. "The Ubiquitin Carboxyl Hydrolase BAP1 Forms a Ternary Complex with YY1 and HCF-1 and Is a Critical Regulator of Gene Expression." Molecular and Cellular Biology 30, no. 21 (2010): 5071–85. http://dx.doi.org/10.1128/mcb.00396-10.

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ABSTRACT The candidate tumor suppressor BAP1 is a deubiquitinating enzyme (DUB) involved in the regulation of cell proliferation, although the molecular mechanisms governing its function remain poorly defined. BAP1 was recently shown to interact with and deubiquitinate the transcriptional regulator host cell factor 1 (HCF-1). Here we show that BAP1 assembles multiprotein complexes containing numerous transcription factors and cofactors, including HCF-1 and the transcription factor Yin Yang 1 (YY1). Through its coiled-coil motif, BAP1 directly interacts with the zinc fingers of YY1. Moreover, H

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Hume, David A. "Probability in transcriptional regulation and its implications for leukocyte differentiation and inducible gene expression." Blood 96, no. 7 (2000): 2323–28. http://dx.doi.org/10.1182/blood.v96.7.2323.

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Abstract The phenotype of individual hematopoietic cells, like all other differentiated mammalian cells, is determined by selective transcription of a subset of the genes encoded within the genome. This overview summarizes the recent evidence that transcriptional regulation at the level of individual cells is best described in terms of the regulation of the probability of transcription rather than the rate. In this model, heterogeneous gene expression among populations of cells arises by chance, and the degree of heterogeneity is a function of the stability of the mRNA and protein products of

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Hume, David A. "Probability in transcriptional regulation and its implications for leukocyte differentiation and inducible gene expression." Blood 96, no. 7 (2000): 2323–28. http://dx.doi.org/10.1182/blood.v96.7.2323.h8002323_2323_2328.

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The phenotype of individual hematopoietic cells, like all other differentiated mammalian cells, is determined by selective transcription of a subset of the genes encoded within the genome. This overview summarizes the recent evidence that transcriptional regulation at the level of individual cells is best described in terms of the regulation of the probability of transcription rather than the rate. In this model, heterogeneous gene expression among populations of cells arises by chance, and the degree of heterogeneity is a function of the stability of the mRNA and protein products of individua

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El Houdaigui, Bilal, Raphaël Forquet, Thomas Hindré, et al. "Bacterial genome architecture shapes global transcriptional regulation by DNA supercoiling." Nucleic Acids Research 47, no. 11 (2019): 5648–57. http://dx.doi.org/10.1093/nar/gkz300.

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Abstract DNA supercoiling acts as a global transcriptional regulator in bacteria, that plays an important role in adapting their expression programme to environmental changes, but for which no quantitative or even qualitative regulatory model is available. Here, we focus on spatial supercoiling heterogeneities caused by the transcription process itself, which strongly contribute to this regulation mode. We propose a new mechanistic modeling of the transcription-supercoiling dynamical coupling along a genome, which allows simulating and quantitatively reproducing in vitro and in vivo transcript

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KUBORI, Tomoko, and Nobuo SHIMAMOTO. "A new model for transcription initiation and its regulation." Seibutsu Butsuri 37, no. 6 (1997): 249–53. http://dx.doi.org/10.2142/biophys.37.249.

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Sarnataro, Sergio, Andrea Riba, and Nacho Molina. "Regulation of transcription reactivation dynamics exiting mitosis." PLOS Computational Biology 17, no. 10 (2021): e1009354. http://dx.doi.org/10.1371/journal.pcbi.1009354.

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Proliferating cells experience a global reduction of transcription during mitosis, yet their cell identity is maintained and regulatory information is propagated from mother to daughter cells. Mitotic bookmarking by transcription factors has been proposed as a potential mechanism to ensure the reactivation of transcription at the proper set of genes exiting mitosis. Recently, mitotic transcription and waves of transcription reactivation have been observed in synchronized populations of human hepatoma cells. However, the study did not consider that mitotic-arrested cell populations progressivel

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Valley, Christopher C., Raphaël Métivier, Natalia M. Solodin та ін. "Differential Regulation of Estrogen-Inducible Proteolysis and Transcription by the Estrogen Receptor α N Terminus". Molecular and Cellular Biology 25, № 13 (2005): 5417–28. http://dx.doi.org/10.1128/mcb.25.13.5417-5428.2005.

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ABSTRACT The ubiquitin-proteasome pathway has emerged as an important regulatory mechanism governing the activity of several transcription factors. While estrogen receptor α (ERα) is also subjected to rapid ubiquitin-proteasome degradation, the relationship between proteolysis and transcriptional regulation is incompletely understood. Based on studies primarily focusing on the C-terminal ligand-binding and AF-2 transactivation domains, an assembly of an active transcriptional complex has been proposed to signal ERα proteolysis that is in turn necessary for its transcriptional activity. Here, w

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Najnin, Tanzira, Sakhawat Hossain Saimon, Garry Sunter, and Jianhua Ruan. "A Network-Based Approach for Improving Annotation of Transcription Factor Functions and Binding Sites in Arabidopsis thaliana." Genes 14, no. 2 (2023): 282. http://dx.doi.org/10.3390/genes14020282.

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Transcription factors are an integral component of the cellular machinery responsible for regulating many biological processes, and they recognize distinct DNA sequence patterns as well as internal/external signals to mediate target gene expression. The functional roles of an individual transcription factor can be traced back to the functions of its target genes. While such functional associations can be inferred through the use of binding evidence from high-throughput sequencing technologies available today, including chromatin immunoprecipitation sequencing, such experiments can be resource-

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Jenkins, Dafyd J., and Dov J. Stekel. "A New Model for Investigating the Evolution of Transcription Control Networks." Artificial Life 15, no. 3 (2009): 259–91. http://dx.doi.org/10.1162/artl.2009.stekel.006.

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Biological systems show unbounded capacity for complex behaviors and responses to their environments. This principally arises from their genetic networks. The processes governing transcription, translation, and gene regulation are well understood, as are the mechanisms of network evolution, such as gene duplication and horizontal gene transfer. However, the evolved networks arising from these simple processes are much more difficult to understand, and it is difficult to perform experiments on the evolution of these networks in living organisms because of the timescales involved. We propose a n

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Neuert, Gregor, Brian Munsky, Rui Zhen Tan, Leonid Teytelman, Mustafa Khammash, and Alexander van Oudenaarden. "Systematic Identification of Signal-Activated Stochastic Gene Regulation." Science 339, no. 6119 (2013): 584–87. http://dx.doi.org/10.1126/science.1231456.

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Although much has been done to elucidate the biochemistry of signal transduction and gene regulatory pathways, it remains difficult to understand or predict quantitative responses. We integrate single-cell experiments with stochastic analyses, to identify predictive models of transcriptional dynamics for the osmotic stress response pathway inSaccharomyces cerevisiae. We generate models with varying complexity and use parameter estimation and cross-validation analyses to select the most predictive model. This model yields insight into several dynamical features, including multistep regulation a

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Guissouma, Hajer, Nathalie Becker, Isabelle Seugnet, and Barbara A. Demeneix. "Transcriptional repression of TRH promoter function by T3: analysis by in vivo gene transfer." Biochemistry and Cell Biology 78, no. 3 (2000): 155–63. http://dx.doi.org/10.1139/o00-009.

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We consider how an integrated in vivo model can be used to study the specific transcriptional effects of specific receptors in neuroendocrine systems. Our example is the role of thyroid receptor (TR) isoforms in mediating negative feedback effects of T3 on TRH (thyrotropin releasing hormone) expression. The in vivo transfection method employed polyethylenimine (PEI) to introduce genes directly into specifc regions of the brains of mice, rats, and Xenopus tadpoles. In the mouse model, the technique has served to examine TR effects on TRH transcription and on the pituitary-thyroid axis end point

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Feng, Zijie, Jian Ma, and Xianxin Hua. "Epigenetic regulation by the menin pathway." Endocrine-Related Cancer 24, no. 10 (2017): T147—T159. http://dx.doi.org/10.1530/erc-17-0298.

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There is a trend of increasing prevalence of neuroendocrine tumors (NETs), and the inherited multiple endocrine neoplasia type 1 (MEN1) syndrome serves as a genetic model to investigate how NETs develop and the underlying mechanisms. Menin, encoded by the MEN1 gene, at least partly acts as a scaffold protein by interacting with multiple partners to regulate cellular homeostasis of various endocrine organs. Menin has multiple functions including regulation of several important signaling pathways by controlling gene transcription. Here, we focus on reviewing the recent progress in elucidating th

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Clayton, Christine. "Regulation of gene expression in trypanosomatids: living with polycistronic transcription." Open Biology 9, no. 6 (2019): 190072. http://dx.doi.org/10.1098/rsob.190072.

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In trypanosomes, RNA polymerase II transcription is polycistronic and individual mRNAs are excised by trans -splicing and polyadenylation. The lack of individual gene transcription control is compensated by control of mRNA processing, translation and degradation. Although the basic mechanisms of mRNA decay and translation are evolutionarily conserved, there are also unique aspects, such as the existence of six cap-binding translation initiation factor homologues, a novel decapping enzyme and an mRNA stabilizing complex that is recruited by RNA-binding proteins. High-throughput analyses have id

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Zhang, Xiaowen, and Rong Li. "BRCA1-Dependent Transcriptional Regulation: Implication in Tissue-Specific Tumor Suppression." Cancers 10, no. 12 (2018): 513. http://dx.doi.org/10.3390/cancers10120513.

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Germ-line mutations in breast cancer susceptibility gene 1 (BRCA1) predominantly predispose women to breast and ovarian cancers. BRCA1 is best known for its functions in maintenance of genomic integrity including repairing DNA double-strand breaks through homologous recombination and suppressing DNA replication stress. However, whether these universally important BRCA1 functions in maintenance of genomic stability are sufficient to account for its tissue-specific tumor-suppressing function remains unclear. Accumulating evidence indicates that there are previously underappreciated roles of BRCA

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Ngondo, Richard Patryk, and Philippe Carbon. "Transcription factor abundance controlled by an auto-regulatory mechanism involving a transcription start site switch." Nucleic Acids Research 42, no. 4 (2013): 2171–84. http://dx.doi.org/10.1093/nar/gkt1136.

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Abstract A transcriptional feedback loop is the simplest and most direct means for a transcription factor to provide an increased stability of gene expression. In this work performed in human cells, we reveal a new negative auto-regulatory mechanism involving an alternative transcription start site (TSS) usage. Using the activating transcription factor ZNF143 as a model, we show that the ZNF143 low-affinity binding sites, located downstream of its canonical TSS, play the role of protein sensors to induce the up- or down-regulation of ZNF143 gene expression. We uncovered that the TSS switch tha

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Duren, Zhana, Xi Chen, Rui Jiang, Yong Wang, and Wing Hung Wong. "Modeling gene regulation from paired expression and chromatin accessibility data." Proceedings of the National Academy of Sciences 114, no. 25 (2017): E4914—E4923. http://dx.doi.org/10.1073/pnas.1704553114.

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The rapid increase of genome-wide datasets on gene expression, chromatin states, and transcription factor (TF) binding locations offers an exciting opportunity to interpret the information encoded in genomes and epigenomes. This task can be challenging as it requires joint modeling of context-specific activation of cis-regulatory elements (REs) and the effects on transcription of associated regulatory factors. To meet this challenge, we propose a statistical approach based on paired expression and chromatin accessibility (PECA) data across diverse cellular contexts. In our approach, we model (

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Zhu, Chunjuan, Guosheng Han, and Feng Jiao. "Dynamical Regulation of mRNA Distribution by Cross-Talking Signaling Pathways." Complexity 2020 (June 17, 2020): 1–11. http://dx.doi.org/10.1155/2020/6402703.

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Gene transcription is a random process in single cells manifested by the observed distribution of mRNA copy numbers in homogeneous cell populations. A central question is to understand how mRNA distribution is modulated under environmental changes. In this work, we initiate a theoretical study on mRNA distribution dynamics for the stochastic transcription model that involves cross-talking signaling pathways to direct gene activation in response to external signals. We first express the distribution in mathematical dynamical formulas under both moderate and high transcriptional upregulations. I

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Friedman, AD, BL Krieder, D. Venturelli, and G. Rovera. "Transcriptional regulation of two myeloid-specific genes, myeloperoxidase and lactoferrin, during differentiation of the murine cell line 32D C13." Blood 78, no. 9 (1991): 2426–32. http://dx.doi.org/10.1182/blood.v78.9.2426.bloodjournal7892426.

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The transcriptional regulation of myeloperoxidase (MPO) and lactoferrin (LF) was examined during terminal myeloid differentiation of the murine cell line 32D C13. The rates of transcription initiation for MPO and LF, determined by an in vitro nuclear run-on assay, increased approximately ninefold. The accumulation of MPO mRNA in 32D C13 cells, determined by Northern blot analysis, correlated temporally with the observed increase in MPO transcription initiation. On the other hand, accumulation of LF mRNA lagged behind the observed increase in LF transcription initiation. In mouse L cells, the L

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Ard, Penny G., Chandrima Chatterjee, Sudeesha Kunjibettu, Leon R. Adside, Lisa E. Gralinski, and Steven B. McMahon. "Transcriptional Regulation of the mdm2 Oncogene by p53 Requires TRRAP Acetyltransferase Complexes." Molecular and Cellular Biology 22, no. 16 (2002): 5650–61. http://dx.doi.org/10.1128/mcb.22.16.5650-5661.2002.

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ABSTRACT The p53 tumor suppressor regulates the cellular response to genetic damage through its function as a sequence-specific transcription factor. Among the most well-characterized transcriptional targets of p53 is the mdm2 oncogene. Activation of mdm2 is critical in the p53 pathway because the mdm2 protein marks p53 for proteosome-mediated degradation, thereby providing a negative-feedback loop. Here we show that the ATM-related TRRAP protein functionally cooperates with p53 to activate mdm2 transcription. TRRAP is a component of several multiprotein acetyltransferase complexes implicated

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Fukayama, S., B. Lanske, J. Guo, H. M. Kronenberg, and F. R. Bringhurst. "Regulation of HSP70 by PTH: a model of gene regulation not mediated by changes in cAMP levels." American Journal of Physiology-Cell Physiology 271, no. 1 (1996): C121—C129. http://dx.doi.org/10.1152/ajpcell.1996.271.1.c121.

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Parathyroid hormone (PTH) activates both adenylate cyclase and phospholipase C in target cells, and cloned PTH/PTH-related protein (PTHrP) receptor can mediate both responses when expressed in host cells such as LLC-PK1 renal epithelial cells. Because calcitonin (CT) is known to augment 70-kDa heat shock protein (HSP70) mRNA by an adenosine 3',5'-cyclic monophosphate (cAMP)-independent mechanism in LLC-PK1 cells, we examined regulation of HSP70 transcription by PTH in these cells. Like CT, human PTH-(1-34) [hPTH-(1-34); 10(-10) to 10(-7) M)] increased porcine HSP70 mRNA and human HSP70 promote

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Swillens, S., and I. Pirson. "Highly sensitive control of transcriptional activity by factor heterodimerization." Biochemical Journal 301, no. 1 (1994): 9–12. http://dx.doi.org/10.1042/bj3010009.

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Several molecular mechanisms have been proposed to explain highly sensitive controls of cellular functions by effector molecules. Here we study an equilibrium model describing the regulation of transcriptional activity through the heterodimerization of transcription factors. We demonstrate that this model involves a new type of biochemical control which accounts for a very high sensitivity.

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Saha, Karabi, and Wenfeng An. "Abstract A013: Transcription initiation and its regulation in mouse L1s." Cancer Immunology Research 12, no. 10_Supplement (2024): A013. http://dx.doi.org/10.1158/2326-6074.tumimm24-a013.

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Abstract Long interspersed elements type 1 (LINE-1s or L1s) are highly abundant non-LTR retrotransposons in mammalian genomes. Apart from an evolutionary role in altering the genomic landscape and gene expression, recent discoveries have revealed the scale and impact of active movement by L1, both in the germline and in somatic niches (e.g., the brain and many cancers). As transcriptional activation is a prerequisite for L1 retrotransposition, it is important to understand how L1 transcription is regulated. L1 transcription is controlled by an internal promoter contained in the 5’ untranslated

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Thalheim, Torsten, Lydia Hopp, Hans Binder, Gabriela Aust, and Joerg Galle. "On the Cooperation between Epigenetics and Transcription Factor Networks in the Specification of Tissue Stem Cells." Epigenomes 2, no. 4 (2018): 20. http://dx.doi.org/10.3390/epigenomes2040020.

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It is generally accepted that epigenetic modifications, such as DNA and histone methylations, affect transcription and that a gene’s transcription feeds back on its epigenetic profile. Depending on the epigenetic modification, positive and negative feedback loops have been described. Here, we study whether such interrelation are mandatory and how transcription factor networks affect it. We apply self-organizing map machine learning to a published data set on the specification and differentiation of murine intestinal stem cells in order to provide an integrative view of gene transcription and D

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Kot, Alexander, Zhendong A. Zhong, Hongliang Zhang, Yu-An Evan Lay, Nancy E. Lane, and Wei Yao. "Sex dimorphic regulation of osteoprogenitor progesterone in bone stromal cells." Journal of Molecular Endocrinology 59, no. 4 (2017): 351–63. http://dx.doi.org/10.1530/jme-17-0076.

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Increasing peak bone mass is a promising strategy to prevent osteoporosis. A mouse model of global progesterone receptor (PR) ablation showed increased bone mass through a sex-dependent mechanism. Cre-Lox recombination was used to generate a mouse model of osteoprogenitor-specific PR inactivation, which recapitulated the high bone mass phenotype seen in the PR global knockout mouse mode. In this work, we employed RNA sequencing analysis to evaluate sex-independent and sex-dependent differences in gene transcription of osteoprogenitors of wild-type and PR conditional knockout mice. PR deletion

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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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Sparling, David P., Beth A. Griesel, and Ann Louise Olson. "Hyperphosphorylation of MEF2A in primary adipocytes correlates with downregulation of human GLUT4 gene promoter activity." American Journal of Physiology-Endocrinology and Metabolism 292, no. 4 (2007): E1149—E1156. http://dx.doi.org/10.1152/ajpendo.00521.2006.

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GLUT4 promoter activity is regulated by hormonal, metabolic, and tissue-specific controls. This complicates the study of GLUT4 gene transcription, as no cell culture model adequately recapitulates these extracellular regulators. While investigating cultured primary adipocytes as a model system for GLUT4 transcription, we observed that GLUT4 mRNA was specifically and rapidly downregulated upon tissue dispersal. Downregulation of GLUT4 mRNA was mediated in part by loss of regulatory control by the trans-acting factors that control GLUT4 transcriptional activity [the myocyte enhancer factor 2 (ME

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Friedman, AD, BL Krieder, D. Venturelli, and G. Rovera. "Transcriptional regulation of two myeloid-specific genes, myeloperoxidase and lactoferrin, during differentiation of the murine cell line 32D C13." Blood 78, no. 9 (1991): 2426–32. http://dx.doi.org/10.1182/blood.v78.9.2426.2426.

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Abstract The transcriptional regulation of myeloperoxidase (MPO) and lactoferrin (LF) was examined during terminal myeloid differentiation of the murine cell line 32D C13. The rates of transcription initiation for MPO and LF, determined by an in vitro nuclear run-on assay, increased approximately ninefold. The accumulation of MPO mRNA in 32D C13 cells, determined by Northern blot analysis, correlated temporally with the observed increase in MPO transcription initiation. On the other hand, accumulation of LF mRNA lagged behind the observed increase in LF transcription initiation. In mouse L cel

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Lin, Jianhong, Tint Lwin, Jianjun Zhao, et al. "Follicular Dendritic Cell (FDC)-Induced Microrna-Mediated up-Regulation of PRDM1 and Down-Regulation of BCL6 in Germinal Center B Lymphocytes: A Potential Mechanism for B-Cell Differentiation." Blood 114, no. 22 (2009): 4588. http://dx.doi.org/10.1182/blood.v114.22.4588.4588.

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Abstract Abstract 4588 B-cell differentiation process is tightly regulated by suppression or induction of specific transcription factors. Among various transcriptional regulators, BCL6 and PRDM-1 are master regulators for germinal center (GC) formation and terminal B-cell differentiation. Dysregulation of BCL6 and PRDM-1 have been associated with lymphomagenesis. However how these transcription factors are regulated and what determines their expression are unclear. Given that follicular dendritic cells (FDC) closely interact with B cells within the GC, provide survival signal to protect B cell

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Bunn, H. F., J. Gu, L. E. Huang, J. W. Park, and H. Zhu. "Erythropoietin: a model system for studying oxygen-dependent gene regulation." Journal of Experimental Biology 201, no. 8 (1998): 1197–201. http://dx.doi.org/10.1242/jeb.201.8.1197.

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The physiological regulation of the red cell mass depends upon enhanced transcription of the erythropoietin (Epo) gene in response to hypoxia. Studies of Epo gene expression have been useful in investigating the mechanism by which cells and tissues sense hypoxia and respond with biologically appropriate alterations in gene expression. It is likely that oxygen sensing involves a heme protein in which cobalt and nickel can substitute for iron in the porphyrin ring. Indirect evidence suggests that the sensor is present in all cells and is a multi-subunit assembly containing an NAD(P)H oxidase cap

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Borsook, D., and S. E. Hyman. "Proenkephalin gene regulation in the neuroendocrine hypothalamus: a model of gene regulation in the CNS." American Journal of Physiology-Endocrinology and Metabolism 269, no. 3 (1995): E393—E408. http://dx.doi.org/10.1152/ajpendo.1995.269.3.e393.

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During the past decade, a great deal of progress has been made in studying the mechanisms by which transcription of neuropeptides is regulated by second messengers and neural activity. Such investigations, which have depended to a great extent on the use of transformed cell lines, are far from complete. Yet a major challenge for the coming decade is to understand the regulation of neuropeptide genes by physiologically and pharmacologically relevant stimuli in appropriate cell types in vivo. The proenkephalin gene, a member of the opioid gene family, has served as a model to study regulated tra

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Guo, Haitao, and Hongwei Huo. "A New Algorithm for Identifying Cis-Regulatory Modules Based on Hidden Markov Model." BioMed Research International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/6274513.

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The discovery of cis-regulatory modules (CRMs) is the key to understanding mechanisms of transcription regulation. Since CRMs have specific regulatory structures that are the basis for the regulation of gene expression, how to model the regulatory structure of CRMs has a considerable impact on the performance of CRM identification. The paper proposes a CRM discovery algorithm called ComSPS. ComSPS builds a regulatory structure model of CRMs based on HMM by exploring the rules of CRM transcriptional grammar that governs the internal motif site arrangement of CRMs. We test ComSPS on three benchm

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Cejas, Pedro J., Louise M. Carlson, Despina Kolonias, et al. "Regulation of RelB Expression during the Initiation of Dendritic Cell Differentiation." Molecular and Cellular Biology 25, no. 17 (2005): 7900–7916. http://dx.doi.org/10.1128/mcb.25.17.7900-7916.2005.

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ABSTRACT The transcription factor RelB is required for proper development and function of dendritic cells (DCs), and its expression is upregulated early during differentiation from a variety of progenitors. We explored this mechanism of upregulation in the KG1 cell line model of a DC progenitor and in the differentiation-resistant KG1a subline. RelB expression is relatively higher in untreated KG1a cells but is upregulated only during differentiation of KG1 by an early enhancement of transcriptional elongation, followed by an increase in transcription initiation. Restoration of protein kinase

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Jung, Hyun Jun, Viswanathan Raghuram, Jae Wook Lee та Mark A. Knepper. "Genome-Wide Mapping of DNA Accessibility and Binding Sites for CREB and C/EBPβ in Vasopressin-Sensitive Collecting Duct Cells". Journal of the American Society of Nephrology 29, № 5 (2018): 1490–500. http://dx.doi.org/10.1681/asn.2017050545.

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Background Renal water excretion is controlled by vasopressin, in part through regulation of the transcription of the aquaporin-2 gene (Aqp2).Methods To identify enhancer regions likely to be involved in the regulation of Aqp2 and other principal cell–specific genes, we used several next generation DNA-sequencing techniques in a well characterized cultured cell model of collecting duct principal cells (mpkCCD). To locate enhancers, we performed the assay for transposase-accessible chromatin using sequencing (ATAC-Seq) to identify accessible regions of DNA and integrated the data with data gene

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Pluta, Aneta, Juan P. Jaworski, and César N. Cortés-Rubio. "Balance between Retroviral Latency and Transcription: Based on HIV Model." Pathogens 10, no. 1 (2020): 16. http://dx.doi.org/10.3390/pathogens10010016.

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The representative of the Lentivirus genus is the human immunodeficiency virus type 1 (HIV-1), the causative agent of acquired immunodeficiency syndrome (AIDS). To date, there is no cure for AIDS because of the existence of the HIV-1 reservoir. HIV-1 infection can persist for decades despite effective antiretroviral therapy (ART), due to the persistence of infectious latent viruses in long-lived resting memory CD4+ T cells, macrophages, monocytes, microglial cells, and other cell types. However, the biology of HIV-1 latency remains incompletely understood. Retroviral long terminal repeat regio

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