Journal articles: 'Non transcriptional'

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Ray, J. Christian J., Jeffrey J. Tabor, and Oleg A. Igoshin. "Non-transcriptional regulatory processes shape transcriptional network dynamics." Nature Reviews Microbiology 9, no. 11 (October 11, 2011): 817–28. http://dx.doi.org/10.1038/nrmicro2667.

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Swami, Meera. "Non-cooperative transcriptional control." Nature Reviews Genetics 11, no. 4 (March 2, 2010): 240. http://dx.doi.org/10.1038/nrg2768.

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Hokello, Joseph, Adhikarimayum Lakhikumar Sharma, and Mudit Tyagi. "Efficient Non-Epigenetic Activation of HIV Latency through the T-Cell Receptor Signalosome." Viruses 12, no. 8 (August 8, 2020): 868. http://dx.doi.org/10.3390/v12080868.

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Human immunodeficiency virus type-1 (HIV-1) can either undergo a lytic pathway to cause productive systemic infections or enter a latent state in which the integrated provirus remains transcriptionally silent for decades. The ability to latently infect T-cells enables HIV-1 to establish persistent infections in resting memory CD4+ T-lymphocytes which become reactivated following the disruption or cessation of intensive drug therapy. The maintenance of viral latency occurs through epigenetic and non-epigenetic mechanisms. Epigenetic mechanisms of HIV latency regulation involve the deacetylation and methylation of histone proteins within nucleosome 1 (nuc-1) at the viral long terminal repeats (LTR) such that the inhibition of histone deacetyltransferase and histone lysine methyltransferase activities, respectively, reactivates HIV from latency. Non-epigenetic mechanisms involve the nuclear restriction of critical cellular transcription factors such as nuclear factor-kappa beta (NF-κB) or nuclear factor of activated T-cells (NFAT) which activate transcription from the viral LTR, limiting the nuclear levels of the viral transcription transactivator protein Tat and its cellular co-factor positive transcription elongation factor b (P-TEFb), which together regulate HIV transcriptional elongation. In this article, we review how T-cell receptor (TCR) activation efficiently induces NF-κB, NFAT, and activator protein 1 (AP-1) transcription factors through multiple signal pathways and how these factors efficiently regulate HIV LTR transcription through the non-epigenetic mechanism. We further discuss how elongation factor P-TEFb, induced through an extracellular signal-regulated kinase (ERK)-dependent mechanism, regulates HIV transcriptional elongation before new Tat is synthesized and the role of AP-1 in the modulation of HIV transcriptional elongation through functional synergy with NF-κB. Furthermore, we discuss how TCR signaling induces critical post-translational modifications of the cyclin-dependent kinase 9 (CDK9) subunit of P-TEFb which enhances interactions between P-TEFb and the viral Tat protein and the resultant enhancement of HIV transcriptional elongation.

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Steensels, Sandra, Jixuan Qiao, and Baran A. Ersoy. "Transcriptional Regulation in Non-Alcoholic Fatty Liver Disease." Metabolites 10, no. 7 (July 9, 2020): 283. http://dx.doi.org/10.3390/metabo10070283.

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Obesity is the primary risk factor for the pathogenesis of non-alcoholic fatty liver disease (NAFLD), the worldwide prevalence of which continues to increase dramatically. The liver plays a pivotal role in the maintenance of whole-body lipid and glucose homeostasis. This is mainly mediated by the transcriptional activation of hepatic pathways that promote glucose and lipid production or utilization in response to the nutritional state of the body. However, in the setting of chronic excessive nutrition, the dysregulation of hepatic transcriptional machinery promotes lipid accumulation, inflammation, metabolic stress, and fibrosis, which culminate in NAFLD. In this review, we provide our current understanding of the transcription factors that have been linked to the pathogenesis and progression of NAFLD. Using publicly available transcriptomic data, we outline the altered activity of transcription factors among humans with NAFLD. By expanding this analysis to common experimental mouse models of NAFLD, we outline the relevance of mouse models to the human pathophysiology at the transcriptional level.

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Ježek, Jan, Daniel G. J. Smethurst, David C. Stieg, Z. A. C. Kiss, Sara E. Hanley, Vidyaramanan Ganesan, Kai-Ti Chang, Katrina F. Cooper, and Randy Strich. "Cyclin C: The Story of a Non-Cycling Cyclin." Biology 8, no. 1 (January 4, 2019): 3. http://dx.doi.org/10.3390/biology8010003.

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The class I cyclin family is a well-studied group of structurally conserved proteins that interact with their associated cyclin-dependent kinases (Cdks) to regulate different stages of cell cycle progression depending on their oscillating expression levels. However, the role of class II cyclins, which primarily act as transcription factors and whose expression remains constant throughout the cell cycle, is less well understood. As a classic example of a transcriptional cyclin, cyclin C forms a regulatory sub-complex with its partner kinase Cdk8 and two accessory subunits Med12 and Med13 called the Cdk8-dependent kinase module (CKM). The CKM reversibly associates with the multi-subunit transcriptional coactivator complex, the Mediator, to modulate RNA polymerase II-dependent transcription. Apart from its transcriptional regulatory function, recent research has revealed a novel signaling role for cyclin C at the mitochondria. Upon oxidative stress, cyclin C leaves the nucleus and directly activates the guanosine 5’-triphosphatase (GTPase) Drp1, or Dnm1 in yeast, to induce mitochondrial fragmentation. Importantly, cyclin C-induced mitochondrial fission was found to increase sensitivity of both mammalian and yeast cells to apoptosis. Here, we review and discuss the biology of cyclin C, focusing mainly on its transcriptional and non-transcriptional roles in tumor promotion or suppression.

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O'Gorman, William, Kon Yew Kwek, Benjamin Thomas, and Alexandre Akoulitchev. "Non-coding RNA in transcription initiation." Biochemical Society Symposia 73 (January 1, 2006): 131–40. http://dx.doi.org/10.1042/bss0730131.

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Diverse classes of non-coding RNAs, including snRNAs (small nuclear RNAs), play fundamental regulatory roles in gene expression. For example, 7SK RNA and the components of the splicing apparatus U1–U6 snRNAs are implicated in the regulation of transcriptional elongation. The first evidence for the involvement of RNA in the regulation of transcriptional initiation is now emerging. TFIIH (transcription factor IIH), a general transcription initiation factor, appears to associate specifically with U1 snRNA, a core splicing component. Reconstituted transcription in vitro demonstrates an increase in the rate of formation of the first phosphodiester bond by RNA polymerase II in presence of U1 snRNA. Reconstituted re-initiation is also stimulated by U1 snRNA. These results suggest that U1 snRNA functions in the regulation of transcription by RNA polymerase II in addition to its role in RNA processing. The implications of these data extend to the development of new technologies that will allow the identification and analysis of diverse RNA species present as regulatory components in transcription-related ribonucleoprotein complexes.

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Poulat, Francis. "Non-Coding Genome, Transcription Factors, and Sex Determination." Sexual Development 15, no. 5-6 (2021): 295–307. http://dx.doi.org/10.1159/000519725.

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In vertebrates, gonadal sex determination is the process by which transcription factors drive the choice between the testicular and ovarian identity of undifferentiated somatic progenitors through activation of 2 different transcriptional programs. Studies in animal models suggest that sex determination always involves sex-specific transcription factors that activate or repress sex-specific genes. These transcription factors control their target genes by recognizing their regulatory elements in the non-coding genome and their binding motifs within their DNA sequence. In the last 20 years, the development of genomic approaches that allow identifying all the genomic targets of a transcription factor in eukaryotic cells gave the opportunity to globally understand the function of the nuclear proteins that control complex genetic programs. Here, the major transcription factors involved in male and female vertebrate sex determination and the genomic profiling data of mouse gonads that contributed to deciphering their transcriptional regulation role will be reviewed.

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Genini, Davide, Ramon Garcia-Escudero, Giuseppina M. Carbone, and Carlo V. Catapano. "Transcriptional and Non-Transcriptional Functions of PPARβ/δ in Non-Small Cell Lung Cancer." PLoS ONE 7, no. 9 (September 25, 2012): e46009. http://dx.doi.org/10.1371/journal.pone.0046009.

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Bouget, François-Yves, Marc Lefranc, Quentin Thommen, Benjamin Pfeuty, Jean-Claude Lozano, Philippe Schatt, Hugo Botebol, and Valérie Vergé. "Transcriptional versus non-transcriptional clocks: A case study in Ostreococcus." Marine Genomics 14 (April 2014): 17–22. http://dx.doi.org/10.1016/j.margen.2014.01.004.

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Chattopadhyay, Saurabh, Gayatri Subramanian, Ying Zhang, Manoj Veleeparambil, and Ganes C. Sen. "Transcriptional and non-transcriptional functions of IRF3 in host defense." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 203.3. http://dx.doi.org/10.4049/jimmunol.198.supp.203.3.

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Abstract Innate immune response is the first line of host defense against microbial infection. Interferon Regulatory Factor 3 (IRF3), a critical transcription factor, is rapidly activated during virus infection to trigger numerous antiviral genes, including the interferons. Our studies have revealed that in addition to triggering these genes, IRF3 activates direct apoptosis of virus-infected cells by a newly discovered antiviral apoptotic pathway, RIPA (Chattopadhyay et al, Immunity 2016, EMBO J, 2010). In RIPA, IRF3 is differentially modified by linear polyubiquitination of two lysine residues. Moreover, a knock-in mouse strain, without the transcriptional activity of IRF3, can still mount antiviral response by its RIPA branch. Importantly, the use of pathway-specific mutants of IRF3 revealed that both transcriptional, and RIPA, branches contribute to the overall antiviral functions of IRF3. To investigate the contribution of the transcriptional branch of IRF3, we screened a shRNA library of the human ISGs. Our screen identified a small subset of novel IRF3-dependent genes, which exhibit antiviral functions in human and mouse cells. These newly-identified ISGs are protective against a wide range of clinically relevant human viruses, e.g. RSV, HPIV3, HSV-1, HCMV. In-depth investigation revealed that these ISGs regulate cellular autophagy pathway to control virus replication. The presentation will highlight how both pathways of IRF3 mount an optimum host response against viral as well as non-viral pathogenesis.

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Ali, Amjad, Ritu Mishra, Harsimrut Kaur, and Akhil Chandra Banerjea. "HIV-1 Tat: An update on transcriptional and non-transcriptional functions." Biochimie 190 (November 2021): 24–35. http://dx.doi.org/10.1016/j.biochi.2021.07.001.

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Dykes, Iain M., and Costanza Emanueli. "Transcriptional and Post-transcriptional Gene Regulation by Long Non-coding RNA." Genomics, Proteomics & Bioinformatics 15, no. 3 (June 2017): 177–86. http://dx.doi.org/10.1016/j.gpb.2016.12.005.

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van Ooijen, Gerben, and Andrew J. Millar. "Non-transcriptional oscillators in circadian timekeeping." Trends in Biochemical Sciences 37, no. 11 (November 2012): 484–92. http://dx.doi.org/10.1016/j.tibs.2012.07.006.

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14

Chen, Yung-Chia Ariel, and Alexei A. Aravin. "Non-coding RNAs in Transcriptional Regulation." Current Molecular Biology Reports 1, no. 1 (February 17, 2015): 10–18. http://dx.doi.org/10.1007/s40610-015-0002-6.

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Carvalho Barbosa, Cristina, Sydnee H. Calhoun, and Hans-Joachim Wieden. "Non-coding RNAs: what are we missing?" Biochemistry and Cell Biology 98, no. 1 (February 2020): 23–30. http://dx.doi.org/10.1139/bcb-2019-0037.

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Over the past two decades, the importance of small non-coding RNAs (sncRNAs) as regulatory molecules has become apparent in all three domains of life (archaea, bacteria, eukaryotes). In fact, sncRNAs play an important role in the control of gene expression at both the transcriptional and the post-transcriptional level, with crucial roles in fine-tuning cell responses during internal and external stress. Multiple pathways for sncRNA biogenesis and diverse mechanisms of regulation have been reported, and although biogenesis and mechanisms of sncRNAs in prokaryotes and eukaryotes are different, remarkable similarities exist. Here, we briefly review and compare the major sncRNA classes that act post-transcriptionally, and focus on recent discoveries regarding the ribosome as a target of regulation and the conservation of these mechanisms between prokaryotes and eukaryotes.

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Hernández-Lemus, Enrique, and María D. Correa-Rodríguez. "Non-Equilibrium Hyperbolic Transport in Transcriptional Regulation." PLoS ONE 6, no. 7 (July 6, 2011): e21558. http://dx.doi.org/10.1371/journal.pone.0021558.

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Barrandon, Charlotte, Béatrice Spiluttini, and Olivier Bensaude. "Non-coding RNAs regulating the transcriptional machinery." Biology of the Cell 100, no. 2 (February 2008): 83–95. http://dx.doi.org/10.1042/bc20070090.

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Feng, Yan-Ling, Jian-Min Dong, and Xu-Lei Tang. "Non-Markovian Effect on Gene Transcriptional Systems." Chinese Physics Letters 33, no. 10 (October 2016): 108701. http://dx.doi.org/10.1088/0256-307x/33/10/108701.

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Strähle, Uwe, and Sepand Rastegar. "Conserved non-coding sequences and transcriptional regulation." Brain Research Bulletin 75, no. 2-4 (March 2008): 225–30. http://dx.doi.org/10.1016/j.brainresbull.2007.11.010.

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Wong, David CS, and John S. O’Neill. "Non-transcriptional processes in circadian rhythm generation." Current Opinion in Physiology 5 (October 2018): 117–32. http://dx.doi.org/10.1016/j.cophys.2018.10.003.

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Jang, Sang-Min, Joo-Hee An, Chul-Hong Kim, Jung-Woong Kim, and Kyung-Hee Choi. "Transcription factor FOXA2-centered transcriptional regulation network in non-small cell lung cancer." Biochemical and Biophysical Research Communications 463, no. 4 (August 2015): 961–67. http://dx.doi.org/10.1016/j.bbrc.2015.06.042.

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Kanai, K., and K. Kataoka. "P128. Phosphorylations regulate transcriptional and non-transcriptional activity of MafA in oncogenic transformation." Differentiation 80 (November 2010): S60. http://dx.doi.org/10.1016/j.diff.2010.09.134.

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Azuma, Kotaro, and Satoshi Inoue. "Genomic and non-genomic actions of estrogen: recent developments." BioMolecular Concepts 3, no. 4 (August 1, 2012): 365–70. http://dx.doi.org/10.1515/bmc-2012-0002.

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AbstractEstrogen affects transcriptional status by activating its corresponding nuclear receptor, the estrogen receptor (ER). It can also induce rapid cellular reactions within a few minutes, and this feature cannot be explained by the transcription-mediated effects of estrogen. The latter mechanisms are called ‘non-genomic actions’ of estrogen. In contrast, the former classic modes of action came to be called ‘genomic actions’. One of the recent developments of research on estrogen was the substantiation of the non-genomic actions of estrogen; these were initially observed and reported as intriguing phenomena more than 40 years ago. The interacting molecules as well as the biological significance of non-genomic actions have now been shown. In the field of genomic actions, invention and spread of new technologies, including high-throughput sequencers, promoted a comprehensive view of estrogen-mediated transcriptional regulation.

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Groh, Matthias, Lara Marques Silva, and Natalia Gromak. "Mechanisms of transcriptional dysregulation in repeat expansion disorders." Biochemical Society Transactions 42, no. 4 (August 1, 2014): 1123–28. http://dx.doi.org/10.1042/bst20140049.

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Approximately 40 human diseases are associated with expansion of repeat sequences. These expansions can reside within coding or non-coding parts of the genes, affecting the host gene function. The presence of such expansions results in the production of toxic RNA and/or protein or causes transcriptional repression and silencing of the host gene. Although the molecular mechanisms of expansion diseases are not well understood, mounting evidence suggests that transcription through expanded repeats plays an essential role in disease pathology. The presence of an expansion can affect RNA polymerase transcription, leading to dysregulation of transcription-associated processes, such as RNA splicing, formation of RNA/DNA hybrids (R-loops), production of antisense, short non-coding and bidirectional RNA transcripts. In the present review, we summarize current advances in this field and discuss possible roles of transcriptional defects in disease pathology.

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Sadka, Avi, Qiaoping Qin, Jianrong Feng, Macarena Farcuh, Lyudmila Shlizerman, Yunting Zhang, David Toubiana, and Eduardo Blumwald. "Ethylene Response of Plum ACC Synthase 1 (ACS1) Promoter is Mediated through the Binding Site of Abscisic Acid Insensitive 5 (ABI5)." Plants 8, no. 5 (May 2, 2019): 117. http://dx.doi.org/10.3390/plants8050117.

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The enzyme 1-amino-cyclopropane-1-carboxylic acid synthase (ACS) participates in the ethylene biosynthesis pathways and it is tightly regulated transcriptionally and post-translationally. Notwithstanding its major role in climacteric fruit ripening, the transcriptional regulation of ACS during ripening is not fully understood. We studied fruit ripening in two Japanese plum cultivars, the climacteric Santa Rosa (SR) and its non-climacteric bud sport mutant, Sweet Miriam (SM). As the two cultivars show considerable difference in ACS expression, they provide a good system for the study of the transcriptional regulation of the gene. To investigate the differential transcriptional regulation of ACS1 genes in the SR and SM, their promoter regions, which showed only minor sequence differences, were isolated and used to identify the binding of transcription factors interacting with specific ACS1 cis-acting elements. Three transcription factors (TFs), abscisic acid-insensitive 5 (ABI5), GLABRA 2 (GL2), and TCP2, showed specific binding to the ACS1 promoter. Synthetic DNA fragments containing multiple cis-acting elements of these TFs fused to β-glucuronidase (GUS), showed the ABI5 binding site mediated ethylene and abscisic acid (ABA) responses of the promoter. While TCP2 and GL2 showed constant and similar expression levels in SM and SR fruit during ripening, ABI5 expression in SM fruits was lower than in SR fruits during advanced fruit ripening states. Overall, the work demonstrates the complex transcriptional regulation of ACS1.

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Ma, Qiuqin, Shihui Long, Zhending Gan, Gianluca Tettamanti, Kang Li, and Ling Tian. "Transcriptional and Post-Transcriptional Regulation of Autophagy." Cells 11, no. 3 (January 27, 2022): 441. http://dx.doi.org/10.3390/cells11030441.

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Autophagy is a widely conserved process in eukaryotes that is involved in a series of physiological and pathological events, including development, immunity, neurodegenerative disease, and tumorigenesis. It is regulated by nutrient deprivation, energy stress, and other unfavorable conditions through multiple pathways. In general, autophagy is synergistically governed at the RNA and protein levels. The upstream transcription factors trigger or inhibit the expression of autophagy- or lysosome-related genes to facilitate or reduce autophagy. Moreover, a significant number of non-coding RNAs (microRNA, circRNA, and lncRNA) are reported to participate in autophagy regulation. Finally, post-transcriptional modifications, such as RNA methylation, play a key role in controlling autophagy occurrence. In this review, we summarize the progress on autophagy research regarding transcriptional regulation, which will provide the foundations and directions for future studies on this self-eating process.

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Buist, Marjorie, David Fuss, and Mojgan Rastegar. "Transcriptional Regulation of MECP2E1-E2 Isoforms and BDNF by Metformin and Simvastatin through Analyzing Nascent RNA Synthesis in a Human Brain Cell Line." Biomolecules 11, no. 8 (August 22, 2021): 1253. http://dx.doi.org/10.3390/biom11081253.

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Methyl CpG binding protein 2 (MeCP2) is the main DNA methyl-binding protein in the brain that binds to 5-methylcytosine and 5-hydroxymethyl cytosine. MECP2 gene mutations are the main origin of Rett Syndrome (RTT), a neurodevelopmental disorder in young females. The disease has no existing cure, however, metabolic drugs such as metformin and statins have recently emerged as potential therapeutic candidates. In addition, induced MECP2-BDNF homeostasis regulation has been suggested as a therapy avenue. Here, we analyzed nascent RNA synthesis versus steady state total cellular RNA to study the transcriptional effects of metformin (an anti-diabetic drug) on MECP2 isoforms (E1 and E2) and BNDF in a human brain cell line. Additionally, we investigated the impact of simvastatin (a cholesterol lowering drug) on transcriptional regulation of MECP2E1/E2-BDNF. Metformin was capable of post-transcriptionally inducing BDNF and/or MECP2E1, while transcriptionally inhibiting MECP2E2. In contrast simvastatin significantly inhibited BDNF transcription without significantly impacting MECP2E2 transcripts. Further analysis of ribosomal RNA transcripts confirmed that the drug neither individually nor in combination affected these fundamentally important transcripts. Experimental analysis was completed in conditions of the presence or absence of serum starvation that showed minimal impact for serum deprival, although significant inhibition of steady state MECP2E1 by simvastatin was only detected in non-serum starved cells. Taken together, our results suggest that metformin controls MECP2E1/E2-BDNF transcriptionally and/or post-transcriptionally, and that simvastatin is a potent transcriptional inhibitor of BDNF. The transcriptional effect of these drugs on MECP2E1/E2-BDNF were not additive under these tested conditions, however, either drug may have potential application for related disorders.

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Simoncini, T., and AR Genazzani. "Non-genomic actions of sex steroid hormones." European Journal of Endocrinology 148, no. 3 (March 1, 2003): 281–92. http://dx.doi.org/10.1530/eje.0.1480281.

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Steroid hormone receptors have been traditionally considered to act via the regulation of transcriptional processes, involving nuclear translocation and binding to specific response elements, and ultimately leading to regulation of gene expression. However, novel non-transcriptional mechanisms of signal transduction through steroid hormone receptors have been identified. These so-called 'non-genomic' effects do not depend on gene transcription or protein synthesis and involve steroid-induced modulation of cytoplasmic or cell membrane-bound regulatory proteins. Several relevant biological actions of steroids have been associated with this kind of signaling. Ubiquitous regulatory cascades such as mitogen-activated protein kinases, the phosphatidylinositol 3-OH kinase and tyrosine kinases are modulated through non-transcriptional mechanisms by steroid hormones. Furthermore, steroid hormone receptor modulation of cell membrane-associated molecules such as ion channels and G-protein-coupled receptors has been shown. TIssues traditionally considered as 'non-targets' for classical steroid actions are instead found to be vividly regulated by non-genomic mechanisms. To this aim, the cardiovascular and the central nervous system provide excellent examples, where steroid hormones induce rapid vasodilatation and neuronal survival via non-genomic mechanisms, leading to relevant pathophysiological consequences. The evidence collected in the past Years indicates that target cells and organs are regulated by a complex interplay of genomic and non-genomic signaling mechanisms of steroid hormones, and the integrated action of these machineries has important functional roles in a variety of pathophysiological processes. The understanding of the molecular basis of the rapid effects of steroids is therefore important, and may in the future turn out to be of relevance for clinical purposes.

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Sen, Rwik, Shivani Malik, Sarah Frankland-Searby, Bhawana Uprety, Shweta Lahudkar, and Sukesh R. Bhaumik. "Rrd1p, an RNA polymerase II-specific prolyl isomerase and activator of phosphoprotein phosphatase, promotes transcription independently of rapamycin response." Nucleic Acids Research 42, no. 15 (August 11, 2014): 9892–907. http://dx.doi.org/10.1093/nar/gku703.

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Abstract Rrd1p (resistance to rapamycin deletion 1) has been previously implicated in controlling transcription of rapamycin-regulated genes in response to rapamycin treatment. Intriguingly, we show here that Rrd1p associates with the coding sequence of a galactose-inducible and rapamycin non-responsive GAL1 gene, and promotes the association of RNA polymerase II with GAL1 in the absence of rapamycin treatment following transcriptional induction. Consistently, nucleosomal disassembly at GAL1 is impaired in the absence of Rrd1p, and GAL1 transcription is reduced in the Δrrd1 strain. Likewise, Rrd1p associates with the coding sequences of other rapamycin non-responsive and inducible GAL genes to promote their transcription in the absence of rapamycin treatment. Similarly, inducible, but rapamycin-responsive, non-GAL genes such as CTT1, STL1 and CUP1 are also regulated by Rrd1p. However, transcription of these inducible GAL and non-GAL genes is not altered in the absence of Rrd1p when the steady-state is reached after long transcriptional induction. Consistently, transcription of the constitutively active genes is not changed in the Δrrd1 strain. Taken together, our results demonstrate a new function of Rrd1p in stimulation of initial rounds of transcription, but not steady-state/constitutive transcription, of both rapamycin-responsive and non-responsive genes independently of rapamycin treatment.

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Khoram, Somayeh A. H., and Huzwah Khaza’ai. "Transcriptional and Non-transcriptional Regulation of Glucose Metabolism and Insulin Sensitivity through Vitamin D." Current Nutrition & Food Science 17, no. 6 (June 9, 2021): 575–82. http://dx.doi.org/10.2174/1573401317666210111105905.

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Enormous progress in the investigation of vitamin D is currently being made from the perspective of basic science to clinical medicine. The typical view of vitamin D function limited to calcium metabolism and bone homeostasis has undergone extensive revision and it has been revealed that vitamin D receptors exist in most tissues of the body. Nowadays, one of the most popular aspects of vitamin D in research area is its role in glucose metabolism and insulin resistance. The functional mechanism of vitamin D in metabolism includes genomic and rapid non-genomic actions that are discussed in this review. Briefly, the modulatory action of vitamin D in the gene expression of insulin signaling compartments and secretion of insulin hormone may point to its role in the pathogenesis and development of type II diabetes. Vitamin D induced activation of the PI3K/AKT pathway is through PTEN-mediated AKT downregulation. Also, allelic variations in VDR and DBP might affect insulin secretion and diabetes occurrence. Vitamin D influences insulin secretion from β-cell through calcium-dependent endopeptidases, which promotes the conversion of pro-insulin to insulin; hence it can be declared that calcium and vitamin D are essential for insulin exocytosis. Hypovitaminosis D in obese individuals is also associated with higher levels of serum parathormone, through which this secondary hyperparathyroidism probably contributes to insulin resistance associated with obesity. Moreover, vitamin D is an immune modulator that may affect inflammation as a contributor to diabetes.

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Speidel, D., H. Helmbold, and W. Deppert. "Dissection of transcriptional and non-transcriptional p53 activities in the response to genotoxic stress." Oncogene 25, no. 6 (October 10, 2005): 940–53. http://dx.doi.org/10.1038/sj.onc.1209126.

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Xu, Jun, Jenny Chong, and Dong Wang. "Strand-specific effect of Rad26 and TFIIS in rescuing transcriptional arrest by CAG trinucleotide repeat slip-outs." Nucleic Acids Research 49, no. 13 (July 1, 2021): 7618–27. http://dx.doi.org/10.1093/nar/gkab573.

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Abstract Transcription induced CAG repeat instability is associated with fatal neurological disorders. Genetic approaches found transcription-coupled nucleotide excision repair (TC-NER) factor CSB protein and TFIIS play critical roles in modulating the repeat stability. Here, we took advantage of an in vitro reconstituted yeast transcription system to investigate the underlying mechanism of RNA polymerase II (Pol II) transcriptional pausing/stalling by CAG slip-out structures and the functions of TFIIS and Rad26, the yeast ortholog of CSB, in modulating transcriptional arrest. We identified length-dependent and strand-specific mechanisms that account for CAG slip-out induced transcriptional arrest. We found substantial R-loop formation for the distal transcriptional pausing induced by template strand (TS) slip-out, but not non-template strand (NTS) slip-out. In contrast, Pol II backtracking was observed at the proximal transcriptional pausing sites induced by both NTS and TS slip-out blockage. Strikingly, we revealed that Rad26 and TFIIS can stimulate bypass of NTS CAG slip-out, but not TS slip-out induced distal pausing. Our biochemical results provide new insights into understanding the mechanism of CAG slip-out induced transcriptional pausing and functions of transcription factors in modulating transcription-coupled CAG repeat instability, which may pave the way for developing potential strategies for the treatment of repeat sequence associated human diseases.

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LI, Yuting, Huan HAN, Jiabao YE, Feng XU, Weiwei ZHANG, and Yongling LIAO. "Regulation mechanism of long non-coding RNA in plant secondary metabolite biosynthesis." Notulae Botanicae Horti Agrobotanici Cluj-Napoca 50, no. 2 (May 23, 2022): 12604. http://dx.doi.org/10.15835/nbha50212604.

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Long non-coding RNAs (lncRNAs) are widely available transcription products of more than 200 nucleotides with unrecognizable coding potential. A large number of lncRNAs have been identified in different plants. lncRNAs are involved in various basic biological processes at the transcriptional, post-transcriptional and epigenetic levels as key regulatory molecules, including in the regulation of flowering time and reproductive organ morphogenesis, and they play important roles in the biosynthesis of plant secondary metabolites. In this paper, we review the research strategies of lncRNAs and lncRNAs related to the biosynthesis of plant secondary metabolites, focusing on the research strategies for studying lncRNAs and the effects of lncRNAs on the biosynthesis of terpenoids, alkaloids and flavonoids, aiming to provide new ideas for the study of the regulation of plant secondary metabolite biosynthesis.

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Escher, Felicitas, Ganna Aleshcheva, Heiko Pietsch, Christian Baumeier, Ulrich M. Gross, Benedikt Norbert Schrage, Dirk Westermann, Claus-Thomas Bock, and Heinz-Peter Schultheiss. "Transcriptional Active Parvovirus B19 Infection Predicts Adverse Long-Term Outcome in Patients with Non-Ischemic Cardiomyopathy." Biomedicines 9, no. 12 (December 14, 2021): 1898. http://dx.doi.org/10.3390/biomedicines9121898.

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Parvovirus B19 (B19V) is the predominant cardiotropic virus currently found in endomyocardial biopsies (EMBs). However, direct evidence showing a causal relationship between B19V and progression of inflammatory cardiomyopathy are still missing. The aim of this study was to analyze the impact of transcriptionally active cardiotropic B19V infection determined by viral RNA expression upon long-term outcomes in a large cohort of adult patients with non-ischemic cardiomyopathy in a retrospective analysis from a prospective observational cohort. In total, the analyzed study group comprised 871 consecutive B19V-positive patients (mean age 50.0 ± 15.0 years) with non-ischemic cardiomyopathy who underwent EMB. B19V-positivity was ascertained by routine diagnosis of viral genomes in EMBs. Molecular analysis of EMB revealed positive B19V transcriptional activity in n = 165 patients (18.9%). Primary endpoint was all-cause mortality in the overall cohort. The patients were followed up to 60 months. On the Cox regression analysis, B19V transcriptional activity was predictive of a worse prognosis compared to those without actively replicating B19V (p = 0.01). Moreover, multivariable analysis revealed transcriptional active B19V combined with inflammation [hazard ratio 4.013, 95% confidence interval 1.515–10.629 (p = 0.005)] as the strongest predictor of impaired survival even after adjustment for age and baseline LVEF (p = 0.005) and independently of viral load. The study demonstrates for the first time the pathogenic clinical importance of B19V with transcriptional activity in a large cohort of patients. Transcriptionally active B19V infection is an unfavourable prognostic trigger of adverse outcome. Our findings are of high clinical relevance, indicating that advanced diagnostic differentiation of B19V positive patients is of high prognostic importance.

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Burenina, O. Y., T. S. Oretskaya, and E. A. Kubareva. "Non-coding RNAs As Transcriptional Regulators In Eukaryotes." Acta Naturae 9, no. 4 (December 1, 2017): 13–25. http://dx.doi.org/10.32607/2075-8251-2017-9-4-13-25.

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Burenina, O. Yu, T. S. Oretskaya, and E. A. Kubareva. "Non-coding RNAs As Transcriptional Regulators In Eukaryotes." Acta Naturae 9, no. 4 (December 15, 2017): 13–25. http://dx.doi.org/10.32607/20758251-2017-9-4-13-25.

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Non-coding RNAs up to 1,000 nucleotides in length are widespread in eukaryotes and fulfil various regulatory functions, in particular during chromatin remodeling and cell proliferation. These RNAs are not translated into proteins: thus, they are non-coding RNAs (ncRNAs). The present review describes the eukaryotic ncRNAs involved in transcription regulation, first and foremost, targeting RNA polymerase II (RNAP II) and/or its major proteinaceous transcription factors. The current state of knowledge concerning the regulatory functions of SRA and TAR RNA, 7SK and U1 snRNA, GAS5 and DHFR RNA is summarized herein. Special attention is given to murine B1 and B2 RNAs and human Alu RNA, due to their ability to bind the active site of RNAP II. Discovery of bacterial analogs of the eukaryotic small ncRNAs involved in transcription regulation, such as 6S RNAs, suggests that they possess a common evolutionary origin.

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Burenina, O. Y., T. S. Oretskaya, and E. A. Kubareva. "Non-coding RNAs As Transcriptional Regulators In Eukaryotes." Acta Naturae 9, no. 4 (December 1, 2017): 13–25. http://dx.doi.org/10.32607/2075851-2017-9-4-13-25.

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Cheng, Shuting, Zhou Jiang, Zhengrong Wang, and Germaine Cornelissen. "Non-transcriptional/translational regulations of the circadian system." Biological Rhythm Research 46, no. 4 (March 23, 2015): 471–81. http://dx.doi.org/10.1080/09291016.2015.1020203.

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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 (April 20, 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 the ENCODE project that provides ChIP-Seq and RNA-Seq data at distinct time points after dexamethasone exposure of human A549 epithelial-like cell line. This study aimed to investigate the temporal interplay between GR binding, enhancer remodeling, and gene expression. By investigating a single distal GR-binding site for each differentially upregulated gene, we show that transcriptional changes follow GR binding, and that the largest enhancer remodeling coincides in time with the highest gene expression changes. A detailed analysis of the time course showed that for upregulated genes, enhancer activation persists after gene expression changes settle. Moreover, genes with the largest change in EP300 binding showed the highest expression dynamics before the peak of EP300 recruitment. Overall, our results show that enhancer remodeling may not directly be driving gene expression dynamics but rather be a consequence of expression activation.

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Truong, Dong-Jiunn Jeffery, Niklas Armbrust, Julian Geilenkeuser, Eva-Maria Lederer, Tobias Heinrich Santl, Maren Beyer, Sebastian Ittermann, et al. "Intron-encoded cistronic transcripts for minimally invasive monitoring of coding and non-coding RNAs." Nature Cell Biology 24, no. 11 (November 2022): 1666–76. http://dx.doi.org/10.1038/s41556-022-00998-6.

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AbstractDespite their fundamental role in assessing (patho)physiological cell states, conventional gene reporters can follow gene expression but leave scars on the proteins or substantially alter the mature messenger RNA. Multi-time-point measurements of non-coding RNAs are currently impossible without modifying their nucleotide sequence, which can alter their native function, half-life and localization. Thus, we developed the intron-encoded scarless programmable extranuclear cistronic transcript (INSPECT) as a minimally invasive transcriptional reporter embedded within an intron of a gene of interest. Post-transcriptional excision of INSPECT results in the mature endogenous RNA without sequence alterations and an additional engineered transcript that leaves the nucleus by hijacking the nuclear export machinery for subsequent translation into a reporter or effector protein. We showcase its use in monitoring interleukin-2 (IL2) after T cell activation and tracking the transcriptional dynamics of the long non-coding RNA (lncRNA) NEAT1 during CRISPR interference-mediated perturbation. INSPECT is a method for monitoring gene transcription without altering the mature lncRNA or messenger RNA of the target of interest.

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Li, Yakun, Lihong Ding, Mei Zhou, Zhixiang Chen, Yanfei Ding, and Cheng Zhu. "Transcriptional Regulatory Network of Plant Cadmium Stress Response." International Journal of Molecular Sciences 24, no. 5 (February 22, 2023): 4378. http://dx.doi.org/10.3390/ijms24054378.

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Cadmium (Cd) is a non-essential heavy metal with high toxicity to plants. Plants have acquired specialized mechanisms to sense, transport, and detoxify Cd. Recent studies have identified many transporters involved in Cd uptake, transport, and detoxification. However, the complex transcriptional regulatory networks involved in Cd response remain to be elucidated. Here, we provide an overview of current knowledge regarding transcriptional regulatory networks and post-translational regulation of the transcription factors involved in Cd response. An increasing number of reports indicate that epigenetic regulation and long non-coding and small RNAs are important in Cd-induced transcriptional responses. Several kinases play important roles in Cd signaling that activate transcriptional cascades. We also discuss the perspectives to reduce grain Cd content and improve crop tolerance to Cd stress, which provides a theoretical reference for food safety and the future research of plant varieties with low Cd accumulation.

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

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Abstract Regulation of MICA expression is incompletely understood, but human MICA can be upregulated in cancer cells, virus-infected cells and rapidly proliferating cells. Binding of MICA to the activating NKG2D receptor on cytotoxic immune cells promotes elimination of the cell expressing MICA. We noted that MICA has tandem promoters that drive overlapping forward transcription. We show that the MICA gene contains a conserved upstream promoter that expresses a non coding transcript. Transcription from the upstream promoter represses transcription from the standard downstream MICA promoter in cis through transcriptional interference. The effect of transcriptional interference depends on the strength of transcription from the upstream promoter and quantitative studies show that it is described by a simple reciprocal repressor function. The time course of transcriptional interference coincides with recruitment at the standard downstream promoter of factors involved in nucleosomal remodeling during transcription. Transcriptional interference is demonstrated in the regulation of MICA expression by the physiological inputs interferon-γ and interleukin-4, that both act through regulatory DNA elements in the upstream promoter. These findings have significant implications for the understanding of MICA expression. Transcription factors activating the downstream promoter will upregulate MICA expression, whereas transcription factors activating the upstream promoter will downregulated MICA expression. A genome-wide analysis indicates that transcriptional interference between tandem intragenic promoters may be involved in regulating the expression of multiple other human genes.

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Mazina, Marina Yu, and Nadezhda E. Vorobyeva. "Chromatin Modifiers in Transcriptional Regulation: New Findings and Prospects." Acta Naturae 13, no. 1 (March 15, 2021): 16–30. http://dx.doi.org/10.32607/actanaturae.11101.

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Histone-modifying and remodeling complexes are considered the main coregulators that affect transcription by changing the chromatin structure. Coordinated action by these complexes is essential for the transcriptional activation of any eukaryotic gene. In this review, we discuss current trends in the study of histone modifiers and chromatin remodelers, including the functional impact of transcriptional proteins/complexes i.e., pioneers; remodeling and modification of non-histone proteins by transcriptional complexes; the supplementary functions of the non-catalytic subunits of remodelers, and the participation of histone modifiers in the pause of RNA polymerase II. The review also includes a scheme illustrating the mechanisms of recruitment of the main classes of remodelers and chromatin modifiers to various sites in the genome and their functional activities.

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Shliakhtunou, Yauheni A., Valery M. Siamionau, and Vyacheslau V. Pobyarzhin. "Transcription phenotype of circulating tumor cells in non-metastatic breast cancer." Carcinogenesis 43, no. 1 (December 17, 2021): 21–27. http://dx.doi.org/10.1093/carcin/bgab112.

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Abstract The presented research is relevant, as breast cancer is the most commonly diagnosed cancer in the female population worldwide, with the exception of skin cancer. The aim of this article is to study the transcription phenotype of circulating tumor cells in non-metastatic breast cancer. The transcriptional phenotype of circulating tumor cells (CTCs) was studied using real-time polymerase chain reaction (PCR). Three-year OS was 79.2, and 90.8 without the expression with p Log-Rank = 0.04. Independent prognostic factors for the recurrence of disease include the presence of CTCs expressing BIRC5 genes and ABC transporter genes in the peripheral blood before the start of special treatment for resectable breast cancer, as well as the preservation of CTCs per se after completion of special anticancer therapy. In patients with breast cancer stage I–IIIC, circulating tumor cells before special treatment have significant heterogeneity, manifested by a different transcriptional phenotype, including both actively growing and stem tumor cells, and cells at the epithelial-to-mesenchymal transition.

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Ibragimov, Airat N., Oleg V. Bylino, and Yulii V. Shidlovskii. "Molecular Basis of the Function of Transcriptional Enhancers." Cells 9, no. 7 (July 5, 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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Castillo, Joseph, Esther Wu, Christopher Lowe, Shrividhya Srinivasan, Ron McCord, Marie-Claire Wagle, Sangeeta Jayakar, et al. "CBP/p300 Drives the Differentiation of Regulatory T Cells through Transcriptional and Non-Transcriptional Mechanisms." Cancer Research 79, no. 15 (June 10, 2019): 3916–27. http://dx.doi.org/10.1158/0008-5472.can-18-3622.

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Klinge, Carolyn M. "Non-coding RNAs: long non-coding RNAs and microRNAs in endocrine-related cancers." Endocrine-Related Cancer 25, no. 4 (April 2018): R259—R282. http://dx.doi.org/10.1530/erc-17-0548.

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The human genome is ‘pervasively transcribed’ leading to a complex array of non-coding RNAs (ncRNAs) that far outnumber coding mRNAs. ncRNAs have regulatory roles in transcription and post-transcriptional processes as well numerous cellular functions that remain to be fully described. Best characterized of the ‘expanding universe’ of ncRNAs are the ~22 nucleotide microRNAs (miRNAs) that base-pair to target mRNA’s 3′ untranslated region within the RNA-induced silencing complex (RISC) and block translation and may stimulate mRNA transcript degradation. Long non-coding RNAs (lncRNAs) are classified as >200 nucleotides in length, but range up to several kb and are heterogeneous in genomic origin and function. lncRNAs fold into structures that interact with DNA, RNA and proteins to regulate chromatin dynamics, protein complex assembly, transcription, telomere biology and splicing. Some lncRNAs act as sponges for miRNAs and decoys for proteins. Nuclear-encoded lncRNAs can be taken up by mitochondria and lncRNAs are transcribed from mtDNA. Both miRNAs and lncRNAs are dysregulated in endocrine cancers. This review provides an overview on the current understanding of the regulation and function of selected lncRNAs and miRNAs, and their interaction, in endocrine-related cancers: breast, prostate, endometrial and thyroid.

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Bakr, Ali, Joschka Hey, Gianluca Sigismondo, Chun-Shan Liu, Ahmed Sadik, Ashish Goyal, Alice Cross, et al. "ID3 promotes homologous recombination via non-transcriptional and transcriptional mechanisms and its loss confers sensitivity to PARP inhibition." Nucleic Acids Research 49, no. 20 (October 28, 2021): 11666–89. http://dx.doi.org/10.1093/nar/gkab964.

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Abstract The inhibitor of DNA-binding 3 (ID3) is a transcriptional regulator that limits interaction of basic helix-loop-helix transcription factors with their target DNA sequences. We previously reported that ID3 loss is associated with mutational signatures linked to DNA repair defects. Here we demonstrate that ID3 exhibits a dual role to promote DNA double-strand break (DSB) repair, particularly homologous recombination (HR). ID3 interacts with the MRN complex and RECQL helicase to activate DSB repair and it facilitates RAD51 loading and downstream steps of HR. In addition, ID3 promotes the expression of HR genes in response to ionizing radiation by regulating both chromatin accessibility and activity of the transcription factor E2F1. Consistently, analyses of TCGA cancer patient data demonstrate that low ID3 expression is associated with impaired HR. The loss of ID3 leads to sensitivity of tumor cells to PARP inhibition, offering new therapeutic opportunities in ID3-deficient tumors.

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Chowdhury, Moumita Roy, Jolly Basak, and Ranjit Prasad Bahadur. "Elucidating the Functional Role of Predicted miRNAs in Post- Transcriptional Gene Regulation Along with Symbiosis in Medicago truncatula." Current Bioinformatics 15, no. 2 (March 10, 2020): 108–20. http://dx.doi.org/10.2174/1574893614666191003114202.

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Background: microRNAs are small non-coding RNAs which inhibit translational and post-transcriptional processes whereas long non-coding RNAs are found to regulate both transcriptional and post-transcriptional gene expression. Medicago truncatula is a well-known model plant for studying legume biology and is also used as a forage crop. In spite of its importance in nitrogen fixation and soil fertility improvement, little information is available about Medicago non-coding RNAs that play important role in symbiosis. Objective: In this study we have tried to understand the role of Medicago ncRNAs in symbiosis and regulation of transcription factors. Methods: We have identified novel miRNAs by computational methods considering various parameters like length, MFEI, AU content, SSR signatures and tried to establish an interaction model with their targets obtained through psRNATarget server. Results: 149 novel miRNAs are predicted along with their 770 target proteins. We have also shown that 51 of these novel miRNAs are targeting 282 lncRNAs. Conclusion: In this study role of Medicago miRNAs in the regulation of various transcription factors are elucidated. Knowledge gained from this study will have a positive impact on the nitrogen fixing ability of this important model plant, which in turn will improve the soil fertility.

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Inazumi, Hideaki, and Koichiro Kuwahara. "NRSF/REST-Mediated Epigenomic Regulation in the Heart: Transcriptional Control of Natriuretic Peptides and Beyond." Biology 11, no. 8 (August 10, 2022): 1197. http://dx.doi.org/10.3390/biology11081197.

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Reactivation of fetal cardiac genes, including those encoding atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), is a key feature of pathological cardiac remodeling and heart failure. Intensive studies on the regulation of ANP and BNP have revealed the involvement of numerous transcriptional factors in the regulation of the fetal cardiac gene program. Among these, we identified that a transcriptional repressor, neuron-restrictive silencer factor (NRSF), also named repressor element-1-silencing transcription factor (REST), which was initially detected as a transcriptional repressor of neuron-specific genes in non-neuronal cells, plays a pivotal role in the transcriptional regulation of ANP, BNP and other fetal cardiac genes. Here we review the transcriptional regulation of ANP and BNP gene expression and the role of the NRSF repressor complex in the regulation of cardiac gene expression and the maintenance of cardiac homeostasis.

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Journal articles on the topic 'Non transcriptional'

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