Journal articles: 'Transcriptional Regulation'

1

Cornut, Maxence, Emilie Bourdonnay, and Thomas Henry. "Transcriptional Regulation of Inflammasomes." International Journal of Molecular Sciences 21, no. 21 (October 29, 2020): 8087. http://dx.doi.org/10.3390/ijms21218087.

Full text

Abstract:

Inflammasomes are multimolecular complexes with potent inflammatory activity. As such, their activity is tightly regulated at the transcriptional and post-transcriptional levels. In this review, we present the transcriptional regulation of inflammasome genes from sensors (e.g., NLRP3) to substrates (e.g., IL-1β). Lineage-determining transcription factors shape inflammasome responses in different cell types with profound consequences on the responsiveness to inflammasome-activating stimuli. Pro-inflammatory signals (sterile or microbial) have a key transcriptional impact on inflammasome genes, which is largely mediated by NF-κB and that translates into higher antimicrobial immune responses. Furthermore, diverse intrinsic (e.g., circadian clock, metabolites) or extrinsic (e.g., xenobiotics) signals are integrated by signal-dependent transcription factors and chromatin structure changes to modulate transcriptionally inflammasome responses. Finally, anti-inflammatory signals (e.g., IL-10) counterbalance inflammasome genes induction to limit deleterious inflammation. Transcriptional regulations thus appear as the first line of inflammasome regulation to raise the defense level in front of stress and infections but also to limit excessive or chronic inflammation.

APA, Harvard, Vancouver, ISO, and other styles

2

Lee, Pauline, Truksa Jaroslav, Hongfan Peng, and Ernest Beutler. "Transcriptional Regulation of Hepcidin by Iron." Blood 110, no. 11 (November 16, 2007): 2664. http://dx.doi.org/10.1182/blood.v110.11.2664.2664.

Full text

Abstract:

Abstract Transcriptional regulation by iron in mammalian systems is poorly understood. Hepcidin, a 25 amino acid peptide that plays a central role in iron homeostasis, is transcriptionally regulated by iron. A region of the murine hepcidin promoter 1.6 to 1.8 kb upstream from the start of translation was recently identified to be important in transcriptional regulation by iron (Truksa J, et al. The distal location of the iron responsive region of the hepcidin promoter. Blood DOI 10.1182/blood-2007-05-091108, 2007). In order to identify transcription factors that might be important in regulation by iron, transcription factor microarray analyses (Panomics TranSignal Protein/DNA Array) were performed with nuclear extracts from livers of mice made iron deficient or iron loaded for 4 weeks. The analyses revealed 43 transcription factors that were upregulated in iron loaded liver nuclear extracts and 39 transcription factors that were upregulated in iron deficient nuclear extracts. In the region of the promoter we had found essential for transcriptional regulation by iron, −1.6 to −1.8 kb, consensus motifs were identified by Genomatix MatInspector for 10 transcription factors that corresponded to transcription factors upregulated in high iron nuclear extracts by array analyses. Similarly, the consensus sequences for 5 transcription factors corresponded to transcription factors identified in iron deficient nuclear extracts. Electrophoretic mobility shift assays were performed with probes across this region of the murine hepcidin promoter. Several probes exhibited differential binding between deficient and high iron nuclear extracts. These include the probe encompassing the CCAAT box and MEL1 motif, a probe containing a HLH motif, and a probe containing a bZIP and COUP motif. The probe containing the CCAAT motif was supershifted with antibodies against CBF, but was not supershifted with antibodies against SMAD4, CEBPα, and COUP. The probe containing a bZIP and COUP motif can be supershifted with antibodies against COUP-Tf and HNF4α, but not with antibodies against SMAD4, CEBPα, and COUP. Our data suggest that CBFA, COUP, and HNF4α are involved in transcriptional regulation of hepcidin by iron.

APA, Harvard, Vancouver, ISO, and other styles

3

Wilson, Nicola K., Fernando J. Calero-Nieto, Rita Ferreira, and Berthold Göttgens. "Transcriptional regulation of haematopoietic transcription factors." Stem Cell Research & Therapy 2, no. 1 (2011): 6. http://dx.doi.org/10.1186/scrt47.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Dutta, Chaitali, Prasanta K. Patel, Adam Rosebrock, Anna Oliva, Janet Leatherwood, and Nicholas Rhind. "The DNA Replication Checkpoint Directly Regulates MBF-Dependent G1/S Transcription." Molecular and Cellular Biology 28, no. 19 (July 28, 2008): 5977–85. http://dx.doi.org/10.1128/mcb.00596-08.

Full text

Abstract:

ABSTRACT The DNA replication checkpoint transcriptionally upregulates genes that allow cells to adapt to and survive replication stress. Our results show that, in the fission yeast Schizosaccharomyces pombe, the replication checkpoint regulates the entire G1/S transcriptional program by directly regulating MBF, the G1/S transcription factor. Instead of initiating a checkpoint-specific transcriptional program, the replication checkpoint targets MBF to maintain the normal G1/S transcriptional program during replication stress. We propose a mechanism for this regulation, based on in vitro phosphorylation of the Cdc10 subunit of MBF by the Cds1 replication-checkpoint kinase. Replacement of two potential phosphorylation sites with phosphomimetic amino acids suffices to promote the checkpoint transcriptional program, suggesting that Cds1 phosphorylation directly regulates MBF-dependent transcription. The conservation of MBF between fission and budding yeast, and recent results implicating MBF as a target of the budding yeast replication checkpoint, suggests that checkpoint regulation of the MBF transcription factor is a conserved strategy for coping with replication stress. Furthermore, the structural and regulatory similarity between MBF and E2F, the metazoan G1/S transcription factor, suggests that this checkpoint mechanism may be broadly conserved among eukaryotes.

APA, Harvard, Vancouver, ISO, and other styles

5

Hahn, Steven. "Transcriptional regulation." EMBO reports 9, no. 7 (June 6, 2008): 612–16. http://dx.doi.org/10.1038/embor.2008.99.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Helntz, Nathaniel. "Transcriptional regulation." Trends in Biochemical Sciences 16 (January 1991): 393. http://dx.doi.org/10.1016/0968-0004(91)90161-n.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Shimizu, Kiminori, Julie K. Hicks, Tzu-Pi Huang, and Nancy P. Keller. "Pka, Ras and RGS Protein Interactions Regulate Activity of AflR, a Zn(II)2Cys6 Transcription Factor in Aspergillus nidulans." Genetics 165, no. 3 (November 1, 2003): 1095–104. http://dx.doi.org/10.1093/genetics/165.3.1095.

Full text

Abstract:

Abstract Sterigmatocystin (ST) is a carcinogenic polyketide produced by several filamentous fungi including Aspergillus nidulans. Expression of ST biosynthetic genes (stc genes) requires activity of a Zn(II)2Cys6 transcription factor, AflR. aflR is transcriptionally and post-transcriptionally regulated by a G-protein/cAMP/protein kinase A (PkaA) signaling pathway involving FlbA, an RGS (regulator of G-protein signaling) protein. Prior genetic data showed that FlbA transcriptional regulation of aflR was PkaA dependent. Here we show that mutation of three PkaA phosphorylation sites in AflR allows resumption of stc expression in an overexpression pkaA background but does not remediate stc expression in a ΔflbA background. This demonstrates negative regulation of AflR activity by phosphorylation and shows that FlbA post-transcriptional regulation of aflR is PkaA independent. AflR nucleocytoplasmic location further supports PkaA-independent regulation of AflR by FlbA. GFP-tagged AflR is localized to the cytoplasm when pkaA is overexpressed but nuclearly located in a ΔflbA background. aflR is also transcriptionally and post-transcriptionally regulated by RasA. RasA transcriptional control of aflR is PkaA independent but RasA post-transcriptional control of AflR is partially mediated by PkaA.

APA, Harvard, Vancouver, ISO, and other styles

8

Desvergne, Béatrice, Liliane Michalik, and Walter Wahli. "Transcriptional Regulation of Metabolism." Physiological Reviews 86, no. 2 (April 2006): 465–514. http://dx.doi.org/10.1152/physrev.00025.2005.

Full text

Abstract:

Our understanding of metabolism is undergoing a dramatic shift. Indeed, the efforts made towards elucidating the mechanisms controlling the major regulatory pathways are now being rewarded. At the molecular level, the crucial role of transcription factors is particularly well-illustrated by the link between alterations of their functions and the occurrence of major metabolic diseases. In addition, the possibility of manipulating the ligand-dependent activity of some of these transcription factors makes them attractive as therapeutic targets. The aim of this review is to summarize recent knowledge on the transcriptional control of metabolic homeostasis. We first review data on the transcriptional regulation of the intermediary metabolism, i.e., glucose, amino acid, lipid, and cholesterol metabolism. Then, we analyze how transcription factors integrate signals from various pathways to ensure homeostasis. One example of this coordination is the daily adaptation to the circadian fasting and feeding rhythm. This section also discusses the dysregulations causing the metabolic syndrome, which reveals the intricate nature of glucose and lipid metabolism and the role of the transcription factor PPARγ in orchestrating this association. Finally, we discuss the molecular mechanisms underlying metabolic regulations, which provide new opportunities for treating complex metabolic disorders.

APA, Harvard, Vancouver, ISO, and other styles

9

Geng, Yanbiao, Peter Laslo, Kevin Barton, and Chyung-Ru Wang. "Transcriptional Regulation ofCD1D1by Ets Family Transcription Factors." Journal of Immunology 175, no. 2 (July 7, 2005): 1022–29. http://dx.doi.org/10.4049/jimmunol.175.2.1022.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Hermsen, Rutger, Sander Tans, and Pieter Rein ten Wolde. "Transcriptional Regulation by Competing Transcription Factor Modules." PLoS Computational Biology 2, no. 12 (2006): e164. http://dx.doi.org/10.1371/journal.pcbi.0020164.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Hermsen, Rutger, Sander J. Tans, and Pieter Rein ten Wolde. "Transcriptional Regulation by Competing Transcription Factor Modules." PLoS Computational Biology preprint, no. 2006 (2005): e164. http://dx.doi.org/10.1371/journal.pcbi.0020164.eor.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Bettegowda, Anilkumar, and Miles F. Wilkinson. "Transcription and post-transcriptional regulation of spermatogenesis." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1546 (May 27, 2010): 1637–51. http://dx.doi.org/10.1098/rstb.2009.0196.

Full text

Abstract:

Spermatogenesis in mammals is achieved by multiple players that pursue a common goal of generating mature spermatozoa. The developmental processes acting on male germ cells that culminate in the production of the functional spermatozoa are regulated at both the transcription and post-transcriptional levels. This review addresses recent progress towards understanding such regulatory mechanisms and identifies future challenges to be addressed in this field. We focus on transcription factors, chromatin-associated factors and RNA-binding proteins necessary for spermatogenesis and/or sperm maturation. Understanding the molecular mechanisms that govern spermatogenesis has enormous implications for new contraceptive approaches and treatments for infertility.

APA, Harvard, Vancouver, ISO, and other styles

13

Matthews, J. L., M. G. Zwick, and M. R. Paule. "Coordinate regulation of ribosomal component synthesis in Acanthamoeba castellanii: 5S RNA transcription is down regulated during encystment by alteration of TFIIIA activity." Molecular and Cellular Biology 15, no. 6 (June 1995): 3327–35. http://dx.doi.org/10.1128/mcb.15.6.3327.

Full text

Abstract:

Transcription of large rRNA precursor and 5S RNA were examined during encystment of Acanthamoeba castellanii. Both transcription units are down regulated almost coordinately during this process, though 5S RNA transcription is not as completely shut down as rRNA transcription. The protein components necessary for transcription of 5S RNA and tRNA were determined, and fractions containing transcription factors comparable to TFIIIA, TFIIIB, and TFIIIC, as well as RNA polymerase III and a 3'-end processing activity, were identified. Regulation of 5S RNA transcription could be recapitulated in vitro, and the activities of the required components were compared. In contrast to regulation of precursor rRNA, there is no apparent change during encystment in the activity of the polymerase dedicated to 5S RNA expression. Similarly, the transcriptional and promoter-binding activities of TFIIIC are not altered in parallel with 5S RNA regulation. TFIIIB transcriptional activity is unaltered in encysting cells. In contrast, both the transcriptional and DNA-binding activities of TFIIIA are strongly reduced in nuclear extracts from transcriptionally inactive cells. These results were analyzed in terms of mechanisms for coordinate regulation of rRNA and 5S RNA expression.

APA, Harvard, Vancouver, ISO, and other styles

14

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 (November 19, 2008): 1262–66. http://dx.doi.org/10.1042/bst0361262.

Full text

Abstract:

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 mechanism that mediates zinc-induced transcriptional up-regulation, involving the transcription factor MTF1 (metal-response element-binding transcription factor 1), has been studied extensively. Gene responses in the opposite direction (reduced mRNA levels in response to increased zinc availability) have been observed in mammalian cells, but a specific transcriptional regulatory process responsible for such a response has yet to be identified. Examples of single zinc-sensitive transcription factors regulating gene expression in opposite directions are emerging. Although zinc-induced transcriptional repression by MTF1 is a possible explanation in some specific instances, such a mechanism cannot account for repression by zinc of all mammalian genes that show this mode of regulation, indicating the existence of as yet uncharacterized mechanisms of zinc-regulated transcription in mammalian cells. In addition, recent findings reveal a role for effects of zinc on mRNA stability in the regulation of specific zinc transporters. Our studies on the regulation of the human gene SLC30A5 (solute carrier 30A5), which codes for the zinc transporter ZnT5, have revealed that this gene provides a model system by which to study both zinc-induced transcriptional down-regulation and zinc-regulated mRNA stabilization.

APA, Harvard, Vancouver, ISO, and other styles

15

Sui, Zhiyuan, Yongjie Zhang, Zhishuai Zhang, Chenguang Wang, Xiaojun Li, Feng Xing, and Mingxing Chu. "Analysis of Lin28B Promoter Activity and Screening of Related Transcription Factors in Dolang Sheep." Genes 14, no. 5 (May 7, 2023): 1049. http://dx.doi.org/10.3390/genes14051049.

Full text

Abstract:

The Lin28B gene is involved in the initiation of puberty, but its regulatory mechanisms remain unclear. Therefore, in this study, we aimed to study the regulatory mechanism of the Lin28B promoter by cloning the Lin28B proximal promoter for bioinformatic analysis. Next, a series of deletion vectors were constructed based on the bioinformatic analysis results for dual-fluorescein activity detection. The transcriptional regulation mechanism of the Lin28B promoter region was analyzed by detecting mutations in transcription factor-binding sites and overexpression of transcription factors. The dual-luciferase assay showed that the Lin28B promoter region −837 to −338 bp had the highest transcriptional activity, and the transcriptional activity of the Lin28B transcriptional regulatory region decreased significantly after Egr1 and SP1 mutations. Overexpression of the Egr1 transcription factor significantly enhanced the transcription of Lin28B, and the results indicated that Egr1 and SP1 play important roles in regulating Lin28B. These results provide a theoretical basis for further research on the transcriptional regulation of sheep Lin28B during puberty initiation.

APA, Harvard, Vancouver, ISO, and other styles

16

Guo, Song, Yunfei Guo, Yuanyuan Chen, Shuaishuai Cui, Chunmei Zhang, and Dahu Chen. "The role of CEMIP in cancers and its transcriptional and post-transcriptional regulation." PeerJ 12 (February 19, 2024): e16930. http://dx.doi.org/10.7717/peerj.16930.

Full text

Abstract:

CEMIP is a protein known for inducing cell migration and binding to hyaluronic acid. Functioning as a hyaluronidase, CEMIP primarily facilitates the breakdown of the extracellular matrix component, hyaluronic acid, thereby regulating various signaling pathways. Recent evidence has highlighted the significant role of CEMIP in different cancers, associating it with diverse pathological states. While identified as a biomarker for several diseases, CEMIP’s mechanism in cancer seems distinct. Accumulating data suggests that CEMIP expression is triggered by chemical modifications to itself and other influencing factors. Transcriptionally, chemical alterations to the CEMIP promoter and involvement of transcription factors such as AP-1, HIF, and NF-κB regulate CEMIP levels. Similarly, specific miRNAs have been found to post-transcriptionally regulate CEMIP. This review provides a comprehensive summary of CEMIP’s role in various cancers and explores how both transcriptional and post-transcriptional mechanisms control its expression.

APA, Harvard, Vancouver, ISO, and other styles

17

Weiss, Mitchell J. "Transcriptional Regulation of Erythropoiesis." Blood 114, no. 22 (November 20, 2009): SCI—7—SCI—7. http://dx.doi.org/10.1182/blood.v114.22.sci-7.sci-7.

Full text

Abstract:

Abstract Abstract SCI-7 Efforts to define the mechanisms of globin gene expression and transcriptional control of erythrocyte formation have provided key insights into our understanding of developmental hematopoiesis. Our group has focused on GATA-1, a zinc finger protein that was initially identified through its ability to bind a conserved cis element that regulates globin gene expression. GATA-1 is essential for erythroid development and mutations in the GATA1 gene are associated with human cytopenias and leukemia. Several general principles have emerged through studies to define the mechanisms of GATA-1 action. First, GATA-1 activates not only globin genes, but also virtually every gene that defines the erythroid phenotype. This observation sparked successful gene discovery efforts to identify new components of erythroid development and physiology. Second, GATA-1 also represses transcription through multiple mechanisms. This property may help to explain how GATA-1 regulates hematopoietic lineage commitment and also how GATA1 mutations contribute to cancer, since several directly repressed targets are proto-oncogenes. Third, GATA-1 regulates not only protein coding genes, but also microRNAs, which in turn, modulate erythropoiesis through post-transcriptional mechanisms. Fourth, GATA-1 interacts with other essential erythroid-specific and ubiquitous transcription factors. These protein interactions regulate gene expression by influencing chromatin modifications and controlling three-dimensional proximity between widely spaced DNA elements. Recently, we have combined transcriptome analysis with ChIP-chip and ChIP-seq studies to correlate in vivo occupancy of DNA by GATA-1 and other transcription factors with mRNA expression genome-wide in erythroid cells. These studies better elucidate how GATA-1 recognizes DNA, discriminates between transcriptional activation versus repression and interacts functionally with other nuclear proteins. I will review published and new aspects of our work in these areas. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

18

Gerbal-Chaloin, Sabine, Martine Daujat, Jean-Marc Pascussi, Lydiane Pichard-Garcia, Marie-Jose Vilarem, and Patrick Maurel. "Transcriptional Regulation ofCYP2C9Gene." Journal of Biological Chemistry 277, no. 1 (October 25, 2001): 209–17. http://dx.doi.org/10.1074/jbc.m107228200.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Guo, Ing-Cherng, Meng-Chun Hu, and Bon-chu Chung. "Transcriptional regulation ofCYP11A1." Journal of Biomedical Science 10, no. 6 (October 2003): 593–98. http://dx.doi.org/10.1007/bf02256309.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Payne, Joshua L., Fahad Khalid, and Andreas Wagner. "RNA-mediated gene regulation is less evolvable than transcriptional regulation." Proceedings of the National Academy of Sciences 115, no. 15 (March 26, 2018): E3481—E3490. http://dx.doi.org/10.1073/pnas.1719138115.

Full text

Abstract:

Much of gene regulation is carried out by proteins that bind DNA or RNA molecules at specific sequences. One class of such proteins is transcription factors, which bind short DNA sequences to regulate transcription. Another class is RNA binding proteins, which bind short RNA sequences to regulate RNA maturation, transport, and stability. Here, we study the robustness and evolvability of these regulatory mechanisms. To this end, we use experimental binding data from 172 human and fruit fly transcription factors and RNA binding proteins as well as human polymorphism data to study the evolution of binding sites in vivo. We find little difference between the robustness of regulatory protein–RNA interactions and transcription factor–DNA interactions to DNA mutations. In contrast, we find that RNA-mediated regulation is less evolvable than transcriptional regulation, because mutations are less likely to create interactions of an RNA molecule with a new RNA binding protein than they are to create interactions of a gene regulatory region with a new transcription factor. Our observations are consistent with the high level of conservation observed for interactions between RNA binding proteins and their target molecules as well as the evolutionary plasticity of regulatory regions bound by transcription factors. They may help explain why transcriptional regulation is implicated in many more evolutionary adaptations and innovations than RNA-mediated gene regulation.

APA, Harvard, Vancouver, ISO, and other styles

21

Powell, Emily, Peter Kuhn, and Wei Xu. "Nuclear Receptor Cofactors in PPARγ-Mediated Adipogenesis and Adipocyte Energy Metabolism." PPAR Research 2007 (2007): 1–11. http://dx.doi.org/10.1155/2007/53843.

Full text

Abstract:

Transcriptional cofactors are integral to the proper function and regulation of nuclear receptors. Members of the peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors are involved in the regulation of lipid and carbohydrate metabolism. They modulate gene transcription in response to a wide variety of ligands, a process that is mediated by transcriptional coactivators and corepressors. The mechanisms by which these cofactors mediate transcriptional regulation of nuclear receptor function are still being elucidated. The rapidly increasing array of cofactors has brought into focus the need for a clear understanding of how these cofactors interact in ligand- and cell-specific manners. This review highlights the differential effects of the assorted cofactors regulating the transcriptional action of PPARγand summarizes the recent advances in understanding the physiological functions of corepressors and coactivators.

APA, Harvard, Vancouver, ISO, and other styles

22

Witzel, Ini-Isabée, Li Fang Koh, and Neil D. Perkins. "Regulation of cyclin D1 gene expression." Biochemical Society Transactions 38, no. 1 (January 19, 2010): 217–22. http://dx.doi.org/10.1042/bst0380217.

Full text

Abstract:

Cyclin D1 is a key regulator of cell proliferation and its expression is subject to both transcriptional and post-transcriptional regulation. In different cellular contexts, different pathways assume a dominant role in regulating its expression, whereas their disregulation can contribute to overexpression of cyclin D1 in tumorigenesis. Here, we discuss the ability of the NF-κB (nuclear factor κB)/IKK [IκB (inhibitor of NF-κB) kinase] pathways to regulate cyclin D1 gene transcription and also consider the newly discovered role of the SNARP (SNIP1/SkIP-associated RNA processing) complex as a co-transcriptional regulator of cyclin D1 RNA stability.

APA, Harvard, Vancouver, ISO, and other styles

23

Disner, Geonildo R., Maria A. P. Falcão, Carla Lima, and Monica Lopes-Ferreira. "In Silico Target Prediction of Overexpressed microRNAs from LPS-Challenged Zebrafish (Danio rerio) Treated with the Novel Anti-Inflammatory Peptide TnP." International Journal of Molecular Sciences 22, no. 13 (July 1, 2021): 7117. http://dx.doi.org/10.3390/ijms22137117.

Full text

Abstract:

miRNAs regulate gene expression post-transcriptionally in various processes, e.g., immunity, development, and diseases. Since their experimental analysis is complex, in silico target prediction is important for directing investigations. TnP is a candidate peptide for anti-inflammatory therapy, first discovered in the venom of Thalassophryne nattereri, which led to miRNAs overexpression in LPS-inflamed zebrafish post-treatment. This work aimed to predict miR-21, miR-122, miR-731, and miR-26 targets using overlapped results of DIANA microT-CDS and TargetScanFish software. This study described 513 miRNAs targets using highly specific thresholds. Using Gene Ontology over-representation analysis, we identified their main roles in regulating gene expression, neurogenesis, DNA-binding, transcription regulation, immune system process, and inflammatory response. miRNAs act in post-transcriptional regulation, but we revealed that their targets are strongly related to expression regulation at the transcriptional level, e.g., transcription factors proteins. A few predicted genes participated concomitantly in many biological processes and molecular functions, such as foxo3a, rbpjb, rxrbb, tyrobp, hes6, zic5, smad1, e2f7, and npas4a. Others were particularly involved in innate immunity regulation: il17a/f2, pik3r3b, and nlrc6. Together, these findings not only provide new insights into the miRNAs mode of action but also raise hope for TnP therapy and may direct future experimental investigations.

APA, Harvard, Vancouver, ISO, and other styles

24

Tower, J., and B. Sollner-Webb. "Polymerase III transcription factor B activity is reduced in extracts of growth-restricted cells." Molecular and Cellular Biology 8, no. 2 (February 1988): 1001–5. http://dx.doi.org/10.1128/mcb.8.2.1001-1005.1988.

Full text

Abstract:

Extracts of cells that are down-regulated for transcription by RNA polymerase I and RNA polymerase III exhibit a reduced in vitro transcriptional capacity. We have recently demonstrated that the down-regulation of polymerase I transcription in extracts of cycloheximide-treated and stationary-phase cells results from a lack of an activated subform of RNA polymerase I which is essential for rDNA transcription. To examine whether polymerase III transcriptional down-regulation occurs by a similar mechanism, the polymerase III transcription factors were isolated and added singly and in pairs to control cell extracts and to extracts of cells that had reduced polymerase III transcriptional activity due to cycloheximide treatment or growth into stationary phase. These down-regulations result from a specific reduction in TFIIIB; TFIIIC and polymerase III activities remain relatively constant. Thus, although transcription by both polymerase III and polymerase I is substantially decreased in extracts of growth-arrested cells, this regulation is brought about by reduction of different kinds of activities: a component of the polymerase III stable transcription complex in the former case and the activated subform of RNA polymerase I in the latter.

APA, Harvard, Vancouver, ISO, and other styles

25

Tower, J., and B. Sollner-Webb. "Polymerase III transcription factor B activity is reduced in extracts of growth-restricted cells." Molecular and Cellular Biology 8, no. 2 (February 1988): 1001–5. http://dx.doi.org/10.1128/mcb.8.2.1001.

Full text

Abstract:

Extracts of cells that are down-regulated for transcription by RNA polymerase I and RNA polymerase III exhibit a reduced in vitro transcriptional capacity. We have recently demonstrated that the down-regulation of polymerase I transcription in extracts of cycloheximide-treated and stationary-phase cells results from a lack of an activated subform of RNA polymerase I which is essential for rDNA transcription. To examine whether polymerase III transcriptional down-regulation occurs by a similar mechanism, the polymerase III transcription factors were isolated and added singly and in pairs to control cell extracts and to extracts of cells that had reduced polymerase III transcriptional activity due to cycloheximide treatment or growth into stationary phase. These down-regulations result from a specific reduction in TFIIIB; TFIIIC and polymerase III activities remain relatively constant. Thus, although transcription by both polymerase III and polymerase I is substantially decreased in extracts of growth-arrested cells, this regulation is brought about by reduction of different kinds of activities: a component of the polymerase III stable transcription complex in the former case and the activated subform of RNA polymerase I in the latter.

APA, Harvard, Vancouver, ISO, and other styles

26

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

27

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

28

Tirosh, Itay. "Transcriptional priming of cytoplasmic post-transcriptional regulation." Transcription 2, no. 6 (November 2011): 258–62. http://dx.doi.org/10.4161/trns.2.6.18608.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Afzal, Zainab, and Robb Krumlauf. "Transcriptional Regulation and Implications for Controlling Hox Gene Expression." Journal of Developmental Biology 10, no. 1 (January 10, 2022): 4. http://dx.doi.org/10.3390/jdb10010004.

Full text

Abstract:

Hox genes play key roles in axial patterning and regulating the regional identity of cells and tissues in a wide variety of animals from invertebrates to vertebrates. Nested domains of Hox expression generate a combinatorial code that provides a molecular framework for specifying the properties of tissues along the A–P axis. Hence, it is important to understand the regulatory mechanisms that coordinately control the precise patterns of the transcription of clustered Hox genes required for their roles in development. New insights are emerging about the dynamics and molecular mechanisms governing transcriptional regulation, and there is interest in understanding how these may play a role in contributing to the regulation of the expression of the clustered Hox genes. In this review, we summarize some of the recent findings, ideas and emerging mechanisms underlying the regulation of transcription in general and consider how they may be relevant to understanding the transcriptional regulation of Hox genes.

APA, Harvard, Vancouver, ISO, and other styles

30

Zhang, Wei, Jun Huang, and David E. Cook. "Histone modification dynamics at H3K27 are associated with altered transcription of in planta induced genes in Magnaporthe oryzae." PLOS Genetics 17, no. 2 (February 3, 2021): e1009376. http://dx.doi.org/10.1371/journal.pgen.1009376.

Full text

Abstract:

Transcriptional dynamic in response to environmental and developmental cues are fundamental to biology, yet many mechanistic aspects are poorly understood. One such example is fungal plant pathogens, which use secreted proteins and small molecules, termed effectors, to suppress host immunity and promote colonization. Effectors are highly expressedin plantabut remain transcriptionally repressedex planta, but our mechanistic understanding of these transcriptional dynamics remains limited. We tested the hypothesis that repressive histone modification at H3-Lys27 underlies transcriptional silencingex planta, and that exchange for an active chemical modification contributes to transcription ofin plantainduced genes. Using genetics, chromatin immunoprecipitation and sequencing and RNA-sequencing, we determined that H3K27me3 provides significant local transcriptional repression. We detail how regions that lose H3K27me3 gain H3K27ac, and these changes are associated with increased transcription. Importantly, we observed that manyin plantainduced genes were marked by H3K27me3 during axenic growth, and detail how altered H3K27 modification influences transcription. ChIP-qPCR duringin plantagrowth suggests that H3K27 modifications are generally stable, but can undergo dynamics at specific genomic locations. Our results support the hypothesis that dynamic histone modifications at H3K27 contributes to fungal genome regulation and specifically contributes to regulation of genes important during host infection.

APA, Harvard, Vancouver, ISO, and other styles

31

Ouellette, A. J., R. Moonka, A. D. Zelenetz, and R. A. Malt. "Regulation of ribosome synthesis during compensatory renal hypertrophy in mice." American Journal of Physiology-Cell Physiology 253, no. 4 (October 1, 1987): C506—C513. http://dx.doi.org/10.1152/ajpcell.1987.253.4.c506.

Full text

Abstract:

Ribosomal synthesis was studied at the transcriptional and translational levels to investigate the mechanisms of ribosome accretion during compensatory renal hypertrophy. As measured by in vitro transcriptional runoff comparisons 6-48 h after surgery, nuclei from the kidney remaining after contralateral nephrectomy show an increase of up to 150% in the rate of synthesis of ribosomal precursor RNA. The rate of rDNA transcription is 40-50% greater than control values as early as 6 h after nephrectomy; by 48 h, the rate returns to normal. In contrast to the stimulated transcription of rDNA and accretion of rRNA, the steady-state levels and the cytoplasmic distribution of ribosomal protein mRNAs S16 and L10 remain unchanged during induced renal growth. Thus coordinate production of adequate protein for increased assembly of ribosomes during induced renal growth appears to be accomplished by increasingly efficient translation of existing ribosomal protein mRNAs or by post-translational stabilization of ribosomal proteins. The rate of rDNA transcription may be regulated by accelerating the transcription of already functioning genes or, more likely, by recruiting transcription units that are transcriptionally inactive in the normal kidney.

APA, Harvard, Vancouver, ISO, and other styles

32

Yoshida, Toshimi, Esther Landhuis, Marei Dose, Idit Hazan, Jiangwen Zhang, Taku Naito, Audrey F. Jackson, et al. "Transcriptional regulation of the Ikzf1 locus." Blood 122, no. 18 (October 31, 2013): 3149–59. http://dx.doi.org/10.1182/blood-2013-01-474916.

Full text

Abstract:

Key Points Multiple enhancers identified at the Ikzf1 locus with shared and distinct epigenetic and transcriptional properties. Transcription factor networks that distinguish between LMPP-specific and T cell–specific Ikzf1 enhancers.

APA, Harvard, Vancouver, ISO, and other styles

33

Nakayama, Koh, and Naoyuki Kataoka. "Regulation of Gene Expression under Hypoxic Conditions." International Journal of Molecular Sciences 20, no. 13 (July 3, 2019): 3278. http://dx.doi.org/10.3390/ijms20133278.

Full text

Abstract:

Eukaryotes are often subjected to different kinds of stress. In order to adjust to such circumstances, eukaryotes activate stress–response pathways and regulate gene expression. Eukaryotic gene expression consists of many different steps, including transcription, RNA processing, RNA transport, and translation. In this review article, we focus on both transcriptional and post-transcriptional regulations of gene expression under hypoxic conditions. In the first part of the review, transcriptional regulations mediated by various transcription factors including Hypoxia-Inducible Factors (HIFs) are described. In the second part, we present RNA splicing regulations under hypoxic conditions, which are mediated by splicing factors and their kinases. This work summarizes and discusses the emerging studies of those two gene expression machineries under hypoxic conditions.

APA, Harvard, Vancouver, ISO, and other styles

34

Keller, Samuel H., Siddhartha G. Jena, Yuji Yamazaki, and Bomyi Lim. "Regulation of spatiotemporal limits of developmental gene expression via enhancer grammar." Proceedings of the National Academy of Sciences 117, no. 26 (June 15, 2020): 15096–103. http://dx.doi.org/10.1073/pnas.1917040117.

Full text

Abstract:

The regulatory specificity of a gene is determined by the structure of its enhancers, which contain multiple transcription factor binding sites. A unique combination of transcription factor binding sites in an enhancer determines the boundary of target gene expression, and their disruption often leads to developmental defects. Despite extensive characterization of binding motifs in an enhancer, it is still unclear how each binding site contributes to overall transcriptional activity. Using live imaging, quantitative analysis, and mathematical modeling, we measured the contribution of individual binding sites in transcriptional regulation. We show that binding site arrangement within the Rho-GTPase componentt48enhancer mediates the expression boundary by mainly regulating the timing of transcriptional activation along the dorsoventral axis ofDrosophilaembryos. By tuning the binding affinity of the Dorsal (Dl) and Zelda (Zld) sites, we show that single site modulations are sufficient to induce significant changes in transcription. Yet, no one site seems to have a dominant role; rather, multiple sites synergistically drive increases in transcriptional activity. Interestingly, Dl and Zld demonstrate distinct roles in transcriptional regulation. Dl site modulations change spatial boundaries oft48, mostly by affecting the timing of activation and bursting frequency rather than transcriptional amplitude or bursting duration. However, modulating the binding site for the pioneer factor Zld affects both the timing of activation and amplitude, suggesting that Zld may potentiate higher Dl recruitment to target DNAs. We propose that such fine-tuning of dynamic gene control via enhancer structure may play an important role in ensuring normal development.

APA, Harvard, Vancouver, ISO, and other styles

35

Desgranges, Zana P., Jinwoo Ahn, Maria B. Lazebnik, Todd Ashworth, Caleb Lee, Richard C. Pestell, Naomi Rosenberg, Carol Prives, and Ananda L. Roy. "Inhibition of TFII-I-Dependent Cell Cycle Regulation by p53." Molecular and Cellular Biology 25, no. 24 (December 15, 2005): 10940–52. http://dx.doi.org/10.1128/mcb.25.24.10940-10952.2005.

Full text

Abstract:

ABSTRACT The multifunctional transcription factor TFII-I is tyrosine phosphorylated in response to extracellular growth signals and transcriptionally activates growth-promoting genes. However, whether activation of TFII-I also directly affects the cell cycle profile is unknown. Here we show that under normal growth conditions, TFII-I is recruited to the cyclin D1 promoter and transcriptionally activates this gene. Most strikingly, upon cell cycle arrest resulting from genotoxic stress and p53 activation, TFII-I is ubiquitinated and targeted for proteasomal degradation in a p53- and ATM (ataxia telangiectasia mutated)-dependent manner. Consistent with a direct role of TFII-I in cell cycle regulation and cellular proliferation, stable and ectopic expression of wild-type TFII-I increases cyclin D1 levels, resulting in accelerated entry to and exit from S phase, and overcomes p53-mediated cell cycle arrest, despite radiation. We further show that the transcriptional regulation of cyclin D1 and cell cycle control by TFII-I are dependent on its tyrosine phosphorylation at positions 248 and 611, sites required for its growth signal-mediated transcriptional activity. Taken together, our data define TFII-I as a growth signal-dependent transcriptional activator that is critical for cell cycle control and proliferation and further reveal that genotoxic stress-induced degradation of TFII-I results in cell cycle arrest.

APA, Harvard, Vancouver, ISO, and other styles

36

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

37

Davies, Kevin M., and Kathy E. Schwinn. "Transcriptional regulation of secondary metabolism." Functional Plant Biology 30, no. 9 (2003): 913. http://dx.doi.org/10.1071/fp03062.

Full text

Abstract:

Plants produce secondary metabolites during development and in response to environmental stimuli such as light or pathogen attack. Transcriptional regulation provides the most important control point for the secondary metabolic pathways studied to date. In this article we review the data on the transcription factors that modulate this regulation. For the phenylpropanoid pathway, much is understood about both the specific sequences in the target genes (cis-elements) that are involved in responses to environmental and developmental stimuli, and the transcription factors involved. Most information is available for the light induction of the genes for hydroxycinnamic acid production, the production of anthocyanins in leaves and floral tissues, and the production of proanthocyanidins in seeds. Some of the functional interactions between the different types of transcription factor are now being elucidated, and upstream regulators of the genes encoding the transcription factors identified. For other secondary metabolic pathways much less is known, although good progress has been made on identifying transcription factors involved in controlling terpenoid indole alkaloid production. The identification of defined transcription factor genes provides tools for modulating both the amount and distribution of secondary metabolites in plants, and the validity of this approach has been well established by transgenic plants with modified flavonoid accumulation patterns.

APA, Harvard, Vancouver, ISO, and other styles

38

Takaoka, Shohei, Marcos E. Jaso-Vera, and Xiangbo Ruan. "Disrupted Post-Transcriptional Regulation of Gene Expression as a Hallmark of Fatty Liver Progression." International Journal of Molecular Sciences 25, no. 20 (October 15, 2024): 11054. http://dx.doi.org/10.3390/ijms252011054.

Full text

Abstract:

It is known that both transcriptional and post-transcriptional mechanisms control messenger RNA (mRNA) levels. Compared to transcriptional regulations, our understanding of how post-transcriptional regulations adapt during fatty liver progression at the whole-transcriptome level is unclear. While traditional RNA-seq analysis uses only reads mapped to exons to determine gene expression, recent studies support the idea that intron-mapped reads can be reliably used to estimate gene transcription. In this study, we analyzed differential gene expression at both the exon and intron levels using two liver RNA-seq datasets from mice that were fed a high-fat diet for seven weeks (mild fatty liver) or thirty weeks (severe fatty liver). We found that the correlation between gene transcription and mature mRNA levels was much lower in mice with mild fatty liver as compared with mice with severe fatty liver. This result indicates broad post-transcriptional regulations for early fatty liver and such regulations are compromised for severe fatty liver. Specifically, gene ontology analysis revealed that genes involved in synapse organization and cell adhesion were transcriptionally upregulated, while their mature mRNAs were unaffected in mild fatty liver. Further characterization of post-transcriptionally suppressed genes in early fatty liver revealed that their mRNAs harbor a significantly longer 3′ UTR, one of the major features that may subject RNA transcripts to nonsense-mediated RNA decay (NMD). We further show that the expression of representative genes that were post-transcriptionally suppressed were upregulated in mice with a hepatocyte-specific defect of NMD. Finally, we provide data supporting a time-dependent decrease in NMD activity in the liver of a diet-induced metabolic-dysfunction-associated fatty liver disease mouse model. In summary, our study supports the conclusion that NMD is essential in preventing unwanted/harmful gene expression at the early stage of fatty liver and such a mechanism is lost due to decreased NMD activity in mice with severe fatty liver.

APA, Harvard, Vancouver, ISO, and other styles

39

Lv, Xiaoyang, Wei Sun, Shuangxia Zou, Ling Chen, Joram M. Mwacharo, and Jinyu Wang. "Characteristics of the BMP7 Promoter in Hu Sheep." Animals 9, no. 11 (October 28, 2019): 874. http://dx.doi.org/10.3390/ani9110874.

Full text

Abstract:

The BMP7 gene is involved in the growth and development of hair follicles but its regulation mechanism is unclear. We studied the regulation mechanism of the BMP7 promoter by cloning the proximal promoter of BMP7 for bioinformatics analysis. A series of missing vectors was then constructed for dual-fluorescein activity detection based on the bioinformatics analysis results. We tested transcription-factor binding-site mutations and transcription factor over-expression to analyze the transcriptional regulation principle of the BMP7 promoter region. The upstream transcriptional regulatory region of the BMP7 gene proximal promoter was predicted by bioinformatics. There were −1216 bp to −1166 bp and −632 bp to −582 bp transcription initiation sites in the upstream transcriptional regulatory region of the BMP7 gene proximal promoter. The CpG islands’ distribution showed that there were many CpG islands at −549 bp to 1 bp. A dual-luciferase assay revealed high activity between −758 bp and −545 bp in the core region and a possible binding site for transcription factors SP1 and EGR1. The transcriptional activity of BMP7 was significantly decreased in the transcriptional regulatory region of the BMP7 after EGR1 and SP1 mutation. Transcription was significantly enhanced by over expression of the EGR1 transcription factor, which strongly suggests that EGR1 and SP1 play important roles in BMP7 regulation.

APA, Harvard, Vancouver, ISO, and other styles

40

Georgitsi, Marianthi, Branka Zukic, Sonja Pavlovic, and George P. Patrinos. "Transcriptional regulation and pharmacogenomics." Pharmacogenomics 12, no. 5 (May 2011): 655–73. http://dx.doi.org/10.2217/pgs.10.215.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Rosen, Evan D., Christopher J. Walkey, Pere Puigserver, and Bruce M. Spiegelman. "Transcriptional regulation of adipogenesis." Genes & Development 14, no. 11 (June 1, 2000): 1293–307. http://dx.doi.org/10.1101/gad.14.11.1293.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

McGee, Sean, L. "AMPK and transcriptional regulation." Frontiers in Bioscience 13, no. 13 (2008): 3022. http://dx.doi.org/10.2741/2907.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Wong, W. W., M. P. Brynildsen, and J. C. Liao. "Transcriptional regulation and metabolism." Biochemical Society Transactions 33, no. 6 (December 1, 2005): 1423. http://dx.doi.org/10.1042/bst20051423.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Wysocka, Joanna. "Enhancers and Transcriptional Regulation." Blood 128, no. 22 (December 2, 2016): SCI—14—SCI—14. http://dx.doi.org/10.1182/blood.v128.22.sci-14.sci-14.

Full text

Abstract:

Abstract Interactions between the genome and its cellular and signaling environments, which ultimately occur at the level of chromatin, are the key to comprehending how cell-type-specific gene expression patterns arise and are maintained during development or are misregulated in disease. Central to the cell type-specific transcriptional regulation are distal cis-regulatory elements called enhancers, which function in a modular way to provide exquisite spatiotemporal control of gene expression during development. We are using a combination of genomic, genetic, biochemical, and single-cell approaches to investigate how enhancers are activated in response to developmental stimuli, how they communicate with target promoters over large genomic distances to regulate transcriptional outputs, what is the role of chromatin modification and remodeling in facilitating or restricting enhancer activity and how regulatory sequence change leads to the phenotypic divergence in humans. I will discuss our latest results on the mechanisms underlying enhancer function and gene regulation in development and disease. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

45

Franceschi, Renny T., Chunxi Ge, Guozhi Xiao, Hernan Roca, and Di Jiang. "Transcriptional Regulation of Osteoblasts." Cells Tissues Organs 189, no. 1-4 (August 27, 2008): 144–52. http://dx.doi.org/10.1159/000151747.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

NAKAHIRA, Yoichi, and Yoshinori TOYOSHIMA. "Transcriptional Regulation in Chloroplasts." Nippon Nōgeikagaku Kaishi 71, no. 11 (1997): 1166–69. http://dx.doi.org/10.1271/nogeikagaku1924.71.1166.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Myers, Lawrence C., and Roger D. Kornberg. "Mediator of Transcriptional Regulation." Annual Review of Biochemistry 69, no. 1 (June 2000): 729–49. http://dx.doi.org/10.1146/annurev.biochem.69.1.729.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

FRANCESCHI, R. T., C. GE, G. XIAO, H. ROCA, and D. JIANG. "Transcriptional Regulation of Osteoblasts." Annals of the New York Academy of Sciences 1116, no. 1 (November 1, 2007): 196–207. http://dx.doi.org/10.1196/annals.1402.081.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Beckerman, R., and C. Prives. "Transcriptional Regulation by P53." Cold Spring Harbor Perspectives in Biology 2, no. 8 (April 28, 2010): a000935. http://dx.doi.org/10.1101/cshperspect.a000935.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Heller, Loreé C., Yong Li, Kevin L. Abrams, and Melissa B. Rogers. "Transcriptional Regulation of theBmp2Gene." Journal of Biological Chemistry 274, no. 3 (January 15, 1999): 1394–400. http://dx.doi.org/10.1074/jbc.274.3.1394.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Transcriptional Regulation'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles