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Journal articles on the topic 'Promoter opening'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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1

Murakami, Kenji, Pierre-Jean Mattei, Ralph E. Davis, Huiyan Jin, Craig D. Kaplan, and Roger D. Kornberg. "Uncoupling Promoter Opening from Start-Site Scanning." Molecular Cell 59, no. 1 (2015): 133–38. http://dx.doi.org/10.1016/j.molcel.2015.05.021.

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2

BURNS, Helen D., Tamara A. BELYAEVA, Stephen J. W. BUSBY, and Stephen D. MINCHIN. "Temperature-dependence of open-complex formation at two Escherichia coli promoters with extended −10 sequences." Biochemical Journal 317, no. 1 (1996): 305–11. http://dx.doi.org/10.1042/bj3170305.

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We have studied the formation of open complexes between purified RNA polymerase from Escherichia coli and DNA fragments carrying the galP1 promoter, a promoter with an extended -10 region. Unusually, these complexes are formed readily at low temperatures. This low-temperature opening is unaffected by deletions of either upstream or downstream promoter sequences. We conclude that low-temperature open-complex formation is due to specific base sequences in and just upstream of the extended -10 region. In contrast, open complexes are not formed at low temperatures with DNA fragments carrying the E

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3

Sandoz, Jérémy, and Frédéric Coin. "Unified promoter opening steps in eukaryotic gene expression." Oncotarget 8, no. 49 (2017): 84614–15. http://dx.doi.org/10.18632/oncotarget.21387.

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4

Kim, Hajin, Guo-Qing Tang, Smita S. Patel, and Taekjip Ha. "Promoter Opening-Closing Dynamics of Mitochondrial RNA Polymerase." Biophysical Journal 100, no. 3 (2011): 65a. http://dx.doi.org/10.1016/j.bpj.2010.12.555.

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5

Nelson, Everette J. R., Laura M. Tuschong, and Dennis D. Hickstein. "Lentiviral Vectors Incorporating Ubiquitous Chromatin Opening Element Driving Canine CD18 Expression." Blood 128, no. 22 (2016): 5890. http://dx.doi.org/10.1182/blood.v128.22.5890.5890.

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Abstract Leukocyte adhesion deficiency type 1 (LAD1) in humans is caused due to mutations in the ITGB2 gene encoding the leukocyte CD18 subunit (b2 integrin). This results in defective leukocyte adhesion and migration leading to recurrent episodes of life-threatening bacterial infection. Canine leukocyte adhesion deficiency (CLAD) represents a disease-specific large animal model of LAD1 in which new therapeutic approaches could be tested. Our previous studies have demonstrated variable efficiency of CD18 expression under the control of several promoters. These include cellular promoters such a

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6

Micorescu, Michael, Sebastian Grünberg, Andreas Franke, Patrick Cramer, Michael Thomm, and Michael Bartlett. "Archaeal Transcription: Function of an Alternative Transcription Factor B from Pyrococcus furiosus." Journal of Bacteriology 190, no. 1 (2007): 157–67. http://dx.doi.org/10.1128/jb.01498-07.

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ABSTRACT The genome of the hyperthermophile archaeon Pyrococcus furiosus encodes two transcription factor B (TFB) paralogs, one of which (TFB1) was previously characterized in transcription initiation. The second TFB (TFB2) is unusual in that it lacks recognizable homology to the archaeal TFB/eukaryotic TFIIB B-finger motif. TFB2 functions poorly in promoter-dependent transcription initiation, but photochemical cross-linking experiments indicated that the orientation and occupancy of transcription complexes formed with TFB2 at the strong gdh promoter are similar to the orientation and occupanc

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7

Barinova, N., E. Zhilina, I. Bass, V. Nikiforov та A. Kulbachinskiy. "Lineage-Specific Amino Acid Substitutions in Region 2 of the RNA Polymerase σ Subunit Affect the Temperature of Promoter Opening". Journal of Bacteriology 190, № 8 (2008): 3088–92. http://dx.doi.org/10.1128/jb.00008-08.

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ABSTRACT Highly conserved amino acid residues in region 2 of the RNA polymerase σ subunit are known to participate in promoter recognition and opening. We demonstrated that nonconserved residues in this region collectively determine lineage-specific differences in the temperature of promoter opening.

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8

Guo, Y., and J. D. Gralla. "Promoter opening via a DNA fork junction binding activity." Proceedings of the National Academy of Sciences 95, no. 20 (1998): 11655–60. http://dx.doi.org/10.1073/pnas.95.20.11655.

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9

He, Yuan, Chunli Yan, Jie Fang, et al. "Near-atomic resolution visualization of human transcription promoter opening." Acta Crystallographica Section A Foundations and Advances 73, a1 (2017): a256. http://dx.doi.org/10.1107/s0108767317097483.

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10

He, Yuan, Chunli Yan, Jie Fang, et al. "Near-atomic resolution visualization of human transcription promoter opening." Nature 533, no. 7603 (2016): 359–65. http://dx.doi.org/10.1038/nature17970.

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11

Vorländer, Matthias K., Heena Khatter, Rene Wetzel, Wim J. H. Hagen, and Christoph W. Müller. "Molecular mechanism of promoter opening by RNA polymerase III." Nature 553, no. 7688 (2018): 295–300. http://dx.doi.org/10.1038/nature25440.

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12

Barbaric, Slobodan, Tim Luckenbach, Andrea Schmid, Dorothea Blaschke, Wolfram Hörz, and Philipp Korber. "Redundancy of Chromatin Remodeling Pathways for the Induction of the Yeast PHO5 Promoter in Vivo." Journal of Biological Chemistry 282, no. 38 (2007): 27610–21. http://dx.doi.org/10.1074/jbc.m700623200.

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Induction of the yeast PHO5 and PHO8 genes leads to a prominent chromatin transition at their promoter regions as a prerequisite for transcription activation. Although induction of PHO8 is strictly dependent on Snf2 and Gcn5, there is no chromatin remodeler identified so far that would be essential for the opening of PHO5 promoter chromatin. Nonetheless, the nonessential but significant involvement of cofactors can be identified if the chromatin opening kinetics are delayed in the respective mutants. Using this approach, we have tested individually all 15 viable Snf2 type ATPase deletion mutan

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13

Kulbachinskiy, A., I. Bass, E. Bogdanova, A. Goldfarb, and V. Nikiforov. "Cold Sensitivity of Thermophilic and Mesophilic RNA Polymerases." Journal of Bacteriology 186, no. 22 (2004): 7818–20. http://dx.doi.org/10.1128/jb.186.22.7818-7820.2004.

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ABSTRACT RNA polymerase from mesophilic Deinococcus radiodurans displays the same cold sensitivity of promoter opening as RNA polymerase from the closely related thermophilic Thermus aquaticus. This suggests that, contrary to the accepted view, cold sensitivity of promoter opening by thermophilic RNA polymerases may not be a consequence of their thermostability.

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14

Dienemann, Christian, Björn Schwalb, Sandra Schilbach, and Patrick Cramer. "Promoter Distortion and Opening in the RNA Polymerase II Cleft." Molecular Cell 73, no. 1 (2019): 97–106. http://dx.doi.org/10.1016/j.molcel.2018.10.014.

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15

Kamali-Moghaddam, Masood, and E. Peter Geiduschek. "Thermoirreversible and Thermoreversible Promoter Opening by TwoEscherichia coliRNA Polymerase Holoenzymes." Journal of Biological Chemistry 278, no. 32 (2003): 29701–9. http://dx.doi.org/10.1074/jbc.m304604200.

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16

Bandwar, Rajiv P., and Smita S. Patel. "The Energetics of Consensus Promoter Opening by T7 RNA Polymerase." Journal of Molecular Biology 324, no. 1 (2002): 63–72. http://dx.doi.org/10.1016/s0022-2836(02)01034-3.

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17

Lee, Bo Bae, Hyeonju Woo, Min Kyung Lee, et al. "Core promoter activity contributes to chromatin-based regulation of internal cryptic promoters." Nucleic Acids Research 49, no. 14 (2021): 8097–109. http://dx.doi.org/10.1093/nar/gkab639.

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Abstract During RNA polymerase II (RNA Pol II) transcription, the chromatin structure undergoes dynamic changes, including opening and closing of the nucleosome to enhance transcription elongation and fidelity. These changes are mediated by transcription elongation factors, including Spt6, the FACT complex, and the Set2-Rpd3S HDAC pathway. These factors not only contribute to RNA Pol II elongation, reset the repressive chromatin structures after RNA Pol II has passed, thereby inhibiting aberrant transcription initiation from the internal cryptic promoters within gene bodies. Notably, the inter

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18

Fenton, Mike S., Shun Jin Lee та Jay D. Gralla. "Escherichia coli promoter opening and −10 recognition: mutational analysis of σ70". EMBO Journal 19, № 5 (2000): 1130–37. http://dx.doi.org/10.1093/emboj/19.5.1130.

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19

Korber, Philipp, Tim Luckenbach, Dorothea Blaschke, and Wolfram Hörz. "Evidence for Histone Eviction in trans upon Induction of the Yeast PHO5 Promoter." Molecular and Cellular Biology 24, no. 24 (2004): 10965–74. http://dx.doi.org/10.1128/mcb.24.24.10965-10974.2004.

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ABSTRACT The yeast PHO5 promoter is a model system for the role of chromatin in eukaryotic gene regulation. Four positioned nucleosomes in the repressed state give way to an extended DNase I hypersensitive site upon induction. Recently this hypersensitive site was shown to be devoid of histone DNA contacts. This raises the mechanistic question of how histones are removed from the promoter. A displacement in trans or movement in cis, the latter according to the well established nucleosome sliding mechanism, are the major alternatives. In this study, we embedded the PHO5 promoter into the contex

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20

Kassavetis, George A., Ashok Kumar, Garth A. Letts, and E. Peter Geiduschek. "A post-recruitment function for the RNA polymerase III transcription–initiation factor IIIB." Proceedings of the National Academy of Sciences 95, no. 16 (1998): 9196–201. http://dx.doi.org/10.1073/pnas.95.16.9196.

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Transcription factor (TF) IIIB, which directs RNA polymerase (pol) III to its promoters, is made up of three components: the TATA box-binding protein, the TFIIB-related Brf, and the pol III-specific B′′. Certain mutations in Saccharomyces cerevisiae Brf and B′′ retain TFIIIB transcription factor activity with supercoiled DNA but are inactive with linear duplex DNA. Further analysis shows that these inactive TFIIIB–DNA complexes bind pol III and position it appropriately over the transcriptional start site but do not form DNA strand-separated open promoter complexes. It is proposed that the nor

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21

Zhang, Nan, Vidya C. Darbari, Robert Glyde, Xiaodong Zhang, and Martin Buck. "The bacterial enhancer-dependent RNA polymerase." Biochemical Journal 473, no. 21 (2016): 3741–53. http://dx.doi.org/10.1042/bcj20160741c.

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Transcription initiation is highly regulated in bacterial cells, allowing adaptive gene regulation in response to environment cues. One class of promoter specificity factor called sigma54 enables such adaptive gene expression through its ability to lock the RNA polymerase down into a state unable to melt out promoter DNA for transcription initiation. Promoter DNA opening then occurs through the action of specialized transcription control proteins called bacterial enhancer-binding proteins (bEBPs) that remodel the sigma54 factor within the closed promoter complexes. The remodelling of sigma54 o

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22

Hertel, Christina Bech, Gernot Längst, Wolfram Hörz, and Philipp Korber. "Nucleosome Stability at the Yeast PHO5 and PHO8 Promoters Correlates with Differential Cofactor Requirements for Chromatin Opening." Molecular and Cellular Biology 25, no. 24 (2005): 10755–67. http://dx.doi.org/10.1128/mcb.25.24.10755-10767.2005.

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ABSTRACT The coregulated PHO5 and PHO8 genes in Saccharomyces cerevisiae provide typical examples for the role of chromatin in promoter regulation. It has been a long-standing question why the cofactors Snf2 and Gcn5 are essential for full induction of PHO8 but dispensable for opening of the PHO5 promoter. We show that this discrepancy may result from different stabilities of the two promoter chromatin structures. To test this hypothesis, we used our recently established yeast extract in vitro chromatin assembly system, which generates the characteristic PHO5 promoter chromatin. Here we show t

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23

Wang, Shuwen, Chunguang Hu, and Jiyue Zhu. "Transcriptional Silencing of a Novel hTERT Reporter Locus during In Vitro Differentiation of Mouse Embryonic Stem Cells." Molecular Biology of the Cell 18, no. 2 (2007): 669–77. http://dx.doi.org/10.1091/mbc.e06-09-0840.

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The human telomerase reverse transcriptase hTERT is highly expressed in undifferentiated embryonic cells and silenced in the majority of somatic cells. To investigate the mechanisms of hTERT silencing, we have developed a novel reporter using a bacterial artificial chromosome (BAC) that contained the entire hTERT gene and its neighboring loci, hCRR9 and hXtrp2. Firefly and Renilla luciferases were used to monitor transcription from the hTERT and hCRR9 promoters, respectively. In mouse embryonic stem cells stably integrated with the BAC reporter, both hTERT and hCRR9 promoters were highly expre

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24

Tang, Guo-Qing, and Smita S. Patel. "T7 RNA Polymerase-Induced Bending of Promoter DNA Is Coupled to DNA Opening†." Biochemistry 45, no. 15 (2006): 4936–46. http://dx.doi.org/10.1021/bi0522910.

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25

Wang, W., M. Carey, and J. Gralla. "Polymerase II promoter activation: closed complex formation and ATP-driven start site opening." Science 255, no. 5043 (1992): 450–53. http://dx.doi.org/10.1126/science.1310361.

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26

Cook, Victoria M., and Pieter L. deHaseth. "Strand Opening-deficientEscherichia coliRNA Polymerase Facilitates Investigation of Closed Complexes with Promoter DNA." Journal of Biological Chemistry 282, no. 29 (2007): 21319–26. http://dx.doi.org/10.1074/jbc.m702232200.

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27

Palacios, Daniela, Dennis Summerbell, Peter W. J. Rigby, and Joan Boyes. "Interplay between DNA Methylation and Transcription Factor Availability: Implications for Developmental Activation of the Mouse Myogenin Gene." Molecular and Cellular Biology 30, no. 15 (2010): 3805–15. http://dx.doi.org/10.1128/mcb.00050-10.

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ABSTRACT During development, gene activation is stringently regulated to restrict expression only to the correct cell type and correct developmental stage. Here, we present mechanistic evidence that suggests DNA methylation contributes to this regulation by suppressing premature gene activation. Using the mouse Myogenin promoter as an example of the weak CpG island class of promoters, we find that it is initially methylated but becomes demethylated as development proceeds. Full hypersensitive site formation of the Myogenin promoter requires both the MEF2 and SIX binding sites, but binding to o

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28

Yu, Liuning, and Randall H. Morse. "Chromatin Opening and Transactivator Potentiation by RAP1 in Saccharomyces cerevisiae." Molecular and Cellular Biology 19, no. 8 (1999): 5279–88. http://dx.doi.org/10.1128/mcb.19.8.5279.

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ABSTRACT Transcriptional activators function in vivo via binding sites that may be packaged into chromatin. Here we show that whereas the transcriptional activator GAL4 is strongly able to perturb chromatin structure via a nucleosomal binding site in yeast, GCN4 does so poorly. Correspondingly, GCN4 requires assistance from an accessory protein, RAP1, for activation of the HIS4 promoter, whereas GAL4 does not. The requirement for RAP1 for GCN4-mediated HIS4activation is dictated by the DNA-binding domain of GCN4 and not the activation domain, suggesting that RAP1 assists GCN4 in gaining access

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29

Shidlovskii, Yulii V., Oleg V. Bylino, Alexander V. Shaposhnikov, et al. "Subunits of the PBAP Chromatin Remodeler Are Capable of Mediating Enhancer-Driven Transcription in Drosophila." International Journal of Molecular Sciences 22, no. 6 (2021): 2856. http://dx.doi.org/10.3390/ijms22062856.

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The chromatin remodeler SWI/SNF is an important participant in gene activation, functioning predominantly by opening the chromatin structure on promoters and enhancers. Here, we describe its novel mode of action in which SWI/SNF factors mediate the targeted action of an enhancer. We studied the functions of two signature subunits of PBAP subfamily, BAP170 and SAYP, in Drosophila. These subunits were stably tethered to a transgene reporter carrying the hsp70 core promoter. The tethered subunits mediate transcription of the reporter in a pattern that is generated by enhancers close to the insert

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30

Buck, M., D. Bose, P. Burrows, et al. "A second paradigm for gene activation in bacteria." Biochemical Society Transactions 34, no. 6 (2006): 1067–71. http://dx.doi.org/10.1042/bst0341067.

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Control of gene expression is key to development and adaptation. Using purified transcription components from bacteria, we employ structural and functional studies in an integrative manner to elaborate a detailed description of an obligatory step, the accessing of the DNA template, in gene expression. Our work focuses on a specialized molecular machinery that utilizes ATP hydrolysis to initiate DNA opening and permits a description of how the events triggered by ATP hydrolysis within a transcriptional activator can lead to DNA opening and transcription. The bacterial EBPs (enhancer binding pro

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31

Duan, Zhijun, George Stamatoyannopoulos та Qiliang Li. "Role of NF-Y in In Vivo Regulation of the γ-Globin Gene". Molecular and Cellular Biology 21, № 9 (2001): 3083–95. http://dx.doi.org/10.1128/mcb.21.9.3083-3095.2001.

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ABSTRACT The duplicated CCAAT box is required for γ gene expression. We report here that the transcriptional factor NF-Y is recruited to the duplicated CCAAT box in vivo. A mutation of the duplicated CCAAT box that severely disrupts the NF-Y binding also reduces the accessibility level of the γ gene promoter, affects the assembly of basal transcriptional machinery, and increases the recruitment of GATA-1 to the locus control region (LCR) and the proximal promoter and the recruitment of transcription cofactor CBP/p300 to the LCR. These findings suggest that recruitment of NF-Y to the duplicated

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Wigneshweraraj, Siva R., Patricia C. Burrows, Konstantin Severinov та Martin Buck. "Stable DNA Opening within Open Promoter Complexes Is Mediated by the RNA Polymerase β′-Jaw Domain". Journal of Biological Chemistry 280, № 43 (2005): 36176–84. http://dx.doi.org/10.1074/jbc.m506416200.

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DNA opening for transcription-competent open promoter complex (OC) formation by the bacterial RNA polymerase (RNAP) relies upon a complex network of interactions between the structurally conserved and flexible modules of the catalytic β and β′-subunits, RNAP-associated σ-subunit, and the DNA. Here, we show that one such module, the β′-jaw, functions to stabilize the OC. In OCs formed by the major σ70-RNAP, the stabilizing role of the β′-jaw is not restricted to any particular melted DNA segment. In contrast, in OCs formed by the major variant σ54-RNAP, the β′-jaw and a conserved σ54 regulatory

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33

Rubin, Joel E., Peter Pasceri, Xiumei Wu, Philippe Leboulch та James Ellis. "Locus control region activity by 5′HS3 requires a functional interaction with β-globin gene regulatory elements: expression of novel β/γ-globin hybrid transgenes". Blood 95, № 10 (2000): 3242–49. http://dx.doi.org/10.1182/blood.v95.10.3242.

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Abstract The human β-globin locus control region (LCR) contains chromatin opening and transcriptional enhancement activities that are important to include in β-globin gene therapy vectors. We previously used single-copy transgenic mice to map chromatin opening activity to the 5′HS3 LCR element. Here, we test novel hybrid globin genes to identify β-globin gene sequences that functionally interact with 5′HS3. First, we show that an 850-base pair (bp) 5′HS3 element activates high-level β-globin gene expression in fetal livers of 17 of 17 transgenic mice, including 3 single-copy animals, but fails

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34

Rubin, Joel E., Peter Pasceri, Xiumei Wu, Philippe Leboulch та James Ellis. "Locus control region activity by 5′HS3 requires a functional interaction with β-globin gene regulatory elements: expression of novel β/γ-globin hybrid transgenes". Blood 95, № 10 (2000): 3242–49. http://dx.doi.org/10.1182/blood.v95.10.3242.010k27_3242_3249.

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The human β-globin locus control region (LCR) contains chromatin opening and transcriptional enhancement activities that are important to include in β-globin gene therapy vectors. We previously used single-copy transgenic mice to map chromatin opening activity to the 5′HS3 LCR element. Here, we test novel hybrid globin genes to identify β-globin gene sequences that functionally interact with 5′HS3. First, we show that an 850-base pair (bp) 5′HS3 element activates high-level β-globin gene expression in fetal livers of 17 of 17 transgenic mice, including 3 single-copy animals, but fails to repro

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35

Plachetka, Annette, Olesya Chayka, Carola Wilczek, Svitlana Melnik, Constanze Bonifer та Karl-Heinz Klempnauer. "C/EBPβ Induces Chromatin Opening at a Cell-Type-Specific Enhancer". Molecular and Cellular Biology 28, № 6 (2008): 2102–12. http://dx.doi.org/10.1128/mcb.01943-07.

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ABSTRACT We have used the chicken mim-1 gene as a model to study the mechanisms by which transcription factors gain initial access to their target sites in compacted chromatin. The expression of mim-1 is restricted to the myelomonocytic lineage of the hematopoietic system where it is regulated synergistically by the Myb and CCAAT/enhancer binding protein (C/EBP) factors. Myb and C/EBPβ cooperate at two distinct cis elements of mim-1, the promoter and a cell-type-specific enhancer, both of which are associated with DNase I hypersensitive sites in myelomonocytic cells but not in mim-1-nonexpress

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36

Hatta, Mitsutoki, and Lisa Ann Cirillo. "Chromatin Opening and Stable Perturbation of Core Histone:DNA Contacts by FoxO1." Journal of Biological Chemistry 282, no. 49 (2007): 35583–93. http://dx.doi.org/10.1074/jbc.m704735200.

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FoxO1, a member of the forkhead rabdomyosarcoma (FoxO) subfamily of transcription factors, binds DNA via a highly conserved winged-helix “forkhead box” motif used by other regulatory proteins to mediate their effects through chromatin binding and remodeling. To examine how FoxO1 regulates target genes in chromatin, we studied the binding of purified recombinant FoxO1 protein to nucleosome particles and chromatin arrays containing the insulin-like growth factor-binding protein 1 promoter. We found that FoxO1 is able to bind to its cognate sites within the insulin-like growth factor-binding prot

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Unarta, Ilona Christy, Siqin Cao, Shintaroh Kubo, et al. "Role of bacterial RNA polymerase gate opening dynamics in DNA loading and antibiotics inhibition elucidated by quasi-Markov State Model." Proceedings of the National Academy of Sciences 118, no. 17 (2021): e2024324118. http://dx.doi.org/10.1073/pnas.2024324118.

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To initiate transcription, the holoenzyme (RNA polymerase [RNAP] in complex with σ factor) loads the promoter DNA via the flexible loading gate created by the clamp and β-lobe, yet their roles in DNA loading have not been characterized. We used a quasi-Markov State Model (qMSM) built from extensive molecular dynamics simulations to elucidate the dynamics of Thermus aquaticus holoenzyme’s gate opening. We showed that during gate opening, β-lobe oscillates four orders of magnitude faster than the clamp, whose opening depends on the Switch 2’s structure. Myxopyronin, an antibiotic that binds to S

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Ertel, Franziska, A. Barbara Dirac-Svejstrup, Christina Bech Hertel, Dorothea Blaschke, Jesper Q. Svejstrup, and Philipp Korber. "In Vitro Reconstitution of PHO5 Promoter Chromatin Remodeling Points to a Role for Activator-Nucleosome Competition In Vivo." Molecular and Cellular Biology 30, no. 16 (2010): 4060–76. http://dx.doi.org/10.1128/mcb.01399-09.

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ABSTRACT The yeast PHO5 promoter is a classical model for studying the role of chromatin in gene regulation. To enable biochemical dissection of the mechanism leading to PHO5 activation, we reconstituted the process in vitro. Positioned nucleosomes corresponding to the repressed PHO5 promoter state were assembled using a yeast extract-based in vitro system. Addition of the transactivator Pho4 yielded an extensive DNase I-hypersensitive site resembling induced PHO5 promoter chromatin. Importantly, this remodeling was energy dependent. In contrast, little or no chromatin remodeling was detected

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39

Albert, T., J. Mautner, J. O. Funk, K. Hörtnagel, A. Pullner, and D. Eick. "Nucleosomal structures of c-myc promoters with transcriptionally engaged RNA polymerase II." Molecular and Cellular Biology 17, no. 8 (1997): 4363–71. http://dx.doi.org/10.1128/mcb.17.8.4363.

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Organization of DNA into chromatin has been shown to contribute to a repressed state of gene transcription. Disruption of nucleosomal structure is observed in response to gene induction, suggesting a model in which RNA polymerase II (pol II) is recruited to the promoter upon reorganization of nucleosomes. Here we show that induction of c-myc transcription correlates with the disruption of two nucleosomes in the upstream promoter region. This nucleosomal disruption, however, is not necessary for the binding of pol II to the promoter. Transcriptionally engaged pol II complexes can be detected wh

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40

Kassavetis, G. A. "The RNA polymerase III transcription initiation factor TFIIIB participates in two steps of promoter opening." EMBO Journal 20, no. 11 (2001): 2823–34. http://dx.doi.org/10.1093/emboj/20.11.2823.

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41

Grünberg, Sebastian, Linda Warfield, and Steven Hahn. "Architecture of the RNA polymerase II preinitiation complex and mechanism of ATP-dependent promoter opening." Nature Structural & Molecular Biology 19, no. 8 (2012): 788–96. http://dx.doi.org/10.1038/nsmb.2334.

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42

Lin, Yin Chun, Wai S. Choi, and Jay D. Gralla. "TFIIH XPB mutants suggest a unified bacterial-like mechanism for promoter opening but not escape." Nature Structural & Molecular Biology 12, no. 7 (2005): 603–7. http://dx.doi.org/10.1038/nsmb949.

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43

Cailotto, Frederic, Pascal Reboul, Sylvie Sebillaud, Patrick Netter, Jean-Yves Jouzeau та Arnaud Bianchi. "Calcium Input Potentiates the Transforming Growth Factor (TGF)-β1-dependent Signaling to Promote the Export of Inorganic Pyrophosphate by Articular Chondrocyte". Journal of Biological Chemistry 286, № 22 (2011): 19215–28. http://dx.doi.org/10.1074/jbc.m110.175448.

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Transforming growth factor (TGF)-β1 stimulates extracellular PPi (ePPi) generation and promotes chondrocalcinosis, which also occurs secondary to hyperparathyroidism-induced hypercalcemia. We previously demonstrated that ANK was up-regulated by TGF-β1 activation of ERK1/2 and Ca2+-dependent protein kinase C (PKCα). Thus, we investigated mechanisms by which calcium could affect ePPi metabolism, especially its main regulating proteins ANK and PC-1 (plasma cell membrane glycoprotein-1). We stimulated articular chondrocytes with TGF-β1 under extracellular (eCa2+) or cytosolic Ca2+ (cCa2+) modulati

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Yarragudi, Arunadevi, Tsuyoshi Miyake, Rong Li, and Randall H. Morse. "Comparison of ABF1 and RAP1 in Chromatin Opening and Transactivator Potentiation in the Budding Yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 24, no. 20 (2004): 9152–64. http://dx.doi.org/10.1128/mcb.24.20.9152-9164.2004.

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ABSTRACT Autonomously replicating sequence binding factor 1 (ABF1) and repressor/activator protein 1 (RAP1) from budding yeast are multifunctional, site-specific DNA-binding proteins, with roles in gene activation and repression, replication, and telomere structure and function. Previously we have shown that RAP1 can prevent nucleosome positioning in the vicinity of its binding site and have provided evidence that this ability to create a local region of “open” chromatin contributes to RAP1 function at the HIS4 promoter by facilitating binding and activation by GCN4. Here we examine and direct

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Oleggini, Roberta, and Armando Di Donato. "Lysyl oxidase regulates MMTV promoter: indirect evidence of histone H1 involvement." Biochemistry and Cell Biology 89, no. 6 (2011): 522–32. http://dx.doi.org/10.1139/o11-049.

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Lysyl oxidase (LOX) is the enzyme that facilitates the cross-linking of collagen and elastin, although other functions for this enzyme have been indicated. Of these other functions, we describe herein the ability of LOX to regulate several gene promoters, like collagen III, elastin, and cyclin D1. We have previously demonstrated a specific binding between LOX and histone H1, in vitro. Therefore, we investigated whether LOX would affect the mouse mammary tumor virus (MMTV) promoter and its glucocorticoid regulation, which depends on the phophorylation status of histone H1. Our results show that

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Lavelle, Donald, Kestas Vaitkus, Maria Hankewych, Mahipal Singh та Joseph DeSimone. "Changes in Globin Gene Methylation and Covalent Histone Modifications of Chromatin Associated with the ε-, γ-, and β-Globin Promoters of the Baboon (P. Anubis) during Development." Blood 104, № 11 (2004): 1206. http://dx.doi.org/10.1182/blood.v104.11.1206.1206.

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Abstract The pattern of globin gene expression during development is conserved in all simian primates, but not in prosimians or other species. Therefore knowledge of the mechanisms regulating globin gene expression in animal models such as the baboon (P. anubis) is directly applicable to human. This investigation addressed the role of chromatin structure in developmental regulation of globin gene expression. DNA methylation of the ε- and γ-gene promoters and covalent histone modifications in chromatin associated with the ε- γ- and β-globin gene promoters have been investigated in 40d fetal pri

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Alekseev, Sergey, Zita Nagy, Jérémy Sandoz, et al. "Transcription without XPB Establishes a Unified Helicase-Independent Mechanism of Promoter Opening in Eukaryotic Gene Expression." Molecular Cell 65, no. 3 (2017): 504–14. http://dx.doi.org/10.1016/j.molcel.2017.01.012.

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Kassavetis, George A., Shulin Han, Souad Naji, and E. Peter Geiduschek. "The Role of Transcription Initiation Factor IIIB Subunits in Promoter Opening Probed by Photochemical Cross-linking." Journal of Biological Chemistry 278, no. 20 (2003): 17912–17. http://dx.doi.org/10.1074/jbc.m300743200.

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Nemeth, Michael J., David M. Bodine, Lisa J. Garrett та Christopher H. Lowrey. "An Erythroid-Specific Chromatin Opening Element Reorganizes β-Globin Promoter Chromatin Structure and Augments Gene Expression". Blood Cells, Molecules, and Diseases 27, № 4 (2001): 767–80. http://dx.doi.org/10.1006/bcmd.2001.0448.

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Logquist, Alan K., Han Li, Martin lmboden та Marvin R. Paule. "Promoter opening (melting) and transcription initiation by RNA polymerase I requires neither nucleotideβ,γhydrolysis norprotein phosphorylation". Nucleic Acids Research 21, № 14 (1993): 3233–38. http://dx.doi.org/10.1093/nar/21.14.3233.

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