Relevant bibliographies by topics / Chromatin-remodelling

Academic literature on the topic 'Chromatin-remodelling'

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Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Chromatin-remodelling"

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Meyer, Peter. "Chromatin remodelling." Current Opinion in Plant Biology 4, no. 5 (October 2001): 457–62. http://dx.doi.org/10.1016/s1369-5266(00)00200-4.

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Ho, Lena, and Gerald R. Crabtree. "Chromatin remodelling during development." Nature 463, no. 7280 (January 2010): 474–84. http://dx.doi.org/10.1038/nature08911.

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Flaus, A., I. Whitehouse, C. Stockdale, K. Havas, M. Bruno, N. Wiechens, and T. A. Owen-Hughes. "Pathways for remodelling chromatin." Biochemical Society Transactions 30, no. 5 (October 1, 2002): A97. http://dx.doi.org/10.1042/bst030a097.

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Owen-Hughes, T. "Pathways for remodelling chromatin." Biochemical Society Transactions 31, no. 5 (October 1, 2003): 893–905. http://dx.doi.org/10.1042/bst0310893.

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The alteration of chromatin structure plays an integral role in gene regulation. One means by which eukaryotes manipulate chromatin structure involves the use of ATP-dependent chromatin-remodelling enzymes. It appears likely that these enzymes play a widespread role in the regulation of many nuclear processes. Recently, significant progress has been made in defining the alterations to chromatin structure that these enzymes generate. The ability to alter nucleosome positioning may be a common feature of all ATP-dependent remodelling enzymes, but the spectrum of positions to which nucleosomes are relocated varies. Mounting evidence supports the ability of remodelling enzymes to translocate along DNA. This provides a means by which they could alter both the twist and writhe of DNA on the surface of nucleosomes, and so accelerate nucleosome repositioning.
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Willard, Huntington F., and Helen K. Salz. "Remodelling chromatin with RNA." Nature 386, no. 6622 (March 1997): 228–29. http://dx.doi.org/10.1038/386228a0.

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Whitehouse, I., A. Flaus, K. Havas, and T. Owen-Hughes. "Mechanisms for ATP-dependent chromatin remodelling." Biochemical Society Transactions 28, no. 4 (August 1, 2000): 376–79. http://dx.doi.org/10.1042/bst0280376.

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Gene regulation involves the generation of a local chromatin topology that is conducive to transcription. Several classes of chromatin remodelling activity have been shown to play a role in this process. ATP-dependent chromatin-remodelling activities use energy derived from the hydrolysis of ATP to alter the structure of chromatin, making it more accessible for transcription factor binding. The yeast SWI-SWF complex is the founding member of this family of ATP-dependent chromatin-remodelling activities. We have developed a model system to study the ability of the SWI-SWF complex to alter chromatin structure. Using this system, we find that SWI-SWF is able to alter the position of nucleosomes along the DNA. This is consistent with recent reports that other ATP-dependent chromatin-remodelling activities can alter the positions of nucleosomes along DNA. This suggests that nucleosome mobilization may be a general feature of the activity of ATP-dependent chromatin-remodelling activities. Some of the mechanisms by which nucleosomes may be moved along DNA are discussed.
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Sundaramoorthy, Ramasubramian, and Tom Owen-Hughes. "Chromatin remodelling comes into focus." F1000Research 9 (August 20, 2020): 1011. http://dx.doi.org/10.12688/f1000research.21933.1.

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ATP-dependent chromatin remodelling enzymes are molecular machines that act to reconfigure the structure of nucleosomes. Until recently, little was known about the structure of these enzymes. Recent progress has revealed that their interaction with chromatin is dominated by ATPase domains that contact DNA at favoured locations on the nucleosome surface. Contacts with histones are limited but play important roles in modulating activity. The ATPase domains do not act in isolation but are flanked by diverse accessory domains and subunits. New structures indicate how these subunits are arranged in multi-subunit complexes providing a framework from which to understand how a common motor is applied to distinct functions.
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Strzyz, Paulina. "R loops regulate chromatin remodelling." Nature Reviews Molecular Cell Biology 16, no. 12 (November 18, 2015): 703. http://dx.doi.org/10.1038/nrm4094.

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Allison, Susan J. "Chromatin remodelling in diabetic nephropathy." Nature Reviews Nephrology 12, no. 8 (July 18, 2016): 444. http://dx.doi.org/10.1038/nrneph.2016.106.

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Flintoft, Louisa. "Chromatin remodelling finds its niche." Nature Reviews Genetics 7, no. 1 (January 2006): 5. http://dx.doi.org/10.1038/nrg1784.

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Dissertations / Theses on the topic "Chromatin-remodelling"

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Gelius, Birgitta. "Chromatin remodelling and gene regulation /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-89428-16-1/.

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Fisher, Alex. "Chromatin remodelling in light signalling." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/29749.

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Plants selectively deplete incident light of red (R) wavelength, relative to far-red (FR) wavelength light. Consequently, the relative proportions of R and FR (R:FR ratio) act as an indicator of surrounding vegetation and plants, via the phytochrome photoreceptors, are capable of detecting this. Low R:FR ratio is interpreted as surrounding competition and results in plants eliciting, what is known as, the shade avoidance response. This involves a host of both phenotypic and molecular changes, including increased hypocotyl growth, earlier flowering time and changes in gene expression. The fundamental mechanisms underlying R:FR-mediated changes in gene expression are not fully characterised. Given that increasing evidence in Arabidopsis suggests that the structure of chromatin is integral in the regulation of gene expression in response to environmental stimuli, it was investigated to see if this was the case in R:FR ratio signalling. Here, DNaseI sensitivity assays demonstrate that the shade avoidance genes ATHB2, PIL1 and XTH15 all undergo gross changes in chromatin structure in plants grown in light/dark cycles and treated with low R:FR ratio. These low R:FR induced changes in DNaseI sensitivity are conspicuously absent when plants are grown in continuous light, suggesting an involvement of the circadian clock. Complementary to this, the use of ChIP has identified the coding region of PIL1 to show increased association with hyper-acetylated H3K9 and possibly H3K14 in response to low R:FR ratio. Together, this work demonstrates that changes in R:FR ratio induce changes in gene expression that are correlated with changes in chromatin structure and histone modifications and that these changes could be regulated by the circadian clock. In addition, the identification and construction of multiple mutant and transgenic lines expressing altered levels of chromatin modifying protein was attempted.
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Guyver, Carly Jane. "Chromatin remodelling in T cell tuning." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439671.

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Mastorakis, Emmanouil. "Chromatin remodelling during plant-pathogen interactions." Thesis, University of Warwick, 2017. http://wrap.warwick.ac.uk/101423/.

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Plants - including commercially important crops - are exposed to numerous pathogens often resulting in significant loss of yield. Understanding the underlying mechanisms of pathogen recognition and defence strategies is key in successfully ensuring food security. Research on plant-pathogen interactions has mainly focused on the gene networks after pathogen perception as well the identification of resistance genes. Latest research suggests that chromatin remodelling, including nucleosome displacement and DNA or histone-modifying enzymes are important in plant immunity. This thesis focuses on chromatin remodelling as the mechanism by which plants mount an effective immune response. The thesis also investigates the role of histone acetylation as one of several chromatin remodelling mechanisms. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) are two classes of histone modifying enzymes that antagonistically govern the acetylation levels of histones in gene promoters and gene bodies ultimately affecting gene expression. HAG1 was identified as an important positive regulator of plant immunity in the interaction with Pst DC3000. A proteomic approach allowed the identification of TOPLESS family members as HAG1 interactors. Considering that chromatin remodelling is an important aspect of plant immunity, it was hypothesised that pathogens have evolved mechanisms to interfere with such processes. To this end, this thesis will present a comprehensive approach towards identifying Pst DC3000 Type-III effectors with the ability to interfere with chromatin remodelling. HopO1-1 was initially identified as an effector with chromatin binding properties, however, further experiments pointed more strongly towards this effector’s involvement in processes such as translation and photosynthesis. Overall, this thesis contributes towards a better understanding of the roles of histone acetylation and HAG1 histone acetyltransferase in plant immunity and sheds light into which Pst DC3000 effectors could be potentially involved in chromatin remodelling processes.
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Jang, Boyun. "Analysis of chromatin targeting modules in the chromatin remodelling enzyme NURF." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5204/.

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Drosophila nucleosome remodelling factor (NURF) is one of the founding members of the ISWI family of ATP-dependent chromatin remodelling enzymes and mediates energy-dependent nucleosome sliding leading to transcription regulation. In previous work (Wysocka et al., 2006), NURF was shown to be recruited to gene targets by binding specific histone modifications. The largest subunit of NURF, NURF301, contains a bromodomain and three PHD finger domains that have the ability to recognize specific histone modifications. Here we determine the histone binding-specificities of these domains, and how NURF histone binding is influenced by histone modification "cross-talk". This has been analyzed by histone peptide library array assays and our study shows that the PHD2 domain specifically recognizes the histone H3K4me3 mark. This binding can be inhibited by phosphorylation of H3 Thr 3, while enhanced by acetylation of H3 Lys 9 and phosphorylation of Ser 10. The binding specificities of bromodomain, PHD and PHD1 domains were also determined. These data were confirmed by peptide pull-down, Biacore and immunofluorescence microscopy assays. Moreover, two different NURF301-A/B and NURF301-C isoforms were CTAP-tagged by recombineering, and we used chromatin immunoprecipitation coupled sequencing (ChIP-Seq) to profile the genome-wide distribution of NURF in vivo. Therefore, our results identify regulatory mechanisms of histone modifications directing recruitment of ATP-dependent chromatin remodelling enzymes.
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Bassett, A. R. "SUMOylation and chromatin remodelling in Drosophila melanogaster." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596455.

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The thesis describes the analysis of the function of the small ubiquitin-like modifier (SUMO) in Drosophila melanogaster, and a potential effector of such modification, the chromatin remodelling factor dATRX. A substrate of SUMO modification, the transcriptional repressor Tramtrack 69 was verified, and the site of SUMO modification narrowed to a single lysine residue. Mutation of this prevented SUMOylation, and the functional consequence of this was analysed in a variety of assays, including transcriptional repression, subcellular localisation, degradation and overexpression in fly tissues. The ETS-domain transcription factor Pointed was also identified as a potential SUMO substrate and the functional consequences of such a modification analysed in a similar manner. The role of SUMOylation in the intact fly was analysed through clonal loss of function and overexpression phenotypes in both adult and larval fly tissues, implicating it in wing and eye development and melanotic tumour formation. The similarities to the phenotypes of mutation in dISW1, another chromatin remodelling factor are discussed. SUMO was shown to be a strong suppressor of position effect variegation (PEV) and potential mechanisms for its action are discussed. The mechanism by which SUMOylation acts is addressed through analysis of SUMO interacting proteins using a yeast two-hybrid screen. This identified the chromatin remodelling complexes NuRD and dATRX and the histone methyltransferase pR-Set7 as potential effectors of SUMO modification, which were verified by GST-pulldown assay. They were shown to interact with wild type SUMO but not a mutant form that is unable to repress transcription, suggesting a possible role in transcriptional repression by SUMO.
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Durley, Samuel C. "Chromatin remodelling in Sacchromyces cerevisiae by RSC." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/56801/.

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RSC is a member of the multi-subunit SWI/SNF family of ATPase-dependent chromatin remodellers and it is implicated in transcriptional regulation and DNA repair in Saccharomyces cerevisiae. The central ATPase subunit, Sth1, translocates nucleosomes in vitro and mutations in human RSC sub-unit orthologues are implicated in human disease. RSC is found in two isoforms, defined by the presence of either the Rsc1 or Rsc2 subunits, and these appear to confer distinct remodelling functions in different genomic contexts. At the MAT locus, Rsc1 and Rsc2 appear to mediate different forms of nucleosome positioning which are required for efficient mating type switching. Elsewhere in the genome, it has been suggested that RSC can create partially un-wrapped nucleosomes in order to facilitate transcription factor binding. This thesis uses indirect-end-label analysis and chromatin-sequencing technologies to dissect the chromatin remodelling functions of RSC and to determine the roles of Rsc1, Rsc2 and their subdomains. The work presented here suggests that four chromatin-remodelling outcomes arise from RSC activity. Firstly, RSC alters the positions of a tract of nucleosomes abutting HO endonuclease-induced double-strand DNA breaks both at MAT and non-MAT loci in a Rsc1-dependent manner. This activity can be transferred from Rsc1 to Rsc2 by swapping BAH domains. Secondly, RSC can aggregate nucleosomes into a large nuclease-resistant structure, termed an alphasome, in a Rsc2- and Rsc7-dependent manner. Thirdly, RSC positions nucleosomes at tRNA genes in a manner that requires both Rsc1 and Rsc2. Finally, chromatin particles consistent with previously described un-wound nucleosomes are confirmed to be present in specific promoter regions. Although Rsc1- and Rsc2- dependent subsets of these promoters could be identified, and associations with binding motifs for particular transcriptions factors were discovered, it was ultimately not possible to unambiguously define why some gene promoters depend on one RSC sub-unit rather than the other.
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Cavellán, Erica. "Chromatin remodelling in Pol I and III transcription." Doctoral thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-991.

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Compaction of chromosomes in the eukaryotic cell is due to interactions between DNA and proteins and interactions between proteins. These two types of interaction form a dynamic structure, known as "chromatin". The condensation of chromatin must be carefully regulated, since the structure is an obstacle for factors that need access to the DNA. An extensive range of components, one group of which is the ATP-dependent chromatin remodel-ling complexes, controls the accessibility of DNA. These complexes have been studied in a variety of eukaryotic systems, and their functions in major events in the cell, such as replication, DNA-repair and transcription have been established, as have their roles in the assembly and maintenance of chromatin. All of the complexes contain a highly conserved ATPase, which belongs to the SWI2/SNF2 family of proteins, one group of which is known as the ISWI proteins. There are two forms of ISWI in human, known as "SNF2h" and "SNF2l".

We have identified a human SNF2h-assembly, B-WICH, that consists of SNF2h, William’s syndrome transcription factor (WSTF), nuclear myosin (NM1), and a number of additional nuclear proteins including the Myb-binding protein 1a (Myb bp1a), SF3b155/SAP155, the RNA helicase II/Guα, the proto-oncogene Dek, and the Cockayne Syndrome protein B (CSB). The 45S rRNA, 5S rRNA and 7SL RNA are all parts of the B-WICH assembly. The formation of B-WICH depends on active transcription, and is implicated in the regulation of both RNA transcription by both pol I and pol III. The B-WICH provides a link between RNA and the chromatin structure.

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Lee, Huay-Leng. "Glucocorticoid receptor mediated MMTV chromatin remodelling in vivo." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq28504.pdf.

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Cavellán, Erica. "Chromatin remodelling in Pol I and III transcription /." Stockholm : Wenner-Gren Institute for Experimental Biology, Stockholm university, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-991.

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Books on the topic "Chromatin-remodelling"

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Radzioch, Danuta, ed. Chromatin Remodelling. InTech, 2013. http://dx.doi.org/10.5772/50815.

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Donev, Rossen. Chromatin Remodelling and Immunity. Elsevier Science & Technology, 2017.

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Donev, Rossen. Chromatin Remodelling and Immunity. Elsevier Science & Technology, 2017.

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Alvarez-Venegas, Raúl, Clelia De la Peña, and Juan Armando Casas-Mollano. Epigenetics in Plants of Agronomic Importance : Fundamentals and Applications: Transcriptional Regulation and Chromatin Remodelling in Plants. Springer, 2016.

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Alvarez-Venegas, Raúl, Clelia De la Peña, and Juan Armando Casas-Mollano. Epigenetics in Plants of Agronomic Importance : Fundamentals and Applications: Transcriptional Regulation and Chromatin Remodelling in Plants. Springer, 2014.

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Alvarez-Venegas, Raúl, Juan Armando Casas-Mollano, and Clelia De-la-Peña. Epigenetics in Plants of Agronomic Importance : Fundamentals and Applications: Transcriptional Regulation and Chromatin Remodelling in Plants. Springer, 2019.

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Eisen, Tim. The patient with renal cell cancer. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.

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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.
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Book chapters on the topic "Chromatin-remodelling"

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Wotton, David, and Jacqueline C. Merrill. "SUMO and Chromatin Remodelling." In SUMO Regulation of Cellular Processes, 59–76. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2649-1_4.

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De La Fuente, Rabindranath, Claudia Baumann, Feikun Yang, and Maria M. Viveiros. "Chromatin Remodelling in Mammalian Oocytes." In Oogenesis, 447–78. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470687970.ch18.

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de Campos Vidal, Benedicto, Marina B. Felisbino, and Maria Luiza S. Mello. "Image Analysis of Chromatin Remodelling." In Methods in Molecular Biology, 99–108. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-706-8_9.

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Madders, Eleanor C. E. T., and Jason L. Parsons. "Base Excision Repair in Chromatin and the Requirement for Chromatin Remodelling." In Advances in Experimental Medicine and Biology, 59–75. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41283-8_5.

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Miller, Anzy, and Brian Hendrich. "Chromatin Remodelling Proteins and Cell Fate Decisions in Mammalian Preimplantation Development." In Chromatin Regulation of Early Embryonic Lineage Specification, 3–14. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-63187-5_2.

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Lodde, V., A. M. Luciano, F. Franciosi, R. Labrecque, and M. A. Sirard. "Accumulation of Chromatin Remodelling Enzyme and Histone Transcripts in Bovine Oocytes." In Results and Problems in Cell Differentiation, 223–55. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60855-6_11.

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Vagnarelli, Paola. "Repo-Man at the Intersection of Chromatin Remodelling, DNA Repair, Nuclear Envelope Organization, and Cancer Progression." In Cancer Biology and the Nuclear Envelope, 401–14. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8032-8_18.

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R., Elena, Luis Torres, Rosa Zaragoza, and Juan R. "The Role of Id2 in the Regulation of Chromatin Structure and Gene Expression." In Chromatin Remodelling. InTech, 2013. http://dx.doi.org/10.5772/54969.

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Zahorakova, Daniela. "Rett Syndrome." In Chromatin Remodelling. InTech, 2013. http://dx.doi.org/10.5772/55020.

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Gong, Lili, Edward Wang, and Shiaw-Yih Li. "Chromatin Remodeling in DNA Damage Response and Human Aging." In Chromatin Remodelling. InTech, 2013. http://dx.doi.org/10.5772/55272.

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Conference papers on the topic "Chromatin-remodelling"

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Huang, Rui, Simon P. Langdon, David J. Harrison, and Dana Faratian. "Abstract 4085: The roles of HDACs in chromatin remodelling and response to chemotherapy in cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4085.

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Mooney, B., S. Das, R. Klinger, B. Moran, K. Wynne, W. Gallagher, T. Ni Chonghaile, G. Cagney, A. Bracken, and D. O’Connor. "PO-090 Expression of the cocaine- and amphetamine-regulated transcript (CART) recruits SWI/SNF chromatin remodelling complexes to the oestrogen receptor." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.132.

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O'Connor, DP, B. Mooney, S. Das, R. Klinger, B. Moran, T. Ni Chonghaile, G. Cagney, A. Bracken, and WM Gallagher. "Abstract P5-05-07: Expression of the cocaine- and amphetamine-regulated transcript (CART) recruits SWI/SNF chromatin remodelling complexes to the estrogen receptor." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p5-05-07.

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