Relevant bibliographies by topics / Chromatin

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Chromatin'

Author: Grafiati
Published: 4 June 2021
Last updated: 27 July 2024

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Journal articles on the topic "Chromatin"

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Mishra, Prashant K., Sultan Ciftci-Yilmaz, David Reynolds, Wei-Chun Au, Lars Boeckmann, Lauren E. Dittman, Ziad Jowhar, et al. "Polo kinase Cdc5 associates with centromeres to facilitate the removal of centromeric cohesin during mitosis." Molecular Biology of the Cell 27, no. 14 (July 15, 2016): 2286–300. http://dx.doi.org/10.1091/mbc.e16-01-0004.

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Sister chromatid cohesion is essential for tension-sensing mechanisms that monitor bipolar attachment of replicated chromatids in metaphase. Cohesion is mediated by the association of cohesins along the length of sister chromatid arms. In contrast, centromeric cohesin generates intrastrand cohesion and sister centromeres, while highly cohesin enriched, are separated by >800 nm at metaphase in yeast. Removal of cohesin is necessary for sister chromatid separation during anaphase, and this is regulated by evolutionarily conserved polo-like kinase (Cdc5 in yeast, Plk1 in humans). Here we address how high levels of cohesins at centromeric chromatin are removed. Cdc5 associates with centromeric chromatin and cohesin-associated regions. Maximum enrichment of Cdc5 in centromeric chromatin occurs during the metaphase-to-anaphase transition and coincides with the removal of chromosome-associated cohesin. Cdc5 interacts with cohesin in vivo, and cohesin is required for association of Cdc5 at centromeric chromatin. Cohesin removal from centromeric chromatin requires Cdc5 but removal at distal chromosomal arm sites does not. Our results define a novel role for Cdc5 in regulating removal of centromeric cohesins and faithful chromosome segregation.
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Daban, Joan-Ramon. "The energy components of stacked chromatin layers explain the morphology, dimensions and mechanical properties of metaphase chromosomes." Journal of The Royal Society Interface 11, no. 92 (March 6, 2014): 20131043. http://dx.doi.org/10.1098/rsif.2013.1043.

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The measurement of the dimensions of metaphase chromosomes in different animal and plant karyotypes prepared in different laboratories indicates that chromatids have a great variety of sizes which are dependent on the amount of DNA that they contain. However, all chromatids are elongated cylinders that have relatively similar shape proportions (length to diameter ratio approx. 13). To explain this geometry, it is considered that chromosomes are self-organizing structures formed by stacked layers of planar chromatin and that the energy of nucleosome–nucleosome interactions between chromatin layers inside the chromatid is approximately 3.6 × 10 −20 J per nucleosome, which is the value reported by other authors for internucleosome interactions in chromatin fibres. Nucleosomes in the periphery of the chromatid are in contact with the medium; they cannot fully interact with bulk chromatin within layers and this generates a surface potential that destabilizes the structure. Chromatids are smooth cylinders because this morphology has a lower surface energy than structures having irregular surfaces. The elongated shape of chromatids can be explained if the destabilizing surface potential is higher in the telomeres (approx. 0.16 mJ m −2 ) than in the lateral surface (approx. 0.012 mJ m −2 ). The results obtained by other authors in experimental studies of chromosome mechanics have been used to test the proposed supramolecular structure. It is demonstrated quantitatively that internucleosome interactions between chromatin layers can justify the work required for elastic chromosome stretching (approx. 0.1 pJ for large chromosomes). The high amount of work (up to approx. 10 pJ) required for large chromosome extensions is probably absorbed by chromatin layers through a mechanism involving nucleosome unwrapping.
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Chen, Yu-Fan, Chia-Ching Chou, and Marc R. Gartenberg. "Determinants of Sir2-Mediated, Silent Chromatin Cohesion." Molecular and Cellular Biology 36, no. 15 (May 16, 2016): 2039–50. http://dx.doi.org/10.1128/mcb.00057-16.

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Cohesin associates with distinct sites on chromosomes to mediate sister chromatid cohesion. Single cohesin complexes are thought to bind by encircling both sister chromatids in a topological embrace. Transcriptionally repressed chromosomal domains in the yeastSaccharomyces cerevisiaerepresent specialized sites of cohesion where cohesin binds silent chromatin in a Sir2-dependent fashion. In this study, we investigated the molecular basis for Sir2-mediated cohesion. We identified a cluster of charged surface residues of Sir2, collectively termed the EKDK motif, that are required for cohesin function. In addition, we demonstrated that Esc8, a Sir2-interacting factor, is also required for silent chromatin cohesion. Esc8 was previously shown to associate with Isw1, the enzymatic core of ISW1 chromatin remodelers, to form a variant of the ISW1a chromatin remodeling complex. WhenESC8was deleted or the EKDK motif was mutated, cohesin binding at silenced chromatin domains persisted but cohesion of the domains was abolished. The data are not consistent with cohesin embracing both sister chromatids within silent chromatin domains. Transcriptional silencing remains largely intact in strains lackingESC8or bearing EKDK mutations, indicating that silencing and cohesion are separable functions of Sir2 and silent chromatin.
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Giménez-Abián, J. F., D. J. Clarke, A. M. Mullinger, C. S. Downes, and R. T. Johnson. "A postprophase topoisomerase II-dependent chromatid core separation step in the formation of metaphase chromosomes." Journal of Cell Biology 131, no. 1 (October 1, 1995): 7–17. http://dx.doi.org/10.1083/jcb.131.1.7.

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Metaphase chromatids are believed to consist of loops of chromatin anchored to a central scaffold, of which a major component is the decatenatory enzyme DNA topoisomerase II. Silver impregnation selectively stains an axial element of metaphase and anaphase chromatids; but we find that in earlier stages of mitosis, silver staining reveals an initially single, folded midline structure, which separates at prometaphase to form two chromatid axes. Inhibition of topoisomerase II prevents this separation, and also prevents the contraction of chromatids that occurs when metaphase is arrested. Immunolocalization of topoisomerase II alpha reveals chromatid cores analogous to those seen with silver staining. We conclude that the chromatid cores in early mitosis form a single structure, constrained by DNA catenations, which must separate before metaphase chromatids can be resolved.
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Muñoz, Sofía, Francesca Passarelli, and Frank Uhlmann. "Conserved roles of chromatin remodellers in cohesin loading onto chromatin." Current Genetics 66, no. 5 (April 10, 2020): 951–56. http://dx.doi.org/10.1007/s00294-020-01075-x.

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Abstract Cohesin is a conserved, ring-shaped protein complex that topologically entraps DNA. This ability makes this member of the structural maintenance of chromosomes (SMC) complex family a central hub of chromosome dynamics regulation. Besides its essential role in sister chromatid cohesion, cohesin shapes the interphase chromatin domain architecture and plays important roles in transcriptional regulation and DNA repair. Cohesin is loaded onto chromosomes at centromeres, at the promoters of highly expressed genes, as well as at DNA replication forks and sites of DNA damage. However, the features that determine these binding sites are still incompletely understood. We recently described a role of the budding yeast RSC chromatin remodeler in cohesin loading onto chromosomes. RSC has a dual function, both as a physical chromatin receptor of the Scc2/Scc4 cohesin loader complex, as well as by providing a nucleosome-free template for cohesin loading. Here, we show that the role of RSC in sister chromatid cohesion is conserved in fission yeast. We discuss what is known about the broader conservation of the contribution of chromatin remodelers to cohesin loading onto chromatin.
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Stephens, Andrew D., Julian Haase, Leandra Vicci, Russell M. Taylor, and Kerry Bloom. "Cohesin, condensin, and the intramolecular centromere loop together generate the mitotic chromatin spring." Journal of Cell Biology 193, no. 7 (June 27, 2011): 1167–80. http://dx.doi.org/10.1083/jcb.201103138.

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Sister chromatid cohesion provides the mechanistic basis, together with spindle microtubules, for generating tension between bioriented chromosomes in metaphase. Pericentric chromatin forms an intramolecular loop that protrudes bidirectionally from the sister chromatid axis. The centromere lies on the surface of the chromosome at the apex of each loop. The cohesin and condensin structural maintenance of chromosomes (SMC) protein complexes are concentrated within the pericentric chromatin, but whether they contribute to tension-generating mechanisms is not known. To understand how pericentric chromatin is packaged and resists tension, we map the position of cohesin (SMC3), condensin (SMC4), and pericentric LacO arrays within the spindle. Condensin lies proximal to the spindle axis and is responsible for axial compaction of pericentric chromatin. Cohesin is radially displaced from the spindle axis and confines pericentric chromatin. Pericentric cohesin and condensin contribute to spindle length regulation and dynamics in metaphase. Together with the intramolecular centromere loop, these SMC complexes constitute a molecular spring that balances spindle microtubule force in metaphase.
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SIMPSON, R. T. "Chromatin Research Surveyed: Chromatin." Science 243, no. 4895 (March 3, 1989): 1220. http://dx.doi.org/10.1126/science.243.4895.1220.

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Lawrimore, Josh, Ayush Doshi, Brandon Friedman, Elaine Yeh, and Kerry Bloom. "Geometric partitioning of cohesin and condensin is a consequence of chromatin loops." Molecular Biology of the Cell 29, no. 22 (November 2018): 2737–50. http://dx.doi.org/10.1091/mbc.e18-02-0131.

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SMC (structural maintenance of chromosomes) complexes condensin and cohesin are crucial for proper chromosome organization. Condensin has been reported to be a mechanochemical motor capable of forming chromatin loops, while cohesin passively diffuses along chromatin to tether sister chromatids. In budding yeast, the pericentric region is enriched in both condensin and cohesin. As in higher-eukaryotic chromosomes, condensin is localized to the axial chromatin of the pericentric region, while cohesin is enriched in the radial chromatin. Thus, the pericentric region serves as an ideal model for deducing the role of SMC complexes in chromosome organization. We find condensin-mediated chromatin loops establish a robust chromatin organization, while cohesin limits the area that chromatin loops can explore. Upon biorientation, extensional force from the mitotic spindle aggregates condensin-bound chromatin from its equilibrium position to the axial core of pericentric chromatin, resulting in amplified axial tension. The axial localization of condensin depends on condensin’s ability to bind to chromatin to form loops, while the radial localization of cohesin depends on cohesin’s ability to diffuse along chromatin. The different chromatin-tethering modalities of condensin and cohesin result in their geometric partitioning in the presence of an extensional force on chromatin.
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Ghaddar, Nagham, Pierre Luciano, Vincent Géli, and Yves Corda. "Chromatin assembly factor-1 preserves genome stability in ctf4∆ cells by promoting sister chromatid cohesion." Cell Stress 7, no. 9 (September 11, 2023): 69–89. http://dx.doi.org/10.15698/cst2023.09.289.

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Chromatin assembly and the establishment of sister chromatid cohesion are intimately connected to the progression of DNA replication forks. Here we examined the genetic interaction between the heterotrimeric chromatin assembly factor-1 (CAF-1), a central component of chromatin assembly during replication, and the core replisome component Ctf4. We find that CAF-1 deficient cells as well as cells affected in newly-synthesized H3-H4 histones deposition during DNA replication exhibit a severe negative growth with ctf4∆ mutant. We dissected the role of CAF-1 in the maintenance of genome stability in ctf4∆ yeast cells. In the absence of CTF4, CAF-1 is essential for viability in cells experiencing replication problems, in cells lacking functional S-phase checkpoint or functional spindle checkpoint, and in cells lacking DNA repair pathways involving homologous recombination. We present evidence that CAF-1 affects cohesin association to chromatin in a DNA-damage-dependent manner and is essential to maintain cohesion in the absence of CTF4. We also show that Eco1-catalyzed Smc3 acetylation is reduced in absence of CAF-1. Furthermore, we describe genetic interactions between CAF-1 and essential genes involved in cohesin loading, cohesin stabilization, and cohesin component indicating that CAF-1 is crucial for viability when sister chromatid cohesion is affected. Finally, our data indicate that the CAF-1-dependent pathway required for cohesion is functionally distinct from the Rtt101-Mms1-Mms22 pathway which functions in replicated chromatin assembly. Collectively, our results suggest that the deposition by CAF-1 of newly-synthesized H3-H4 histones during DNA replication creates a chromatin environment that favors sister chromatid cohesion and maintains genome integrity.
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Stanyte, Rugile, Johannes Nuebler, Claudia Blaukopf, Rudolf Hoefler, Roman Stocsits, Jan-Michael Peters, and Daniel W. Gerlich. "Dynamics of sister chromatid resolution during cell cycle progression." Journal of Cell Biology 217, no. 6 (April 25, 2018): 1985–2004. http://dx.doi.org/10.1083/jcb.201801157.

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Faithful genome transmission in dividing cells requires that the two copies of each chromosome’s DNA package into separate but physically linked sister chromatids. The linkage between sister chromatids is mediated by cohesin, yet where sister chromatids are linked and how they resolve during cell cycle progression has remained unclear. In this study, we investigated sister chromatid organization in live human cells using dCas9-mEGFP labeling of endogenous genomic loci. We detected substantial sister locus separation during G2 phase irrespective of the proximity to cohesin enrichment sites. Almost all sister loci separated within a few hours after their respective replication and then rapidly equilibrated their average distances within dynamic chromatin polymers. Our findings explain why the topology of sister chromatid resolution in G2 largely reflects the DNA replication program. Furthermore, these data suggest that cohesin enrichment sites are not persistent cohesive sites in human cells. Rather, cohesion might occur at variable genomic positions within the cell population.
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Dissertations / Theses on the topic "Chromatin"

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Jurisic, Anamarija. "Développement d'une approche méthodologique basée sur la biotinylation in vivo de protéines de la chromatine - Application à l’étude des interactions entre des domaines chromosomiques et une protéine de l'enveloppe nucléaire dans des cellules individuelles." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS349.

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Les arguments en faveur d’un rôle important de l'architecture des chromosomes en interphase pour la régulation des gènes et la maintenance du génome s’accumulent rapidement. Au cours de l'interphase, les chromosomes sont positionnés de façon non aléatoire l’un par rapport à l'autre et fournissent ainsi des points de repère nucléaires. Deux types d'interactions contribuent probablement à ce positionnement non aléatoire: (i) des domaines subchromosomiques interagissent avec des structures nucléaires telles l'enveloppe nucléaire (EN) et (ii) des interactions intrachromosomiques s’établissent entre des loci situés de façon linéairement distante en cis sur un même chromosome. Contribuant à l’expansion de ce domaine de recherche, nous avons poursuivi le développement d’une technique préalablement établie au laboratoire pour détecter des interactions protéine-protéine. Le développement de cette technique nouvelle a constitué une part de ce travail de thèse accompli sur des cellules humaines. Elle se base sur le marquage par la biotine de composants de la chromatine qui en interphase se trouvent à proximité immédiate de l’EN. Les cellules ont été traitées pour exprimer (i) la biotine ligase BirA fusionnée à l’émerine, une protéine de l’EN, conjointement avec (ii) une variante d’histone, l’histone macroH2A, en fusion avec un peptide accepteur de biotine. L'étiquette biotine déposée sur l’histone macroH2A pendant l'interphase est ensuite détectée par microscopie à fluorescence sur des cellules en mitose étalées sur lames. Les chromosomes mitotiques marqués peuvent en outre être caractérisés par des techniques plus classiques de caryotypage. Nous avons nommé cette technique «topokaryotypage» car elle peut fournir des informations d’ordre à la fois topologique et caryotypique. Son développement pas à pas a nécessité la production d'une lignée cellulaire ad hoc et une optimisation fine du protocole. Ce travail de thèse peut déboucher sur des questions biologiques explorées sur cellules uniques. A titre d’application, une analyse comparative a été réalisée par topokaryotypage sur des cellules cultivées in vitro dans diverses conditions de stress expérimentales. L’utilisation du topocaryotypage pourrait fournir des informations précieuses sur les mécanismes à la base de l’organisation et de la dynamtique des noyaux cellulaires
Evidence is rapidly accumulating that the architecture of interphase chromosomes is important for both gene regulation and genome maintenance. During interphase, chromosomes are nonrandomly positioned with respect to each other and thus they provide nuclear landmarks. Two kinds of interactions are likely to contribute to this nonrandom positioning: (i) subchromosomal domains interact with nuclear structures such as the nuclear envelope (NE) and ii) intrachromosomal interactions take place between linearly distant loci positioned in cis on the same chromosome. As a contribution to this expanding research domain, we have built upon an existing approach previously established in the laboratory to detect protein-protein interactions. The new technique was developed in human cells as part of the present PhD research. It is based on biotin labelling of chromatin components which are in close proximity with the nuclear envelope (NE) in interphase cells. Cells were made to express (i) the biotin ligase BirA fused to the NE protein emerin together with (ii) a fusion between a biotin acceptor peptide and macroH2A, a variant core histone. The biotin label deposited on the macroH2A histone during interphase is then detected by fluorescence microscopy on mitotic cells spread on slides. The biotin-labelled mitotic chromosomes can be further characterized using more classical karyotyping techniques. We refer to this new technique as “Topokaryotyping” since it can provide both topological and karyotypic information. Its step-by-step development has required the establishment of an ad hoc cell line and a fine protocol optimization. This PhD work could pave the way for biological questions explored at a single cell level. As an illustration, a comparative topokaryotyping analysis was performed on cells cultivated in vitro in various experimental stress conditions. It is envisioned that using this technique can provide valuable mechanistic insights relevant to the organization and dynamics of cell nuclei
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Gasser, Regula. "Active chromatin /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10389.

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Belaghzal, Houda. "Chromatin Interaction Dynamics Revealed by Liquid Chromatin Hi-C." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1046.

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Development and application of genomic approaches based on 3C methods combined with increasingly powerful imaging approaches have enabled high-resolution genome-wide analysis of the spatial organization of chromosomes in genome function. In this thesis, I first describe an updated protocol for Hi-C (Hi-C 2.0), integrating recent improvements that significantly contribute to the efficient and high-resolution capture of chromatin interactions. Secondly, I present an assessment of the epigenetic landscape and chromosome conformation around the MYC gene in acute myeloid leukemia (AML) cells before and after small molecule, AI-10-49, treatment. MYC is up-regulated upon inhibition of the RUNX1 repressor by the fusion oncoprotein CBFβ-SMMHC. Treatment of AML cells with AI-10-49 blocks the RUNX1-CBFβ-SMMHC interaction, restoring RUNX1 at MYC regulatory elements. We demonstrate that the established loop is maintained and exchange between activating and repressive chromatin complexes at the regulatory elements, rather than altered chromatin topology, mediates disruption of target gene expression. Finally, Hi-C interaction maps represent the population-averaged steady-states. To understand the forces that promote and maintain the association of loci with specific sub-nuclear structures genome-wide, we developed liquid chromatin Hi-C. Detection of intrinsic locus-locus interaction stabilities and chromatin mobility are enabled by fragmenting chromosomes prior to fixation and Hi-C, thus removing strong polymeric constraints. Nuclear compartmentalization was found to be stable for average fragment lengths are 10-25 kb while fragmentation below 6kb led to a gradual loss of spatial genome organization. Dissolution kinetics of chromatin interactions vary widely for different domains and are analyzed in detail in the final chapter of this thesis., with lamin-associated domains being most stable, and speckle-associated loci most dynamic.
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Besnard, Emilie. "Modifications de l'organisation de la chromatine liées à l’entrée en sénescence et son impact sur la réplication du génome." Thesis, Montpellier 1, 2010. http://www.theses.fr/2010MON1T008.

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L'entrée en sénescence, considérée comme un arrêt irréversible du cycle, se caractérise par une modification de l'organisation de la chromatine formant de véritables foyers d' hétérochromatine spécifiques (SAHF) coordonnée à une modification d'expression génique et à un déclin progressif de la compétence à répliquer le génome. Ainsi, au cours de ma thèse, j'ai voulu comprendre en quoi ces changements d'organisation du génome pouvaient influer sur la distribution et l'activation des origines d e réplication lors de l'entrée en sénescence réplicative ou déclenchée de façon prématurée par l'inhibition d'un modulateur de chromatine, la protéine à activité Histone AcétylTransférase p300. Pour étudier ces régulations, j'ai utilisé le peignage moléculaire d'ADN réplicatif qui permet de suivre les fourches de réplication et d'évaluer la distribution moyenne des origines. De plus, à l'aide de la purification de brins naissants aux origines de réplication couplée à un séquençage haut débit, nous avons cartographié la position de ces origines sur l'ensemble du génome humain et étudier un ensemble de facteurs pouvant intervenir dans ce déterminisme. Grâce à cette étude, nous avons pu suivre finement les modifications d'activité des origines associées à l'entrée en sénescence. De plus, afin de mieux comprendre les mécanismes d'activation des origines de réplication, nous avons étudié en collaboration avec l'équipe du Dr Fisher, le rôle de Cdk1 et de Cdk2 dans l'activation des origines dans le modèle Xénope
Senescence entry, considered as an irreversible cell cycle arrest, is characterized by modifications of chromatin organization forming specific heterochromatin foci (SAHF) coordinated to modification of gene expression and the progressive loss of capacity to replicate the genome. During my PhD, we investigated whether these changes in genome organization might induce modifications in the distribution and the activity of replication origins during replicative senescence entry and in prematurely induced senescence by inhibition of a chromatin modulator, the Histone AcetylTransferase p300. To study these regulations, we used the replicating DNA combing allowing to follow the progression of replication forks and to evaluate the mean distribution of origins. By using the nascent strand purification assay coupled to deep sequencing, we mapped the position of replication origins in the whole human genome and studied some factors which could be involve d with this determinism. Thanks to this study, we followed finely the modifications of activity of replication origins associated to senescence entry. Moreover, in order to better understand the mechanisms of activation of origins, we studied in collaboration with Dr Fisher's team, the role of Cdk1 and Cdk2, in the activity of replication origins in the Xenopus model
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Clynes, David Alexander. "Signalling to chromatin." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496840.

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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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Marie, Corentine. "The role of Chd7 & Chd8 chromatin remodelers in oligodendrogenesis and (re)myelination." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066365/document.

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Les oligodendrocytes (OLs) sont les cellules myélinisantes du système nerveux central, s’enroulant autour des axones et permettant la conduction saltatoire du potentiel d’action. Dans la Sclérose en Plaques, des gaines de myélines sont détruites et l’efficacité de la remyélinisation par les précurseurs d’oligodendrocytes (OPCs) diminue avec la progression de la maladie. Une meilleure compréhension du mécanisme qui contrôle la génération des OPCs et leur différentiation est donc essentielle pour développer des thérapies efficaces de remyélinisation. L’oligodendrogenèse, qui comprend les étapes de génération des OPCs, de différenciation et de maturation des OLs, est un processus contrôlé par des facteurs de transcription spécifiques incluant Ascl1, Olig2 and Sox10 mais le mécanisme impliqué est encore peu connu. Sachant que les facteurs du remodelage de la chromatine sont des régulateurs nécessaires à la formation de la boucle promoter-enhancer permettant l’initiation de la transcription, nous nous sommes focalisé sur Chd7 (Chromodomain-Helicase-DNA-Binding 7), un membre de la famille de protéine CHD. Dans une première étude, nous avons montré que Chd7 est hautement enrichi dans le lignage oligodendroglial avec un pic d’expression pendant la différenciation des OLs. Nous avons également montré que la délétion conditionnelle de Chd7 diminuait la différentiation des OLs pendant la (re)myélinisation. Dans un seconde étude, nous avons utilisé des techniques de génomique sur les OPCs purifiés pour étudier la régulation par Chd7 de gènes impliqués dans la différenciation, la survie et la prolifération des OPCs. Dans ce but, nous avons générer des délétions inductible de Chd7 spécifiquement dans les OPCs (Chd7iKO) et nous avons analysé le transcriptome (RNA-seq) d’OPCs purifiés à partir de cerveaux de souris P7 comparé à des contrôles. Nous avons trouvé que Chd7 activait l’expression des gènes impliqué dans la différenciation des OPCs et la myélinisation et inhibait l’apoptose, sans montré de défaut de prolifération. Pour aller plus loin, nous avons étudié Chd8, un paralogue de Chd7, et nous avons montré qu’il est exprimé dans le lignage oligodendrocytaire avec un pic d’expression dans les OL en différenciation, similairement à Chd7. Les données de fixation (ChIP-seq) de Chd7 et Chd8 indiquent que ces deux facteurs du remodelage de la chromatine se fixent sur des gènes communs reliés au processus de différenciation, de survie et de prolifération des OPCs. Intégrant ces données avec celles de facteurs transcriptionnels clés dans l’oligodendrogenèse (Olig2, Ascl1 et Sox10), nous avons construit un modèle de la régulation de l’expression de gènes contrôlés dans le temps et impliqué dans chacune des étapes de la différenciation des oligodendrocytes
Oligodendrocytes (OLs) are myelin-forming cells of the central nervous system wrapping axons and allowing the saltatory conduction of action potentials. In Multiple sclerosis (MS), myelin sheath is destroyed and effective remyelination by oligodendrocyte precursor cells (OPCs) diminishes with disease progression. Therefore, a better understanding of the mechanisms controlling OPC generation and differentiation is essential to develop efficient remyelinating therapies. Oligodendrogenesis, involving the steps of OPC generation, OPC differentiation and maturation of OLs, is a process controlled by specific transcription factors including Ascl1, Olig2 and Sox10 but the mechanisms involved are poorly understood. As it is known that chromatin remodelers are regulatory factors necessary in the formation of the promoter-enhancer loop prior to transcription, we focused our study on Chd7 (Chromodomain-Helicase-DNA-Binding 7), a member of the CHD protein family. In a first study, we showed that Chd7 is highly enriched in the oligodendroglial lineage cells with a peak of expression during OL differentiation and that Chd7 OPC-conditional deletion impairs OL differentiation during (re)myelination. In a second study, we used unbiased genome wide technics in purified OPCs to study Chd7 regulation of genes involved in OPC differentiation, proliferation and survival. To this aim, we have generated OPC-specific inducible Chd7 knock-out (Chd7-iKO) and analyse the transcriptome (RNA-seq) of purified OPCs from P7 mouse cortices compared to control littermates. We found that Chd7 promote the expression genes involved in OPC differentiation and myelination and inhibits apoptosis, without affecting OPC proliferation. Furthermore, we investigated Chd8, a paralog of Chd7, showing that it is expressed in the oligodendroglial lineage with a peak of expression in differentiating oligodendrocytes, similar to Chd7. Genome wide binding (ChIP-seq) profiling for Chd7 and Chd8 indicate that these two chromatin remodelers bind to common genes related to OPC differentiation, survival and proliferation. Integrating these datasets with other key transcriptional regulators of oligodendrogenesis (Olig2, Ascl1 & Sox10), we have built a model accounting for the time-controlled regulate expression of genes involved in each step of OL differentiation
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Beurton, Flore. "Étude de l’interaction physique et fonctionnelle entre le complexe histone méthyltransférase SET-2/SET1 et le complexe histone déacétylase SIN-3S dans l’embryon de C. elegans." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSEN017.

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Les complexes histones méthyltransférases SET1, hautement conservés de la levure aux mammifères, sont ciblés aux régions promotrices par la protéine CFP1/CXXC, résultant en l’implémentation de la méthylation de la lysine 4 de l’histone H3 (H3K4me), modification post-traductionnelle influençant l’expression des gènes selon le contexte chromatinien. La présence de plusieurs complexes SET1 distincts dans différents systèmes modèles eucaryotes a compliqué l’étude de leurs fonctions dans un contexte développemental. Caenorhabditis elegans contient une seule protéine homologue de SET1, SET-2, et d’uniques homologues des autres sous-unités du complexe, RBBP5, ASH2, WDR5, DPY30 et CFP1. Cependant, la composition biochimique du complexe n’a pas été décrite. En couplant des expériences de co-immunoprécipitation avec des analyses de spectrométrie de masse, j’ai identifié le complexe SET-2/SET1 dans les embryons de C. elegans. D’autre part, j’ai montré que le complexe SET-2/SET1 co-immunoprécipite aussi un autre complexe conservé modifiant la chromatine et j’ai mis en évidence les interactions mises en jeu entre ces deux complexes. Mon analyse génétique a démontré que les mutants de perte de fonction des sous-unités des deux complexes partagent des phénotypes communs, en cohérence avec des fonctions développementales communes. Le laboratoire a également entrepris des expériences de transcriptomique et d’immunoprécipitation de la chromatine montrant un nouveau rôle de CFP-1 dans le recrutement de ce complexe au niveau de sites spécifiques de la chromatine
The highly conserved SET1 family complexes are targeted by CFP1/CXXC protein to promoter regions through multivalent interactions to implement methylation of histone H3 Ly4 (H3K4me), a modification that correlates with gene expression depending on the chromatin context. The presence of distinct SET1 complexes in multiple eukaryotic model systems has hampered studies aimed at identifying the complete array of functions of SET1/MLL regulatory networks in a developmental context. Caenorhabditis elegans contains one SET1 protein, SET-2, one MLL-like protein, SET-16, and single homologs of RBBP5, ASH2, WDR5, DPY30 and CFP1. The biochemical composition of the complex however, has not been described. Through the use of co-immunoprecipitation coupled to mass spectrometry-based proteomics, I identified the SET-2/SET1 complex in C. elegans embryos. Most importantly, I showed that the SET-2/SET1 complex also co-immunoprecipitates another conserved chromatin-modifying complex and I highlighted the interactions involved between these two complexes. My genetic analysis revealed that loss of function mutants of the two complex subunits share common phenotypes, consistent with common developmental functions. The laboratory has also undertaken transcriptomic and chromatin immunoprecipitation experiments showing that CFP-1 has a role in the binding of this complex at specific chromatin regions
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9

Nothjunge, Stephan [Verfasser], and Stefan [Akademischer Betreuer] Günther. "Chromatin-Interaktionen in Kardiomyozyten." Freiburg : Universität, 2019. http://d-nb.info/1185390979/34.

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Little, Gillian H. "Stat5 binding to chromatin." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/12435.

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Expression of milk proteins including β-lactoglobulin is controlled by prolactin activation of the transcription factor Stat5 via the Janus kinase/Signal transducer and activator of transcription (Jak/STAT) pathway. Stat5 has previously been shown to tetramerise where binding sites are tandemly linked and the proximity of these binding sites appears to be important for these interactions. This work and previous large scale mapping of the β-lactoglobulin promoter shows that the dyad of a strongly positioned nucleosome lies at -184 bp from the transcription start on the promoter of the β-lactoglobulin gene. This brings together two binding sites for Stat5, at the points of entry and exit of DNA from the nucleosome that would otherwise be spaced 185 bp apart, an arrangement that could potentially bring bound Stat5 dimers closer enough to facilitate tetramerisation. The chromatin structure over the active and inactive gene promoter is different; there are two alternative nucleosome positions in the active and only one in the inactive promoter. One of these positioning sites would not allow the tetramerisation interaction to take place. In order to understand better the mechanisms by which the expression of β-lactoglobulin is regulated by Stat5 we set out to investigate the role of these positioned nucleosomes in Stat5 binding in vitro. Stat5A and B binding patterns on both naked DNA and on reconstituted chromatin probes are shown by a series of bandshift experiments using purified recombinant Stat5 produced in a baculovirus expression system. Characterisation of Stat5 reveals the protein to be phosphorylated and able to bind DNA. A mutation, W37A, which removes the ability of Stat5 to form dimer-dimer interactions was employed to further investigate a potential role of tetramerisation influencing Stat5 binding in a chromatin context. This architectural feature could act to control the temporal and tissue specific expression of β-lactoglobulin.
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Books on the topic "Chromatin"

1

David, Allis C., and Wu Carl, eds. Chromatin and chromatin remodeling enzymes. San Diego: Elsevier/Academic Press, 2004.

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Horsfield, Julia, and Judith Marsman, eds. Chromatin. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2140-0.

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van Holde, Kensal E. Chromatin. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3490-6.

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David, Allis C., and Wu Carl, eds. Chromatin and chromatin remodeling enzymes. Amsterdam: Elsevier Academic Press, 2004.

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1942-, Gualerzi Claudio O., Pon Cynthia L. 1942-, and Symposium "Selected Topics on Chromatin Structure and Function" (1985 : University of Camerino), eds. Bacterial chromatin. Berlin: Springer-Verlag, 1986.

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Becker, Peter B. Chromatin Protocols. New Jersey: Humana Press, 1999. http://dx.doi.org/10.1385/1592596819.

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Chellappan, Srikumar P., ed. Chromatin Protocols. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2474-5.

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Zini, Armand, and Ashok Agarwal, eds. Sperm Chromatin. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6857-9.

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Gualerzi, Claudio O., and Cynthia L. Pon, eds. Bacterial Chromatin. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71266-1.

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Morse, Randall H., ed. Chromatin Remodeling. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-477-3.

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Book chapters on the topic "Chromatin"

1

Carlberg, Carsten, and Ferdinand Molnár. "Chromatin." In Human Epigenetics: How Science Works, 15–28. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-22907-8_2.

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Hoyer, Daniel, Eric P. Zorrilla, Pietro Cottone, Sarah Parylak, Micaela Morelli, Nicola Simola, Nicola Simola, et al. "Chromatin." In Encyclopedia of Psychopharmacology, 283–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_743.

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Arnemann, J. "Chromatin." In Springer Reference Medizin, 581–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_3449.

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Arnemann, J. "Chromatin." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_3449-1.

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Brahmachari, Vani, and Shruti Jain. "Chromatin." In Encyclopedia of Systems Biology, 401. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_845.

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Gooch, Jan W. "Chromatin." In Encyclopedic Dictionary of Polymers, 882. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13387.

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Dame, Remus T. "Ultrastructure and Organization of Bacterial Chromosomes." In Bacterial Chromatin, 3–11. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3473-1_1.

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Bell, Stephen D., and Malcolm F. White. "Archaeal Chromatin Organization." In Bacterial Chromatin, 205–17. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3473-1_10.

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Travers, Andrew, and Georgi Muskhelishvili. "The Topology and Organization of Eukaryotic Chromatin." In Bacterial Chromatin, 219–41. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3473-1_11.

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Dorman, Charles J. "Bacterial Chromatin and Gene Regulation." In Bacterial Chromatin, 245–50. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3473-1_12.

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Conference papers on the topic "Chromatin"

1

Adenot, P. G., M. Gèze, P. Debey, and M. S. Szöllösi. "Chromatin ‘‘in real time’’." In The living cell in four dimensions. AIP, 1991. http://dx.doi.org/10.1063/1.40579.

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Emmett, Kevin, Benjamin Schweinhart, and Raul Rabadan. "Multiscale Topology of Chromatin Folding." In 9th EAI International Conference on Bio-inspired Information and Communications Technologies (formerly BIONETICS). ACM, 2016. http://dx.doi.org/10.4108/eai.3-12-2015.2262453.

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Zhong, Jian, Zhenqing Ye, Chad Clark, Samuel Lenz, Justin Nguyen, Huihuang Yan, Keith Robertson, et al. "Abstract 5180: Enhanced and controlled chromatin extraction for chromatin-based epigenetic assays in FFPE tissues." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5180.

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Zhong, Jian, Zhenqing Ye, Chad Clark, Samuel Lenz, Justin Nguyen, Huihuang Yan, Keith Robertson, et al. "Abstract 5180: Enhanced and controlled chromatin extraction for chromatin-based epigenetic assays in FFPE tissues." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5180.

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Kudrin, Roman, and Andrey Mironov. "Inferring chromatin states with stochastic autoencoder." In 2018 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2018. http://dx.doi.org/10.1109/bibm.2018.8621155.

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Tsoy, Olga, Aleksandra Galitsyna, Ekaterina Khrameeva, Sergey Ulianov, Mikhail Gelfand, and Sergey Razin. "The chromatin structure of Dictyostelium discoideum." In 2018 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2018. http://dx.doi.org/10.1109/bibm.2018.8621330.

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MUIR, TOM W. "EXPLORING CHROMATIN BIOLOGY USING PROTEIN CHEMISTRY." In 23rd International Solvay Conference on Chemistry. WORLD SCIENTIFIC, 2014. http://dx.doi.org/10.1142/9789814603836_0005.

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"Consecutive chromatin loops in Dictyostelium discoideum." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-071.

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Rosenfeld, John M., Zirong Li, Konstantin Taganov, Tracy Cooke, Bhaskar Thyagarajan, and Alejandra Solache. "Abstract B58: Implementation of a synthetic reagent to mimic chromatin provides a chromatin immunoprecipitation quantitative control." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-b58.

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Saito, Kan, Konstantin Taganov, John M. Rosenfeld, Nick Asbrock, and Vi Chu. "Abstract 4881: Analysis of long-noncoding RNA interaction at chromatin by chromatin isolation by RNA purification (ChIRP)." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4881.

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Reports on the topic "Chromatin"

1

Kun, Ernest. Molecular Toxicology of Chromatin. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada247307.

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Jeans, C., M. Thelen, and A. Noy. Single Molecule Studies of Chromatin. Office of Scientific and Technical Information (OSTI), February 2006. http://dx.doi.org/10.2172/877892.

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Pandita, Tej K. Chromatin Structure and Breast Cancer Radiosensitivity. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada434814.

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Pandita, Tej K. Chromatin Structure and Breast Cancer Radiosensitivity. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada588290.

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Pandita, Tej K. Chromatin Structure and Breast Cancer Radiosensitivity. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada423679.

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Bradbury, E. M. Neutron scatter studies of chromatin structures related to functions. Office of Scientific and Technical Information (OSTI), January 1991. http://dx.doi.org/10.2172/6000035.

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Bradbury, E. M. Neutron scatter studies of chromatin structures related to functions. Office of Scientific and Technical Information (OSTI), January 1992. http://dx.doi.org/10.2172/7224363.

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Bradbury, E. M. Neutron scatter studies of chromatin structures related to functions. Office of Scientific and Technical Information (OSTI), January 1992. http://dx.doi.org/10.2172/5312037.

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Nordeen, Steven. Classical and Nonclassical Estrogen Receptor Action on Chromatin Templates. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada382501.

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Bradbury, E. M. Neutron scatter studies of chromatin structure related to functions. Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/5445330.

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