Relevant bibliographies by topics / Chromatin Architectural Proteins

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  1. Journal articles
  2. Dissertations / Theses
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  4. Conference papers

Academic literature on the topic 'Chromatin Architectural Proteins'

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Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Chromatin Architectural Proteins"

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McBryant, Steven J., Valerie H. Adams, and Jeffrey C. Hansen. "Chromatin architectural proteins." Chromosome Research 14, no. 1 (February 2006): 39–51. http://dx.doi.org/10.1007/s10577-006-1025-x.

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Thakur, Jitendra, and Steven Henikoff. "Architectural RNA in chromatin organization." Biochemical Society Transactions 48, no. 5 (September 8, 2020): 1967–78. http://dx.doi.org/10.1042/bst20191226.

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RNA plays a well-established architectural role in the formation of membraneless interchromatin nuclear bodies. However, a less well-known role of RNA is in organizing chromatin, whereby specific RNAs have been found to recruit chromatin modifier proteins. Whether or not RNA can act as an architectural molecule for chromatin remains unclear, partly because dissecting the architectural role of RNA from its regulatory role remains challenging. Studies that have addressed RNA's architectural role in chromatin organization rely on in situ RNA depletion using Ribonuclease A (RNase A) and suggest that RNA plays a major direct architectural role in chromatin organization. In this review, we will discuss these findings, candidate chromatin architectural long non-coding RNAs and possible mechanisms by which RNA, along with RNA binding proteins might be mediating chromatin organization.
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Grasser, K. "HMG1 and HU proteins: architectural elements in plant chromatin." Trends in Plant Science 3, no. 7 (July 1, 1998): 260–65. http://dx.doi.org/10.1016/s1360-1385(98)01259-x.

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van Holde, Kensal, and Jordanka Zlatanova. "Chromatin architectural proteins and transcription factors: A structural connection." BioEssays 18, no. 9 (September 1996): 697–700. http://dx.doi.org/10.1002/bies.950180903.

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Zhao, Bo, Yanpeng Xi, Junghyun Kim, and Sibum Sung. "Chromatin architectural proteins regulate flowering time by precluding gene looping." Science Advances 7, no. 24 (June 2021): eabg3097. http://dx.doi.org/10.1126/sciadv.abg3097.

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Chromatin structure is critical for gene expression and many other cellular processes. In Arabidopsis thaliana, the floral repressor FLC adopts a self-loop chromatin structure via bridging of its flanking regions. This local gene loop is necessary for active FLC expression. However, the molecular mechanism underlying the formation of this class of gene loops is unknown. Here, we report the characterization of a group of linker histone-like proteins, named the GH1-HMGA family in Arabidopsis, which act as chromatin architecture modulators. We demonstrate that these family members redundantly promote the floral transition through the repression of FLC. A genome-wide study revealed that this family preferentially binds to the 5′ and 3′ ends of gene bodies. The loss of this binding increases FLC expression by stabilizing the FLC 5′ to 3′ gene looping. Our study provides mechanistic insights into how a family of evolutionarily conserved proteins regulates the formation of local gene loops.
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Driessen, Rosalie P. C., and Remus Th Dame. "Structure and dynamics of the crenarchaeal nucleoid." Biochemical Society Transactions 41, no. 1 (January 29, 2013): 321–25. http://dx.doi.org/10.1042/bst20120336.

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Crenarchaeal genomes are organized into a compact nucleoid by a set of small chromatin proteins. Although there is little knowledge of chromatin structure in Archaea, similarities between crenarchaeal and bacterial chromatin proteins suggest that organization and regulation could be achieved by similar mechanisms. In the present review, we describe the molecular properties of crenarchaeal chromatin proteins and discuss the possible role of these architectural proteins in organizing the crenarchaeal chromatin and in gene regulation.
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Foulger, Larus E., Connie Goh Then Sin, Q. Q. Zhuang, Hugh Smallman, James M. Nicholson, Stanley J. Lambert, Colin D. Reynolds, et al. "Efficient purification of chromatin architectural proteins: histones, HMGB proteins and FKBP3 (FKBP25) immunophilin." RSC Advances 2, no. 28 (2012): 10598. http://dx.doi.org/10.1039/c2ra21758a.

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Alpsoy, Aktan, Surbhi Sood, and Emily C. Dykhuizen. "At the Crossroad of Gene Regulation and Genome Organization: Potential Roles for ATP-Dependent Chromatin Remodelers in the Regulation of CTCF-Mediated 3D Architecture." Biology 10, no. 4 (March 27, 2021): 272. http://dx.doi.org/10.3390/biology10040272.

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In higher order organisms, the genome is assembled into a protein-dense structure called chromatin. Chromatin is spatially organized in the nucleus through hierarchical folding, which is tightly regulated both in cycling cells and quiescent cells. Assembly and folding are not one-time events in a cell’s lifetime; rather, they are subject to dynamic shifts to allow changes in transcription, DNA replication, or DNA damage repair. Chromatin is regulated at many levels, and recent tools have permitted the elucidation of specific factors involved in the maintenance and regulation of the three-dimensional (3D) genome organization. In this review/perspective, we aim to cover the potential, but relatively unelucidated, crosstalk between 3D genome architecture and the ATP-dependent chromatin remodelers with a specific focus on how the architectural proteins CTCF and cohesin are regulated by chromatin remodeling.
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Driessen, Rosalie P. C., and Remus Th Dame. "Nucleoid-associated proteins in Crenarchaea." Biochemical Society Transactions 39, no. 1 (January 19, 2011): 116–21. http://dx.doi.org/10.1042/bst0390116.

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Architectural proteins play an important role in compacting and organizing the chromosomal DNA in all three kingdoms of life (Eukarya, Bacteria and Archaea). These proteins are generally not conserved at the amino acid sequence level, but the mechanisms by which they modulate the genome do seem to be functionally conserved across kingdoms. On a generic level, architectural proteins can be classified based on their structural effect as DNA benders, DNA bridgers or DNA wrappers. Although chromatin organization in archaea has not been studied extensively, quite a number of architectural proteins have been identified. In the present paper, we summarize the knowledge currently available on these proteins in Crenarchaea. By the type of architectural proteins available, the crenarchaeal nucleoid shows similarities with that of Bacteria. It relies on the action of a large set of small, abundant and generally basic proteins to compact and organize their genome and to modulate its activity.
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Brzeski, Jan, and Andrzej Jerzmanowski. "Plant chromatin - epigenetics linked to ATP-dependent remodeling and architectural proteins." FEBS Letters 567, no. 1 (April 9, 2004): 15–19. http://dx.doi.org/10.1016/j.febslet.2004.03.068.

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Dissertations / Theses on the topic "Chromatin Architectural Proteins"

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Riedmann, Caitlyn M. "THE DYNAMIC NATURE OF CHROMATIN." UKnowledge, 2017. http://uknowledge.uky.edu/biochem_etds/31.

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Eukaryotic organisms contain their entire genome in the nucleus of their cells. In order to fit within the nucleus, genomic DNA wraps into nucleosomes, the basic, repeating unit of chromatin. Nucleosomes wrap around each other to form higher order chromatin structures. Here we study many factors that affect, or are effected by, chromatin structure including: (1) how low-dose inorganic arsenic (iAs) changes chromatin structures and their relation to global transcription and splicing patterns, and (2) how chromatin architectural proteins (CAPs) bind to and change nucleosome dynamics and DNA target site accessibility. Despite iAs’s non-mutagenic nature, chronic exposure to low doses of iAs is associated with a higher risk of skin, lung, and bladder cancers. We sought to identify the genome-wide changes to chromatin structure and splicing profiles behind the cell’s adaptive response to iAs and its removal. Furthermore, we extended our investigation into cells that had the iAs insult removed. Our results show that the iAs-induced epithelial to mesenchymal transition and changes to the transcriptome are coupled with changes to the higher order chromatin structure and CAP binding patterns. We hypothesize that CAPs, which bind the entry/exit and linker DNA of nucleosomes, regulate DNA target site accessibility by altering of the rate of spontaneous dissociation of DNA from nucleosome. Therefore, we investigated the effects of the repressive CAP histone H1, the activating CAP high mobility group D1 (HMGD1), and the neural CAP methyl CpG binding protein 2 (MeCP2) on the dynamics of short chromatin arrays and mononucleosomes and their effect on nucleosomal DNA accessibility. Using biochemical and biophysical analyses we show that all CAP-chromatin structures tested were susceptible to chromatin remodeling by ISWI and created more stable higher order structures than if CAPs were absent. Additionally, histone H1 and MeCP2 hinder model transcription factor Gal4 from binding its cognate DNA site within nucleosomal DNA. Overall, we show that chromatin structure is dynamic and changes in response to environmental signals and that CAPs change nucleosome dynamics that help to regulate chromatin structures and impact transcriptional profiles.
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Guo, Haihong [Verfasser], Bernhard [Akademischer Betreuer] Lüscher, and Ferdinand [Akademischer Betreuer] Kappes. "The chromatin architectural protein DEK : assessing its chromatin binding properties / Haihong Guo ; Bernhard Lüscher, Ferdinand Kappes." Aachen : Universitätsbibliothek der RWTH Aachen, 2016. http://d-nb.info/1125911174/34.

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Liu, Jessica Chishow. "Biochemical Characterization of the Domain Architecture of Chromatin Assembly Motor Proteins Human CHD1 and CHD2." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:14226060.

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The sites where the basic unit of chromatin, the nucleosome, is assembled greatly affects the dynamic compaction/decompaction of eukaryotic genetic material and how the DNA is accessed, read, and interpreted. The nucleosome, which consists of ~147 base pairs of DNA wrapped in a left-handed superhelix around an octameric core made up of histone proteins, is the targeted substrate for ATP-dependent protein machineries called chromatin remodelers. Remodelers are essential regulators of DNA accessibility and are often grouped into four families: SWI/SNF, INO80/SWR1, ISWI, and CHD. Though remodelers can act as large multi-subunit complexes, all have a unique core SNF2-like ATPase that utilizes the energy from ATP hydrolysis to translocate along DNA. This DNA translocase activity of the catalytic ATPase domain acts in coordination with auxiliary domains or accessory subunits to disrupt histone-DNA contacts, resulting in distinct remodeling outcomes. Furthermore, the assembly of DNA into nucleosomal arrays is a specialized activity catalyzed by a subset of remodelers. Identifying remodeler proteins responsible for nucleosome assembly and delineating the mechanisms through which remodelers assemble and remodel nucleosomes are key goals in the field of chromatin biology. CHD proteins have important roles in regulating gene expression through their remodeling activities. While yeast cells only have one CHD protein (CHD1), mammalians possess nine proteins (CHD1-9) that are further categorized into subfamilies on the basis of additional sequences flanking the central ATPase domain. CHD2 is in the same subfamily as CHD1 and has been linked to developmental regulation but the enzymatic activity of CHD2 has not been well characterized. Given the homology between human CHD2 and CHD1, which is an important assembly protein in other species (S. cerevisiae and D. melanogaster), we set out to delineate the biochemical properties of human CHD2 and the CHD1 human counterpart. In this dissertation work, we examined the biochemical activities of recombinant human CHD1 and CHD2. We used in vitro chromatin assembly and remodeling assays and showed CHD2 assembles nucleosomal arrays and remodels nucleosomes while CHD1 exhibits less robust activity by comparison. We used radiometric ATPase and electrophoretic mobility gel shift assays to measure the ATPase and DNA-binding activities of human CHD1 and CHD2 and assessed the contribution from conserved accessory domains using systematic protein truncations. We found the N-terminal chromodomains are inhibitory for the ATPase and DNA-binding activities of both CHD1 and CHD2 while providing substrate specificity for the latter. Moreover, we showed the DNA-binding domain of CHD2 enhances its ATPase and remodeling activities. The distinct in vitro activities exhibited by human CHD1 and CHD2 suggest they have non-redundant roles in vivo with important mechanistic implications for remodeling by CHD proteins. In a broader sense, our findings have added to the number of known assembly motor proteins and aids in our understanding of how remodelers have evolved auxiliary domains to carry out specific functions such as chromatin assembly.
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Malashchuk, Ogor. "Epigenetic regulation of skin development and postnatal homeostasis : the role of chromatin architectural protein Ctcf in the control of keratinocyte differentiation and epidermal barrier formation." Thesis, University of Bradford, 2016. http://hdl.handle.net/10454/14791.

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Epigenetic regulatory mechanisms play important roles in the control of lineage-specific differentiation during development. However, mechanisms that regulate higher-order chromatin remodelling and transcription of keratinocyte-specific genes that are clustered in the genome into three distinct loci (Keratin type I/II loci and Epidermal Differentiation Complex (EDC)) during differentiation of the epidermis are poorly understood. By using 3D-Fluorescent In Situ Hybridization (FISH), we determined that in the epidermal keratinocytes, the KtyII and EDC loci are located closely to each other in the nuclear compartment enriched by the nuclear speckles. However, in KtyII locus knockout mice, EDC locus moved away from the KtyII locus flanking regions and nuclear speckles towards the nuclear periphery, which is associated with marked changes in gene expression described previously. Chromatin architectural protein Ctcf has previously been implicated in the control of long-range enhancer-promoter contacts and inter-chromosomal interactions. Ctcf is broadly expressed in the skin including epidermal keratinocytes and hair follicles. Conditional Keratin 14-driven Ctcf ablation in mice results in the increase of the epidermal thickness, proliferation, alterations of the epidermal barrier and the development of epidermal pro-inflammatory response. Epidermal barrier defects in Krt14CreER/Ctcf fl/fl mice are associated with marked changes in gene expression in the EDC and KtyII loci, which become topologically segregated in the nucleus upon Ctcf ablation. Therefore, these data suggest that Ctcf serves as critical determinant regulating higher-order chromatin organization in lineage-specific gene loci in epidermal keratinocytes, which is required for the proper control of gene expression, maintenance of the epidermal barrier and its function.
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Malashchuk, Igor. "Epigenetic Regulation of Skin Development and Postnatal Homeostasis The role of chromatin architectural protein Ctcf in the control of Keratinocyte Differentiation and Epidermal Barrier Formation." Thesis, University of Bradford, 2016. http://hdl.handle.net/10454/14791.

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Epigenetic regulatory mechanisms play important roles in the control of lineage-specific differentiation during development. However, mechanisms that regulate higher-order chromatin remodelling and transcription of keratinocyte-specific genes that are clustered in the genome into three distinct loci (Keratin type I/II loci and Epidermal Differentiation Complex (EDC) during differentiation of the epidermis are poorly understood. By using 3D-Fluorescent In Situ Hybridization (FISH), we determined that in the epidermal keratinocytes, the KtyII and EDC loci are located closely to each other in the nuclear compartment enriched by the nuclear speckles. However, in KtyII locus knockout mice, EDC locus moved away from the KtyII locus flanking regions and nuclear speckles towards the nuclear periphery, which is associated with marked changes in gene expression described previously. Chromatin architectural protein Ctcf has previously been implicated in the control of long-range enhancer-promoter contacts and inter-chromosomal interactions. Ctcf is broadly expressed in the skin including epidermal keratinocytes and hair follicles. Conditional Keratin 14-driven Ctcf ablation in mice results in the increase of the epidermal thickness, proliferation, alterations of the epidermal barrier and the development of epidermal pro-inflammatory response. Epidermal barrier defects in Krt14CreER/Ctcf fl/fl mice are associated with marked changes in gene expression in the EDC and KtyII loci, which become topologically segregated in the nucleus upon Ctcf ablation. Therefore, these data suggest that Ctcf serves as critical determinant regulating higher-order chromatin organization in lineage-specific gene loci in epidermal keratinocytes, which is required for the proper control of gene expression, maintenance of the epidermal barrier and its function.
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Young, Daniel W. "Regulation of Cell Growth and Differentiation within the Context of Nuclear Architecture by the Runx2 Transcription Factor: a Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/19.

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The Runx family of transcription factors performs an essential role in animal development by controlling gene expression programs that mediate cell proliferation, growth and differentiation. The work described in this thesis is concerned with understanding mechanisms by which Runx proteins support this program of gene expression within the architectural context of the mammalian cell nucleus. Multiple aspects of nuclear architecture are influenced by Runx2 proteins including sequence-specific DNA binding at gene regulatory regions, organization of promoter chromatin structure, and higher-order compartmentalization of proteins in nuclear foci. This work provides evidence for several functional activities of Runx2 in relation to architectural parameters of gene. expression for the control of cell growth and differentiation. First, the coordination of SWI/SNF mediated chromatin alterations by Runx2 proteins is found to be a critical component of osteoblast differentiation for skeletal development. Several chromatin modifying enzymes and signaling factors interact with the developmentally essential Runx2 C-terminus. A patent-pending microscopic image analysis strategy invented as part of this thesis work - called intranuclear informatics - has contributed to defining the C-terminal portion of Runx2 as a molecular determinant for the nuclear organization of Runx2 foci and directly links Runx2 function with its organization in the nucleus. Intranuclear informatics also led to the discovery that nuclear organization of Runx2 foci is equivalently restored in progeny cells following mitotic division - a natural perturbation in nuclear structure and function. Additional microscopic studies revealed the sequential and selective reorganization of transcriptional regulators and RNA processing factors during progression of cell division to render progeny cells equivalently competent to support Runx2 mediated gene expression. Molecular studies provide evidence that the Runx proteins have an active role in retaining phenotype by interacting with target gene promoters through sequence-specific DNA binding during cell division to support lineage-specific control of transcriptional programs in progeny cells. Immunolocalization of Runx2 foci on mitotic chromosome spreads revealed several large foci with pairwise symmetry on sister chromatids; these foci co-localize with the RNA polymerase I transcription factor, Upstream Binding Factor (UBFl) at nucleolar organizing regions. A series of experiments were carried out to reveal that Runx2 interacts directly with ribosomal DNA loci in a cell cycle dependent manner; that Runx2 is localized to UBF foci within nucleoli during interphase; that Runx2 attenuates rRNA synthesis; and that this repression of ribosomal gene expression by Runx2 is associated with cell growth inhibition and induction of osteoblast-specific gene expression. This thesis has identified multiple novel mechanisms by which Runx2 proteins function within the hierarchy of nuclear architecture to control cell proliferation, growth and differentiation.
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Kalas, Pamela. "For genes that encode one component of a multimeric protein complex, measuring only one phenotype often gives a biased view of function: SU(VAR)3-9 and chromatin architecture as an example." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/13069.

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Eukaryotic genomes are organized into chromatin, a highly dynamic complex of DNA and proteins, which plays a critical role in the regulation of gene expression. This thesis focuses on the study of a non-histone chromatin protein, the SET domain-containing H3K9 methyltransferase (HMTase) SU(VAR)3-9, and its role in the packaging and regulation of a euchromatic locus, the histone genes cluster (HIS-C). SU(VAR)3-9 was discovered in Drosophila melanogaster, but it is highly conserved from yeast to mammals. It has two conserved domains, the chromo- and the SET domains, and both are required for its function in gene silencing. The SET domain is responsible for the catalytic activity of SU(VAR)3-9, while the exact function of the chromo domain is still unclear. To gain an insight on the role(s) of SU(VAR)3-9 in the regulation of gene silencing, we first characterized a collection of Su(var)3-9 EMS-induced mutants that had been isolated in a genetic screen for strong, dominant suppressors of position-effect variegation (PEV). These mutants were characterized at the molecular, enzymatic, and cellular level, and their effect on gene silencing was also examined. We found that all mutants have single amino acid substitutions in the conserved preSET/SET/postSET domain, and that they all display a dramatic or complete loss of HMTase activity, strongly suggesting that suppression of PEV is linked to SU(VAR)3-9’s ability to methylate H3K9. The HIS-C is a natural, euchromatic target of SU(VAR)3-9, and mutations in Su(var)3-9 can alter its chromatin structure (Ner et al., 2002). To investigate the exact role(s) of SU(VAR)3-9 in the regulation of this locus, we analyzed the effects of a series of Su(var)3-9 missense mutants on the chromatin architecture of the HIS-C and on the expression of the histone genes. We detected a drastic reduction in the levels of H3K9me2 and HP1 associated with the his genes in all Su(var)3-9 missense mutants, although the mutant SU(VAR)3-9s still associate with the HIS-C. In addition, these mutants have elevated amounts of histone H2A and histone H3 RNA, suggesting that the enzyme function of SU(VAR)3-9 is critical for the regulation of the histone genes.
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Šmigová, Jana. "Vztah vyšších chromatinových struktur a genové umlčování." Doctoral thesis, 2012. http://www.nusl.cz/ntk/nusl-305928.

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Book chapters on the topic "Chromatin Architectural Proteins"

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Ando-Kuri, Masami, I. Sarahi M. Rivera, M. Jordan Rowley, and Victor G. Corces. "Analysis of Chromatin Interactions Mediated by Specific Architectural Proteins in Drosophila Cells." In Methods in Molecular Biology, 239–56. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7768-0_14.

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Bustin, Michael, and Raymond Reeves. "High-Mobility-Group Chromosomal Proteins: Architectural Components That Facilitate Chromatin Function." In Progress in Nucleic Acid Research and Molecular Biology, 35–100. Elsevier, 1996. http://dx.doi.org/10.1016/s0079-6603(08)60360-8.

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Lee, Jin-Ho, and Michael Hausmann. "Super-Resolution Radiation Biology: From Bio-Dosimetry towards Nano-Studies of DNA Repair Mechanisms." In DNA - Damages and Repair Mechanisms. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95597.

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Past efforts in radiobiology, radio-biophysics, epidemiology and clinical research strongly contributed to the current understanding of ionizing radiation effects on biological materials like cells and tissues. It is well accepted that the most dangerous, radiation induced damages of DNA in the cell nucleus are double strand breaks, as their false rearrangements cause dysfunction and tumor cell proliferation. Therefore, cells have developed highly efficient and adapted ways to repair lesions of the DNA double strand. To better understand the mechanisms behind DNA strand repair, a variety of fluorescence microscopy based approaches are routinely used to study radiation responses at the organ, tissue and cellular level. Meanwhile, novel super-resolution fluorescence microscopy techniques have rapidly evolved and become powerful tools to study biological structures and bio-molecular (re-)arrangements at the nano-scale. In fact, recent investigations have increasingly demonstrated how super-resolution microscopy can be applied to the analysis of radiation damage induced chromatin arrangements and DNA repair protein recruitment in order to elucidate how spatial organization of damage sites and repair proteins contribute to the control of repair processes. In this chapter, we would like to start with some fundamental aspects of ionizing radiation, their impact on biological materials, and some standard radiobiology assays. We conclude by introducing the concept behind super-resolution radiobiology using single molecule localization microscopy (SMLM) and present promising results from recent studies that show an organized architecture of damage sites and their environment. Persistent homologies of repair clusters indicate a correlation between repair cluster topology and repair pathway at a given damage locus. This overview over recent investigations may motivate radiobiologists to consider chromatin architecture and spatial repair protein organization for the understanding of DNA repair processes.
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Lucchesi, John C. "Aging, cellular senescence and cancer: epigenetic alterations and nuclear remodeling." In Epigenetics, Nuclear Organization & Gene Function, 238–53. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0021.

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Epigenetic modifications correlated with aging and oncogenesis are changes in the pattern of DNA methylation and of histone modifications, and changes in the level of histone variants (H3.3, macroH2A, H2A.Z) and gene mutations. The sirtuins are a set of highly conserved protein deacetylases of particular significance to the aging process. Many cancer types are found to carry mutations in chromatin-modifying genes such as those encoding methyl or acetyl transferases, affecting the histone modifications of promoters and enhancers. The aging process and oncogenesis present a number of changes in the nuclear architecture. Mutations in the lamina-coding genes lead to premature aging syndromes. Mutations in remodeling complexes are found in different cancers. Modifications that affect the architectural protein binding sites at topologically associating domain (TAD) borders can cause the merging of neighboring TADs. The levels of short non-coding RNAs (sncRNAs) are altered in model organisms and are associated with cancer. Changes in the position of chromosome territories often occur in tumor cells. Nevertheless, cellular senescence, due mostly to the absence of telomerase, represents a mechanism of tumor suppression.
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Conference papers on the topic "Chromatin Architectural Proteins"

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Veltri, Robert W., Christhunesa S. Christudass, Sneha Vivekanandhan, David Yeater, and Donald S. Coffey. "Abstract 411: Chromatin regulatory nuclear proteins and nuclear architecture in cell lines derived from curable and incurable metastatic human cancers." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-411.

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