Relevant bibliographies by topics / Structural remodeling

Academic literature on the topic 'Structural remodeling'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Structural remodeling"

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Corradi, Domenico, Sergio Callegari, Roberta Maestri, Stefano Benussi, and Ottavio Alfieri. "Structural remodeling in atrial fibrillation." Nature Clinical Practice Cardiovascular Medicine 5, no. 12 (October 14, 2008): 782–96. http://dx.doi.org/10.1038/ncpcardio1370.

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Irvin, Charles G. "Chronic Rhinosinusitis and Structural Remodeling." American Journal of Respiratory Cell and Molecular Biology 57, no. 3 (September 2017): 265–66. http://dx.doi.org/10.1165/rcmb.2017-0152ed.

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Cohn, Jay N. "Global structural ventricular remodeling: Summation." Journal of Cardiac Failure 8, no. 6 (December 2002): S269—S270. http://dx.doi.org/10.1054/jcaf.2002.129265.

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Harrigan, Timothy P., and James J. Hamilton. "Bone remodeling and structural optimization." Journal of Biomechanics 27, no. 3 (March 1994): 323–28. http://dx.doi.org/10.1016/0021-9290(94)90008-6.

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Ozawa, Hidehiro. "Fine Structural Aspects on Bone Remodeling." Nihon Hotetsu Shika Gakkai Zasshi 42, no. 3 (1998): 359–68. http://dx.doi.org/10.2186/jjps.42.359.

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Weber, Kaarl T., Yao Sun, and Jack P. M. Cleutjens. "Structural Remodeling of the Myocardium Postinfarction." Cardiology in Review 3, no. 1 (January 1995): 53. http://dx.doi.org/10.1097/00045415-199501000-00006.

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Zile, Michael R. "Structural components of cardiomyocyte remodeling: Summation." Journal of Cardiac Failure 8, no. 6 (December 2002): S311—S313. http://dx.doi.org/10.1054/jcaf.2002.129273.

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Kakauridze, N., Z. Tsagareli, and L. Gogiashvili. "Experimental atherosclerosis and lung structural remodeling." Atherosclerosis 275 (August 2018): e126. http://dx.doi.org/10.1016/j.atherosclerosis.2018.06.362.

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Volokh, O. I., N. I. Derkacheva, V. M. Studitsky, and O. S. Sokolova. "Structural studies of chromatin remodeling factors." Molecular Biology 50, no. 6 (November 2016): 812–22. http://dx.doi.org/10.1134/s0026893316060212.

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Sun, Xiaonan, Jalen Alford, and Hongyu Qiu. "Structural and Functional Remodeling of Mitochondria in Cardiac Diseases." International Journal of Molecular Sciences 22, no. 8 (April 17, 2021): 4167. http://dx.doi.org/10.3390/ijms22084167.

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Mitochondria undergo structural and functional remodeling to meet the cell demand in response to the intracellular and extracellular stimulations, playing an essential role in maintaining normal cellular function. Merging evidence demonstrated that dysregulation of mitochondrial remodeling is a fundamental driving force of complex human diseases, highlighting its crucial pathophysiological roles and therapeutic potential. In this review, we outlined the progress of the molecular basis of mitochondrial structural and functional remodeling and their regulatory network. In particular, we summarized the latest evidence of the fundamental association of impaired mitochondrial remodeling in developing diverse cardiac diseases and the underlying mechanisms. We also explored the therapeutic potential related to mitochondrial remodeling and future research direction. This updated information would improve our knowledge of mitochondrial biology and cardiac diseases’ pathogenesis, which would inspire new potential strategies for treating these diseases by targeting mitochondria remodeling.
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Dissertations / Theses on the topic "Structural remodeling"

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Wang, Jingwen M. Eng Massachusetts Institute of Technology. "Trabecular topology : computational structural design inspired by bone remodeling." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/111530.

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Thesis: M. Eng., Massachusetts Institute of Technology, Department of Civil and Environmental Engineering, 2017.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 59-60).
Bone remodeling is the process by which the internal morphology of bones in a healthy person or animal will adapt to the loads under which it is placed. This process makes bone stronger and performs better under daily loadings. It also gives a special topology to the trabecular bone. This thesis proposes a new computational structural design approach inspired by the trabecular bone topology and remodeling process and it can be applied to the 2D, 3D and building-scale structures. It reveals the importance of the connectivity in the structures and provides a innovative bio-inspired method for the future structural topology design.
by Jingwen Wang.
M. Eng.
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2

Li, Li. "Electrophysiological, structural and molecular remodeling of chronically infarcted rabbit heart." online version, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1130882699.

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Атаман, Юрій Олександрович, Юрий Александрович Атаман, Yurii Oleksandrovych Ataman, O. A. Vorozhko, and O. S. Voloshin. "Structural and functional features of myocardial remodeling in professional athletes." Thesis, Сумський державний університет, 2018. http://essuir.sumdu.edu.ua/handle/123456789/71676.

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Hota, Swetansu Kumar. "STRUCTURAL AND FUNCTIONAL ANALYSIS OF THE ISW2 CHROMATIN REMODELING COMPLEX." OpenSIUC, 2011. https://opensiuc.lib.siu.edu/dissertations/431.

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Chromatin remodelers utilize the energy derived from ATP hydrolysis to mobilize nucleosomes. ISWI remodelers mobilize and evenly space nucleosomes to regulate gene expression. ISW2, an ISWI remodeler in yeast, has been shown to reposition nucleosome near promoter regions and represses both mRNA and antisense non coding RNA transcription. ISW2 is composed of four subunits and the catalytic Isw2 subunit consists of several conserved domains. The highly conserved ATPase domain is present at the N-terminus whereas the conserved HAND, SANT and SLIDE domain are towards the carboxyl terminal end of Isw2. Nucleosome mobilization by ISW2 requires both extranucleosomal DNA and the N-terminal tail of histone H4. DNA crosslinking and peptide mapping revealed that the ATPase domain contacts nucleosome two helical turns away (SHL2) from dyad to a site close to the H4 tail, whereas the HAND, SANT and SLIDE domain contact a 30bp stretch of DNA comprising the edge of nucleosome and ~20bp of extranucleosomal DNA. The ATPase domain and the C-terminal domains were investigated for their role in regulation of ISW2 activity both in-vitro and in-vivo. It appears that there are distinct modes of ISW2 regulation by these domains. Mutation of a patch of five acidic amino acids on the region of ATPase domain that contact SHL2 was found to be crucial for both ISW2 remodeling and nucleosome stimulated ATPase activity. Acidic patch mutant ISW2 was unable to mobilize nucleosome or hydrolyze ATP in absence of H4 tail. This indicates that the region of ATPase domain contacting nucleosome at SHL2 and H4 tail act in two separate and independent pathways to regulate ISW2 remodeling. Both HAND and SLIDE domain were shown to crosslink entry/exit site and linker DNA respectively. The roles of C-terminal domains were investigated either by deletion of the individual domain or mutation of conserved basic residues on the surface of these domains that are suspected to interact extranucleosomal with DNA. Deletion of HAND domain had minimal effect on in vitro ISW2 activity, however whole genome transcription analysis revealed one key role of this domain in ISW2 regulation. In absence of HAND domain, ISW2 had minimal role on repression of genes that were RPD3 (co-factor) dependent, however significantly derepressed genes that were RPD3 independent. At these loci, nucleosome positions were altered and ISW2 recruitment was reduced in absence of a functional HAND domain. Thus the HAND domain regulates recruitment and remodeling of ISW2 at those genes where ISW2 acts independent of other cofactors. The SANT domain, C-terminal to HAND domain, appears to control the "step size" of nucleosome remodeling and was found to be required for processive nucleosome remodeling by ISW2. Both H4 tail and SANT domain appear to control two distinct stages of ISW2 remodeling. A long alpha helical spacer separates SANT domain from SLIDE domain. SLIDE domain was found to be the protein-protein interaction domain that interacts with accessory Itc1 subunit to maintain ISW2 complex integrity. The two ways by which SLIDE domain regulate ISW2 is by binding or recruitment of ISW2 to promoter regions and additionally by binding independent regulation of both ATPase and remodeling activity. The remodeling mechanism of ISW2 was further compared with another ISWI type remodeler in yeast, Isw1a; using time resolved nucleosome remodeling combined with high resolution site specific histone DNA crosslinking at six different nucleosomal positions to track the movement of the nucleosomes. Nucleosome remodeled by the same remodeler showed discontinuous nucleosome movement between two tracking points indicating formation of small "bulges". One key difference in remodeling mechanism was that although both ISW2 and Isw1a moved nucleosomes towards longer linker DNA, only Isw1a remodeled nucleosomes "backtracked" ~11bp during remodeling. Backtracking of remodeling was prominently observed at nucleosomal regions in close proximity to translocase binding sites suggesting the potentially different mechanisms shared by similar remodeling complexes.
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Bernardino, Gabriel. "Computational anatomy as a driver of understanding structural and functional cardiac remodeling." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668213.

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We present a statistical shape analysis framework to identify cardiac shape remodelling while accounting for individual´s natural variability and apply it in two clinical applications: comparing triathletes with controls, and comparing individuals who were born small-for-their-gestational-age (SGA) and controls. We were able to identify the shape remodelling due to the practice of endurance sport: it consisted a dilation of the left ventricle and an increase of the left ventricular myocardial mass. In the right ventricle (RV), the increase of volume was concentrated in the outflow. This changes in shape correlated with a better performance during exercise. In SGA, we found subtle differences in the RV that correlated with worse performance during exercise. These differences were bigger when SGA condition was combined with cardiovascular risk factors: smoking and overweight. Finally, we present a geometry processing technique for parcellating the RV cavity in 3 subvolumes for regional analysis without point-to-point correspondence.
Presentamos un framework de análisis estadístico de forma para identificar remodelado cardiaco teniendo en cuenta la variabilidad natural de cada individuo. Utilizamos este framework en dos aplicaciones clínicas: triatletas e individuos nacidos pequeños-para-su-edad-gestacional (SGA). Identificamos el remodelado cardiaco en el caso de los triatletas: consistente en una dilatación del ventrículo izquierdo y un aumento de la masa miocárdica. En el ventrículo derecho (RV) la dilatación estaba concentrada en el tracto de salida. Este remodelado correlaciona con una mejor respuesta al ejercicio. En el análisis de SGA, encontramos sutiles cambios en el RV que correlacionaban con una peor respuesta al ejercicio. Estos cambios de forma fueron mayores si SGA se encontraba combinada con otros factores de riesgo cardiaco: tabaco y sobrepeso. Finalmente, presentamos una parcelación de la cavidad del RV en 3 subvolumenes para el análisis regional del RV cuando no es posible la correspondencia punto-a-punto.
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Lang, Claudia. "Structural analysis and therapeutic modulation of axonal remodeling following spinal cord injury." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-147615.

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Yang, Xiaofang. "Functional and Structural Dissection of the SWI/SNF Chromatin Remodeling Complex: A Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/330.

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The yeast SWI/SNF complex is the prototype of a subfamily of ATP-dependent chromatin remodeling complexes. It consists of eleven stoichiometric subunits including Swi2p/Snf2p, Swi1p, Snf5p, Swi3p, Swp82p, Swp73p, Arp7p, Arp9p, Snf6p, Snf11p, and Swp29p, with a molecular weight of 1.14 mega Daltons. Swi2p/Snf2p, the catalytic subunit of SWI/SNF, is evolutionally conserved from yeast to human cells. Genetic evidence suggests that SWI/SNF is required for the transcriptional regulation of a subset of genes, especially inducible genes. SWI/SNF can be recruited to target promotors by gene specific activators, and in some cases, SWI/SNF facilitates activator binding. Biochemical studies have demonstrated that purified SWI/SNF complex can hydrolyze ATP, and it can use the energy from ATP hydrolysis to generate superhelical torsion, mobilize mononucleosomes, enhance the accessibility of endonucleases to nucleosomal DNA, displace H2A/H2B dimers, induce dinucleosome and altosome formation, or evict nucleosomes. A human homolog of Swi2p/Snf2p, BRG1, is the catalytic subunit of the human SWI/SNF complex. Interestingly, isolated BRG1 alone is able to remodel a mononucleosome substrate. Importantly, mutations in mammalian SWI/SNF core subunits are implicated in tumorigenesis. Therefore, it remains interesting to characterize the role(s) of each subunit for SWI/SNF function. In this thesis project, I dissected SWI/SNF chromatin remodeling function by investigating the role of the SANT domain of the Swi3p subunit. Swi3p is one of the core components of SWI/SNF complex, and it contains an uncharacterized SANT domain that has been found in many chromatin regulatory proteins. Earlier studies suggested that the SANT domain of Ada2p may serve as the histone tail recognition module. For Swi3p, a small deletion of eleven amino acids from the SANT domain caused a growth phenotype similar to that of other swi/snf mutants. In chapter I, I have reviewed recent findings in the function of chromatin remodeling complexes and discuss the molecular mechanism of their action. In chapter II, I characterized the role of the SANT domain of Swi3p. I found that deletion of the SANT domain caused a defect in a genome-wide transcriptional profile, SWI/SNF recruitment, and more interestingly impairment of the SANT domain caused the dissociation of SWI/SNF into several subcomplexes: 1) Swi2p/Arp7p/Arp9p, 2) Swi3p/Swp73p/Snf6p, 3) Snf5p, and 4) Swi1p. Artificial tethering of SWI/SNF onto a LacZ reporter promoter failed to activate the reporter gene in the absence of the SANT domain, although Swi2p can be recruited to the LacZ promoter. We thus demonstrated that the Swi3p SANT domain is critical for Swi3p function and serves as a protein scaffold to integrate these subcomplexes into an intact SWI/SNF complex. In Chapter III, I first characterized the enzymatic activity of the subcomplexes, especially the minimal complex of Swi2p/Arp7p/Arp9p. We found that this minimal subcomplex is fully functional for chromatin remodeling in assays including cruciform formation, restriction enzyme accessibility in mononucleosomal and nucleosomal array substrates, and mononucleosome mobility shift. However, it is defective in ATP-dependent removal of H2A/H2B dimers. Moreover, we found that Swi3p and the N-terminal acidic domain of Swi3p strongly interact with GST-H2A and H2B but not GST-H3 or H4 tails. We purified a SWI/SNF mutant (SWI/SNF-Δ2N) that lacks 200 amino acids within the N-terminal acidic domain of Swi3p. Intriguingly, SWI/SNF-Δ2N failed to catalyze ATP-dependent dimer loss, although this mutant SWI/SNF contains all the subunits and has intact ATP-dependent activity in enhancing restriction enzyme accessibility. These data help to further understand the molecular mechanism of SWI/SNF, and show that H2A/H2B dimer loss is not an obligatory consequence of ATP-dependent DNA translocation, but requires the histone chaperone function of the Swi3p subunit. Based on these findings, we proposed a new model of the structural and functional organization of the SWI/SNF chromatin remodeling machinery: SWI/SNF contains at least four distinct modules that function at distinct stages of the chromatin remodeling process. 1) Swi1p and Snf5p modules directly interact with gene specific activators and function as the recruiter; 2) Swi2p/Arp7p/Arp9p generates energy from ATP hydrolysis and disrupts histone/DNA interactions; and 3) Swi3p/Swp73p/Snf6p may play dual roles by integrating each module into a large remodeling complex, as well as functioning as a histone H2A/H2B chaperone to remove dimers from remodeled nucleosomes. Chapter IV is a perspective from current work in this project. I first discuss the interest in further characterizing the essential role of Snf6p, based on its activation of LacZ reporter on its own. Using in vitro translated protein and co-IP studies, I tried to pinpoint the requirement of the SANT domain for SWI/SNF assembly. I found that Swi3p directly interacts with Swp73p, but not with other subunits. When Swi3p is first incubated with Swp73p, Swi3p also interacts with Snf6p, indicating that Swi3p indirectly interacts with Snf6p, therefore forming a subcomplex of Swi3p/Swp73p/Snf6p. This subcomplex can also be reconstituted using in vitro co-translation. Consistent with the TAP preparation of this subcomplex, partial deletion of the SANT domain of Swi3p does not affect the assembly of Swi3p/Swp73p/Snf6p in vitro. However, the assembly of SWI/SNF complex was not detected in the presence of eight essential in vitro translated subunits or from co-translation of all the subunits. I have discussed the interest in further characterizing the histone chaperone role of the Swi3p N-terminal acidic domain and the role of other core subunits of SWI/SNF such as Snf6p for transcriptional regulation.
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Sen, Payel. "STRUCTURAL AND FUNCTIONAL DELINEATION OF SUBUNITS AND DOMAINS IN THE SACCHAROMYCES CEREVISIAE SWI/SNF COMPLEX." OpenSIUC, 2011. https://opensiuc.lib.siu.edu/dissertations/432.

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Chromatin remodelers are ATP-dependent multisubunit assemblies that regulate transcription and other processes by altering DNA-histone contacts. The mechanism of action is based on the transduction of energy released by ATP hydrolysis to translocation on DNA and ultimately the movement of histones in cis or trans. Though the critical ATP burning and translocation activities are fulfilled by a conserved ATPase domain in the catalytic subunit, there are accessory domains and subunits that are speculated to regulate these activities. Important questions in the field center around the identification of these domains and subunits, whether they affect complex formation, substrate affinity or a critical step in remodeling. If they do affect remodeling, what is the structural basis of the regulatory activity. In this study, these questions have been addressed using the prototype remodeler SWI/SNF from budding yeast. ySWI/SNF is a 12 subunit complex that includes the catalytic subunit Swi2/Snf2. It affects 6% of the yeast genome being primarily involved in gene activation. We employed a systematic protein or domain deletion strategy and characterized the mutant complexes in vitro and in vivo. A key finding was that SWI/SNF is organized in distinct structural modules and that the Snf2 module regulates most of its activities. Snf2 is a central subunit in this module and the function of conserved regions within Snf2 were studied. The N terminus preceding the HSA and ATPase domain has three major roles - complex assembly, recruitment and regulation of catalytic activity. A novel SnAC domain located C terminal to ATPase domain was identified to play critical role in coupling ATP hydrolysis to nucleosome movement by acting as a histone anchor. Finally the tandem AT-hooks between SnAC and bromodomain serve as DNA binding domains but also affect ATPase activity and nucleosome mobilization independent of its binding activity. Taken together, this study provides a comprehensive overview of the function of regulatory domains in SWI/SNF.
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Manning, Benjamin J. "ATP-Dependent Heterochromatin Remodeling: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/795.

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Eukaryotic DNA is incorporated into the nucleoprotein structure of chromatin. This structure is essential for the proper storage, maintenance, regulation, and function of the genomes’ constituent genes and genomic sequences. Importantly, cells generate discrete types of chromatin that impart distinct properties on genomic loci; euchromatin is an open and active compartment of the genome, and heterochromatin is a restricted and inactive compartment. Heterochromatin serves many purposes in vivo, from heritably silencing key gene loci during embryonic development, to preventing aberrant DNA repeat recombination. Despite this generally repressive role, the DNA contained within heterochromatin must still be repaired and replicated, creating a need for regulated dynamic access into silent heterochromatin. In this work, we discover and characterize activities that the ATP-dependent chromatin remodeling enzyme SWI/SNF uses to disrupt repressive heterochromatin structure. First, we find two specific physical interactions between the SWI/SNF core subunit Swi2p and the heterochromatin structural protein Sir3p. We find that disrupting these physical interactions results in a SWI/SNF complex that can hydrolyze ATP and slide nucleosomes like normal, but is defective in its ability to evict Sir3p off of heterochromatin. In vivo, we find that this Sir3p eviction activity is required for proper DNA replication, and for establishment of silent chromatin, but not for SWI/SNF’s traditional roles in transcription. These data establish new roles for ATP-dependent chromatin remodeling in regulating heterochromatin. Second, we discover that SWI/SNF can disrupt heterochromatin structures that contain all three Sir proteins: Sir2p, Sir3p and Sir4p. This new disruption activity requires nucleosomal contacts that are essential for silent chromatin formation in vivo. We find that SWI/SNF evicts all three heterochromatin proteins off of chromatin. Surprisingly, we also find that the presence of Sir2p and Sir4p on chromatin stimulates SWI/SNF to evict histone proteins H2A and H2B from nucleosomes. Apart from discovering a new potential mechanism of heterochromatin dynamics, these data also establish a new paradigm of chromatin remodeling enzyme regulation by nonhistone proteins present on the substrate.
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Manning, Benjamin J. "ATP-Dependent Heterochromatin Remodeling: A Dissertation." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/795.

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Eukaryotic DNA is incorporated into the nucleoprotein structure of chromatin. This structure is essential for the proper storage, maintenance, regulation, and function of the genomes’ constituent genes and genomic sequences. Importantly, cells generate discrete types of chromatin that impart distinct properties on genomic loci; euchromatin is an open and active compartment of the genome, and heterochromatin is a restricted and inactive compartment. Heterochromatin serves many purposes in vivo, from heritably silencing key gene loci during embryonic development, to preventing aberrant DNA repeat recombination. Despite this generally repressive role, the DNA contained within heterochromatin must still be repaired and replicated, creating a need for regulated dynamic access into silent heterochromatin. In this work, we discover and characterize activities that the ATP-dependent chromatin remodeling enzyme SWI/SNF uses to disrupt repressive heterochromatin structure. First, we find two specific physical interactions between the SWI/SNF core subunit Swi2p and the heterochromatin structural protein Sir3p. We find that disrupting these physical interactions results in a SWI/SNF complex that can hydrolyze ATP and slide nucleosomes like normal, but is defective in its ability to evict Sir3p off of heterochromatin. In vivo, we find that this Sir3p eviction activity is required for proper DNA replication, and for establishment of silent chromatin, but not for SWI/SNF’s traditional roles in transcription. These data establish new roles for ATP-dependent chromatin remodeling in regulating heterochromatin. Second, we discover that SWI/SNF can disrupt heterochromatin structures that contain all three Sir proteins: Sir2p, Sir3p and Sir4p. This new disruption activity requires nucleosomal contacts that are essential for silent chromatin formation in vivo. We find that SWI/SNF evicts all three heterochromatin proteins off of chromatin. Surprisingly, we also find that the presence of Sir2p and Sir4p on chromatin stimulates SWI/SNF to evict histone proteins H2A and H2B from nucleosomes. Apart from discovering a new potential mechanism of heterochromatin dynamics, these data also establish a new paradigm of chromatin remodeling enzyme regulation by nonhistone proteins present on the substrate.
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Books on the topic "Structural remodeling"

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Reiter, Thomas J. Functional adaption of bone and application in optimal structural design. Dusseldorf: VDI Verlag, 1996.

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Chinchalkar, Shirish. Parallel structural optimization applied to bone remodeling on distributed memory machines. Ithaca, N.Y: Cornell Theory Center, Cornell University, 1993.

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Zongjin, Li. Structural renovation in concrete. London: Taylor & Francis, 2009.

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Robert, Bowles, ed. Structural aspects of building conservation. 2nd ed. Boston: Elsevier Butterworth-Heinemann, 2004.

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Structural aspects of building conservation. London: McGraw-Hill, 1995.

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Saint-Petersburg-2005, International Scientific-Practical Conference. Rekonstrukt︠s︡ii︠a︡--Sankt-Peterburg-2005: Mezhdunarodnai︠a︡ nauchno-prakticheskai︠a︡ konferent︠s︡ii︠a︡ : sbornik dokladov. Sankt-Peterburg: Peterburgskiĭ gos. arkhitekturno-stroitelʹnyĭ universitet, 2005.

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Chromatin remodeling: Methods and protocols. New York: Humana Press, 2012.

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1964-, Marinaro Nidia, ed. Casas de barrio: Se adormecen, despiertan y se iluminan. [Buenos Aires?]: Nobuko, 2011.

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Rubió, Ignasi Solà-Morales. Architettura minimale a Barcelona: Costruire sulla città costruita = Minimal architecture in Barcelona : building on the built city. Milano: Electa, 1986.

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Altınoluk, Ülkü. Eski yapılar, yeni fonksiyonlar. Şişli, İstanbul: Türkiye Turing ve Otomobil Kurumu, 1987.

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Book chapters on the topic "Structural remodeling"

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Zayat, K. A. "Remodeling." In Structural Wood Detailing in CAD Format, 214–16. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-2104-0_34.

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Gerdes, A. Martin, and Xuejun Wang. "Structural Remodeling of Cardiac Myocytes in Hypertrophy and Progression to Failure." In Cardiac Remodeling and Failure, 183–93. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9262-8_12.

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Barth, Andreas S., and Gordon F. Tomaselli. "Repolarization Remodeling in Structural Heart Disease." In Cardiac Repolarization, 77–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-22672-5_3.

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Tribulová, Narcis, L’udmila Okruhlicová, Dalia Varon, Mordechai Manoach, Ol’ga Pechaňová, Iveta Bernatová, Peter Weismann, Miroslav Barančík, Ján Styk, and Ján Slezák. "Structural Substrates Involved in the Development of Severe Arrhythmias in Hypertensive Rat and Aged Guinea Pig Hearts." In Cardiac Remodeling and Failure, 377–400. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9262-8_27.

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Torrealba, Natalia, Pablo Aranguiz, Camila Alonso, Beverly A. Rothermel, and Sergio Lavandero. "Mitochondria in Structural and Functional Cardiac Remodeling." In Advances in Experimental Medicine and Biology, 277–306. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55330-6_15.

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Wagoner, David R. Van. "Electrical and Structural Remodeling in Atrial Fibrillation." In Atrial Fibrillation, 57–68. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-163-5_5.

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Weber, K. T., Y. Sun, and J. P. M. Cleutjens. "Structural remodeling of the infarcted rat heart." In Myocardial Ischemia: Mechanisms, Reperfusion, Protection, 489–99. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-8988-9_30.

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Jakobs, Tatjana C. "Analysis of Morphology and Structural Remodeling of Astrocytes." In Neuromethods, 129–43. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0381-8_6.

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DeMello, Walmor C. "Structural and Electrophysiological Remodeling of the Failing Heart." In Renin Angiotensin System and Cardiovascular Disease, 81–91. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-186-8_7.

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Janicki, Joseph S., Suresh C. Tyagi, Beatriz B. Matsubara, and Scott E. Campbell. "Structural and Functional Consequences of Myocardial Collagen Remodeling." In Cardiac Adaptation and Failure, 279–89. Tokyo: Springer Japan, 1994. http://dx.doi.org/10.1007/978-4-431-67014-8_20.

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Conference papers on the topic "Structural remodeling"

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Elowsson Rendin, Linda, Anna Löfdahl, Liang Xiong, Barbora Michaliková, Xiaohong Zhou, Göran Dellgren, and Gunilla Westergren-Thorsson. "Altered ECM niche in IPF affect structural remodeling." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3376.

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Zhu, Qiang, Zhangli Peng, and Robert J. Asaro. "Investigation of RBC Remodeling With a Multiscale Model." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13121.

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Erythrocyte (red blood cell, or RBC) possesses one of the simplest and best characterized molecular architectures among all cells. It contains cytosol enclosed inside a composite membrane consisting of a fluidic lipid bilayer reinforced by a single layer of protein skeleton pinned to it. In its normal state, this system demonstrates tremendous structural stability, manifested in its ability to sustain large dynamic deformations during circulation. On the other hand, it has been illustrated in experiments that triggered by mechanical loads structural remodeling may occur. A canonical example of this remodeling is vesiculation, referring to the partial separation of the lipid bilayer from the protein skeleton and the formation of vesicles that contain lipids only.
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Shazly, Tarek, and Alexander Rachev. "The Effects of Arterial Tissue Reorganization on the Geometrical Outputs of Pressure- and Flow-Induced Remodeling: A Theoretical Study." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80086.

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Arterial remodeling in response to sustained alterations in blood pressure and/or flow induces changes in vessel geometry, structure, and composition. In conditions of hypertension and elevated blood flow, remodeling results in increased vessel mass that is distributed in a manner to maintain the local mechanical environment of the vascular cells at a baseline state. A majority of theoretical studies on remodeling have assumed that new mass is formed via a proportional production of load-bearing constituents, namely elastin, collagen, and smooth muscle. Therefore, when the vascular tissue is considered as a constrained mixture of these structural components, their mass fractions do not change as a result of remodeling. However, increased arterial mass is primarily attributed to smooth muscle cell hypertrophy and upregulated collagen production, implying a change in the mass fractions of all constituents and therefore the tissue mechanical properties [1]. Moreover, few papers account for remodeling-induced changes in the configuration and/or orientation of collagen fibers, both of which may also alter tissue mechanical properties. The objective of this study is to build a mathematical model that enables evaluation of the effects of mass redistribution among structural components and changes in collagen fiber configuration on the geometrical outputs of arterial remodeling.
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Cheong, Vee San, Aadil Mumith, Melanie Coathup, Gordon Blunn, and Paul Fromme. "Bone remodeling in additive manufactured porous implants changes the stress distribution." In Health Monitoring of Structural and Biological Systems IX, edited by Paul Fromme and Zhongqing Su. SPIE, 2020. http://dx.doi.org/10.1117/12.2558093.

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Valinoti, Maddalena, Graziano Vito Lozupone, Paolo Sabbatani, Roberto Mantovan, Stefano Severi, and Cristiana Corsi. "Analysis of the electrical patterns and structural remodeling in atrial fibrillation." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7320012.

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Cox, L. G. E., C. C. van Donkelaar, B. van Rietbergen, and K. Ito. "Mechanoregulated Bone Remodeling May Explain Bone Structural Changes Observed in Osteoarthritis." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19583.

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Osteoarthritis (OA) affects both the articular cartilage and the subchondral bone. It is a complicated disease, associated with conditions varying from obesity and strenuous exercise to joint malalignment, anterior cruciate ligament (ACL) injury, and even metabolic bone diseases. Patients suffer from chronic joint pain and limitation of motion, and no cure is yet available. For many years, medical therapies have been focused on cartilage, because bone changes were thought not to play a major role in the OA disease process. However, it has been shown that bone changes occur in an early stage of OA, and that alterations to subchondral bone can lead to cartilage degeneration [1]. Therefore, currently the bone is considered as a therapeutic target as well.
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Rajabzadeh-Oghaz, Hamidreza, Anusha Ramesh Chandra, Liza Gutierrez, Ferdinand Schweser, Ciprian N. Ionita, Adnan H. Siddiqui, and Vincent Tutino. "High-resolution MRI of the mouse cerebral vasculature to study hemodynamic-induced vascular remodeling." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor Gimi and Andrzej Krol. SPIE, 2019. http://dx.doi.org/10.1117/12.2511772.

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Wu, Yin, Hung-Fat Tse, and Ed X. Wu. "Diffusion Tensor MRI Study of Myocardium Structural Remodeling after Infarction in Porcine Model." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.259840.

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Wu, Yin, Hung-Fat Tse, and Ed X. Wu. "Diffusion Tensor MRI Study of Myocardium Structural Remodeling after Infarction in Porcine Model." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4397590.

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Haskett, Darren, Marie Fouts, Urs Utzinger, Doug Larson, Mohamad Azhar, and Jonathan Vande Geest. "The Effects of Angiotensin II Infusion on the Mechanical Response and Microstructural Organization of Mouse Aorta." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19635.

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Vascular diseases such as aneurysm and aortic dissection account for almost 16,000 deaths in the United States annually. In both of these diseases vascular inflammation is a common pathogenic factor. Another common pathologic feature of vascular disease includes structural matrix remodeling. It is also increasingly believed that inflammation may play a key role in the formation and progression of atherosclerotic vascular disease. Angiotensin II (AngII), a potent vasopressor, is also a strong inducer of vascular inflammation and aortic remodeling in atherosclerosis-prone mice. Based on this knowledge studies have been conducted using subcutaneous AngII infusion in order to produce aortic remodeling and aneurysm formation, with acute thoracic and abdominal aortic dissections [1].
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