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Статті в журналах з теми "Remodelled genes"
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Germain, Adeline, Jeanne-Marie Perotin, Gonzague Delepine, Myriam Polette, Gaëtan Deslée, and Valérian Dormoy. "Whole-Exome Sequencing of Bronchial Epithelial Cells Reveals a Genetic Print of Airway Remodelling in COPD." Biomedicines 10, no. 7 (July 15, 2022): 1714. http://dx.doi.org/10.3390/biomedicines10071714.
Повний текст джерелаАнотація:
The remodelling of the airways is a hallmark of chronic obstructive pulmonary disease, but it is highly heterogeneous and erratically distributed in the airways. To assess the genetic print of remodelling in chronic obstructive pulmonary disease (COPD), we performed a comparative whole-exome sequencing analysis on microdissected bronchial epithelia. Lung resections from four non-COPD and three COPD subjects (ex-smokers and current smokers) were formalin-fixed paraffin-embedded (FFPE). Non-remodelled and remodelled bronchial epithelia were isolated by laser microdissection. Genomic DNA was captured and sequenced. The comparative quantitative analysis identified a list of 109 genes as having variants in remodelled epithelia and 160 genes as having copy number alterations in remodelled epithelia, mainly in COPD patients. The functional analysis highlighted cilia-associated processes. Therefore, bronchial-remodelled epithelia appeared genetically more altered than non-remodelled epithelia. Characterizing the unique molecular print of airway remodelling in respiratory diseases may help uncover additional factors contributing to epithelial dysfunctions, ultimately providing additional targetable proteins to correct epithelial remodelling and improve lung function.
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Li, Mengyao, Su Mon Aye, Maizbha Uddin Ahmed, Mei-Ling Han, Chen Li, Jiangning Song, John D. Boyce, et al. "Pan-transcriptomic analysis identified common differentially expressed genes of Acinetobacter baumannii in response to polymyxin treatments." Molecular Omics 16, no. 4 (2020): 327–38. http://dx.doi.org/10.1039/d0mo00015a.
Повний текст джерелаАнотація:
Our pan-transcriptomic study for polymyxin-treated A. baumannii identified that the remodelled outer membrane, up-regulated efflux pumps and down-regulated fatty acid biosynthesis might be essential for early responses to polymyxins in A. baumannii.
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Ou, Yaqing, and James O. McInerney. "Eukaryote Genes Are More Likely than Prokaryote Genes to Be Composites." Genes 10, no. 9 (August 28, 2019): 648. http://dx.doi.org/10.3390/genes10090648.
Повний текст джерелаАнотація:
The formation of new genes by combining parts of existing genes is an important evolutionary process. Remodelled genes, which we call composites, have been investigated in many species, however, their distribution across all of life is still unknown. We set out to examine the extent to which genomes from cells and mobile genetic elements contain composite genes. We identify composite genes as those that show partial homology to at least two unrelated component genes. In order to identify composite and component genes, we constructed sequence similarity networks (SSNs) of more than one million genes from all three domains of life, as well as viruses and plasmids. We identified non-transitive triplets of nodes in this network and explored the homology relationships in these triplets to see if the middle nodes were indeed composite genes. In total, we identified 221,043 (18.57%) composites genes, which were distributed across all genomic and functional categories. In particular, the presence of composite genes is statistically more likely in eukaryotes than prokaryotes.
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Kuleesha, Yadav, Wee Choo Puah, and Martin Wasser. "A model of muscle atrophy based on live microscopy of muscle remodelling in Drosophila metamorphosis." Royal Society Open Science 3, no. 2 (February 2016): 150517. http://dx.doi.org/10.1098/rsos.150517.
Повний текст джерелаАнотація:
Genes controlling muscle size and survival play important roles in muscle wasting diseases. In Drosophila melanogaster metamorphosis, larval abdominal muscles undergo two developmental fates. While a doomed population is eliminated by cell death, another persistent group is remodelled and survives into adulthood. To identify and characterize genes involved in the development of remodelled muscles, we devised a workflow consisting of in vivo imaging, targeted gene perturbation and quantitative image analysis. We show that inhibition of TOR signalling and activation of autophagy promote developmental muscle atrophy in early, while TOR and yorkie activation are required for muscle growth in late pupation. We discovered changes in the localization of myonuclei during remodelling that involve anti-polar migration leading to central clustering followed by polar migration resulting in localization along the midline. We demonstrate that the Cathepsin L orthologue Cp1 is required for myonuclear clustering in mid, while autophagy contributes to central positioning of nuclei in late metamorphosis. In conclusion, studying muscle remodelling in metamorphosis can provide new insights into the cell biology of muscle wasting.
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Wang, Yuzhe, Shiyu Li, Mengge Liu, Jiajia Wang, Zhengbin Fei, Feng Wang, Zhenyou Jiang, Wenhua Huang, and Hanxiao Sun. "Rhodosporidium toruloides sir2-like genes remodelled the mitochondrial network to improve the phenotypes of ageing cells." Free Radical Biology and Medicine 134 (April 2019): 64–75. http://dx.doi.org/10.1016/j.freeradbiomed.2018.12.036.
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Ahmedien, Diaa Ahmed Mohamed. "Bio-pixels: A stem cell-based interactive–generative interface designed to redefine technologies of self-making in new media arts." Convergence: The International Journal of Research into New Media Technologies 26, no. 5-6 (November 29, 2019): 1367–90. http://dx.doi.org/10.1177/1354856519890096.
Повний текст джерелаАнотація:
Bio-pixels is a stem cell-based interactive–generative interface designed to investigate the concept of ‘self-making’. The project uses stem cells as a biological prototype of an identity-free substance and defines in vivo stem cell differentiation processes as nature’s self-making technology. It therefore considers in vitro-induced differentiation processes as artificial self-making technologies that were recontextualized through the interactions between the world of genes and the world of bits. The project’s system was functionally built based on three operational principles derived from convergence technologies that facilitate a mutual functional shift between bio-media and digital media and reveal the extent to which this shift leads to a reconciliation between our biological and narrative identities. Empirically, the project remodelled visual maps of cellular activities during the induced differentiation processes by which cells acquire their identity. Finally, a generative biological–digital mirror was architected by which the viewers see their faces resynthesized as the result of the interactions between the artificial remodelled differentiation processes and the participants’ activities at the project’s physical place and its Twitter page. Within this context, Bio-pixels highlights the consequences of today’s bioinformatics on in vitro artificial processes of self-making through which the public can control, enhance or resynthesize their identities.
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Dalla Torre, Marco, Daniele Pittari, Alessandra Boletta, Laura Cassina, Roberto Sitia, and Tiziana Anelli. "Mitochondria remodeling during endometrial stromal cell decidualization." Life Science Alliance 7, no. 12 (October 4, 2024): e202402627. http://dx.doi.org/10.26508/lsa.202402627.
Повний текст джерелаАнотація:
Upon hormonal stimulation, uterine endometrial stromal cells undergo a dramatic morpho-functional metamorphosis that allows them to secrete large amounts of matrix proteins, cytokines, and growth factors. This step, known as decidualization, is crucial for embryo implantation. We previously demonstrated how the secretory pathway is remodelled during this process. Here we show that hormonal stimulation rapidly induces the expression of many mitochondrial genes, encoded in both the mitochondrial and the nuclear genomes. Altogether, the mitochondrial network quadruples its size and establishes more contacts with the ER. This new organization results in the increased respiratory capacity of decidualized cells. These findings reveal how achieving an efficient secretory phenotype requires a radical metabolic rewiring.
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Reik, Wolf, Fatima Santos, Kohzoh Mitsuya, Hugh Morgan, and Wendy Dean. "Epigenetic asymmetry in the mammalian zygote and early embryo: relationship to lineage commitment?" Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1436 (August 29, 2003): 1403–9. http://dx.doi.org/10.1098/rstb.2003.1326.
Повний текст джерелаАнотація:
Epigenetic asymmetry between parental genomes and embryonic lineages exists at the earliest stages of mammalian development. The maternal genome in the zygote is highly methylated in both its DNA and its histones and most imprinted genes have maternal germline methylation imprints. The paternal genome is rapidly remodelled with protamine removal, addition of acetylated histones, and rapid demethylation of DNA before replication. A minority of imprinted genes have paternal germline methylation imprints. Methylation and chromatin reprogramming continues during cleavage divisions, but at the blastocyst stage lineage commitment to inner cell mass (ICM) or trophectoderm (TE) fate is accompanied by a dramatic increase in DNA and histone methylation, predominantly in the ICM. This may set up major epigenetic differences between embryonic and extraembryonic tissues, including in X–chromosome inactivation and perhaps imprinting. Maintaining epigenetic asymmetry appears important for development as asymmetry is lost in cloned embryos, most of which have developmental defects, and in particular an imbalance between extraembryonic and embryonic tissue development.
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Chen, Xinxin, Jun Wang, Donna Woltring, Steve Gerondakis, and M. Frances Shannon. "Histone Dynamics on the Interleukin-2 Gene in Response to T-Cell Activation." Molecular and Cellular Biology 25, no. 8 (April 15, 2005): 3209–19. http://dx.doi.org/10.1128/mcb.25.8.3209-3219.2005.
Повний текст джерелаАнотація:
ABSTRACT Several models have been proposed for the mechanism of chromatin remodelling across the promoters of inducible genes in mammalian cells. The most commonly held model is one of cooccupation where histone proteins are modified by acetylation or phosphorylation and nucleosomes are remodelled, allowing the assembly of transcription factor complexes. Using chromatin immunoprecipitation, we observed an apparent decrease of histone acetylation and phosphorylation signals at the proximal promoter region of the inducible interleukin-2 and granulocyte-macrophage colony-stimulating factor genes in response to T-cell activation. We showed that this apparent decrease was due to a loss of histone H3 and H4 proteins corresponding to a decrease in nucleosome occupation of the promoter. This histone loss is reversible; it is dependent on the continual presence of appropriate activating signals and transcription factors and is not dependent on the acetylation status of the histone proteins. These data show for the first time that histone proteins are lost from a mammalian promoter upon activation of transcription and support a model of activation-dependent disassembly and reassembly of nucleosomes.
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PRAJAPATI, SURENDRA K., RICHARD CULLETON, and OM P. SINGH. "Protein trafficking in Plasmodium falciparum-infected red cells and impact of the expansion of exported protein families." Parasitology 141, no. 12 (July 30, 2014): 1533–43. http://dx.doi.org/10.1017/s0031182014000948.
Повний текст джерелаАнотація:
SUMMARYErythrocytes are extensively remodelled by the malaria parasite following invasion of the cell. Plasmodium falciparum encodes numerous virulence-associated and host-cell remodelling proteins that are trafficked to the cytoplasm, the cell membrane and the surface of the infected erythrocyte. The export of soluble proteins relies on a sequence directing entry into the secretory pathways in addition to an export signal. The export signal consisting of five amino acids is termed the Plasmodium export element (PEXEL) or the vacuole transport signal (VTS). Genome mining studies have revealed that PEXEL/VTS carrying protein families have expanded dramatically in P. falciparum compared with other malaria parasite species, possibly due to lineage-specific expansion linked to the unique requirements of P. falciparum for host-cell remodelling. The functional characterization of such genes and gene families may reveal potential drug targets that could inhibit protein trafficking in infected erythrocytes. This review highlights some of the recent advances and key knowledge gaps in protein trafficking pathways in P. falciparum-infected red cells and speculates on the impact of exported gene families in the trafficking pathway.
Дисертації з теми "Remodelled genes"
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Sussfeld, Duncan. "Identifying remote homology and gene remodelling using network-based approaches." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL112.
Повний текст джерелаАнотація:
L'augmentation toujours plus importante de données génomiques et métagénomiques appelle de nouveaux développements méthodologiques et bio-informatiques, afin de caractériser avec davantage de précision les phénomènes évolutifs dans leur ensemble. En particulier, certaines des méthodes usuelles pour étudier l'évolution des (familles de) gènes s'avèrent inadaptées lorsque la parenté entre séquences n'est que partiellement supportée. Ainsi, la définition et la reconstruction de familles de gènes se heurtent à l'obstacle de l'homologie distante, qui passe sous le seuil de détection des alignements de séquences. De même, les mécanismes d'évolution combinatoire, tels que les fusions et fissions de gènes, remettent en cause les représentations purement arborescentes de l'évolution des familles de gènes. L'application de méthodes complémentaires basées sur les réseaux de similarité de séquences permet de contourner certaines de ces lacunes, en proposant une représentation holistique des similarités entre gènes. La détection et l'analyse d'homologues très divergents de familles de gènes fortement conservées dans des jeux de données environnementaux est notamment facilitée par la recherche itérative d'homologie fondée sur les réseaux. Cette fouille itérative de métagénomes révèle une immense diversité de variants environnementaux dans ces familles, qui divergent de la diversité connue tant par leur séquence que par la structure des protéines qu'ils encodent, et elle permet de suggérer des pistes pour guider de futures explorations de la matière noire microbienne. En outre, en prenant en compte des liens d'homologie partielle entre séquences génétiques, les réseaux de similarité de séquences permettent une identification systématique des évènements de fusion et de fission de gènes. Il devient ainsi possible d'évaluer l'impact de ces processus au cours de l'évolution de lignées biologiques d'intérêt, permettant de comparer le rôle qu'ils ont joué lors de l'émergence de phénotypes multicellulaires complexes dans plusieurs telles lignées. Plus généralement, ces approches basées sur les réseaux illustrent l'intérêt de prendre en compte une pluralité de modèles pour étudier une plus grande variété de processus évolutifsThe ever-increasing accumulation of genomic and metagenomic data calls for new methodological developments in bioinformatics, in order to characterise evolutionary phenomena as a whole with better accuracy. In particular, some of the canonical methods to study the evolution of genes and gene families may be ill-suited when the relatedness of sequences is only partially supported. For instance, the definition and reconstruction of gene families face the hurdle of remote homology, which falls beneath the detection thresholds of sequence alignments. Likewise, combinatorial mechanisms of evolution, such as gene fusion and gene fission, challenge the purely tree-based representations of gene family evolution. The use of complementary methods based on sequence similarity networks allows us to circumvent some of these shortcomings, by offering a more holistic representation of similarities between genes. The detection and analysis of highly divergent homologues of strongly conserved families in environmental sequence datasets, in particular, is facilitated by iterative homology search protocols based on networks. This iterative mining of metagenomes reveals an immense diversity of environmental variants in these families, diverging from the known diversity in primary sequence as well as in the tertiary structure of the proteins they encode. It is thus able to suggest possible directions of future explorations into microbial dark matter. Furthermore, by factoring in relationships of partial homology between gene sequences, sequence similarity networks allow for a systematic identification of gene fusion and fission events. It thus becomes possible to assess the effects of these processes on the evolution of biological lineages of interest, enabling us for instance to compare the role that they played in the emergence of complex multicellular phenotypes between several such lineages. More generally, these network-based approaches illustrate the benefits of taking a plurality of models into account, in order to study a broader range of evolutionary processes
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Kreher, Judith [Verfasser], and Alexander [Akademischer Betreuer] Brehm. "Function of the ATP-dependent chromatin remodeler Mi-2 in the regulation of ecdysone dependent genes in Drosophila melanogaster / Judith Kreher. Betreuer: Alexander Brehm." Marburg : Philipps-Universität Marburg, 2015. http://d-nb.info/1070623962/34.
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(6635906), Erin L. Sorlien. "The Chromatin Remodeler and Tumor Suppress Chd5 Promotes Expression and Processing of Transcripts During Development of the Zebrafish Neural System." Thesis, 2019.
Знайти повний текст джерелаАнотація:
Vertebrate neurogenesis is a multistep process that coordinates complex signaling pathways and chromatin-based regulatory machinery to generate highly specialized cells (Hsieh and Zhao 2016; Urban and Guillemot 2014; Alunni and Bally-Cuif 2016; Yao and Jin 2014; Schmidt, Strahle, and Scholpp 2013). Epigenetic factors play a fundamental role in underwriting neurogenesis in part by contributing to control of gene expression in differentiating neurons. A mechanistic understanding of the epigenetic machinery underlying neurogenesis in vertebrates is necessary both to fully understand biogenesis of neural tissue in this subphylum as well as to develop effective therapeutic strategies to treat diseased or damaged neural tissue.
An example of an epigenetic factor that is important for both neuronal differentiation and disease states is CHD5, a vertebrate-specific member of the CHD family of ATP-dependent chromatin remodeling proteins. Chromodomain / Helicase / DNA-binding (CHD) proteins play a variety of roles in vertebrate development, and misregulation or loss of CHD proteins has been linked to numerous diseases (Mayes et al. 2014; Marfella and Imbalzano 2007; Bartholomew 2014). CHD5 is expressed primarily in neural tissue, where it is thought to contribute to neurogenesis, and has been strongly linked to tumor suppression (Thompson et al. 2003; Vestin and Mills 2013). Loss of CHD5 plays a significant role in development of neuroblastoma, a devastating tumor that is a leading cause of cancer-related death in children (Jiang, Stanke, and Lahti 2011; Maris and Matthay 1999). Consistent with the disease phenotype associated with loss of CHD5, reduced expression of CHD5 impairs differentiation of neuronal cells (Egan et al. 2013b). However, ablation of CHD5 in mice surprisingly resulted in no detectable defects in brain development (Li et al. 2014; Zhuang et al. 2014). A subsequent report revealed that mice conditionally ablated for CHD5 in neural tissue exhibit symptoms consistent with an autism spectrum disorder (Pisansky et al. 2017). Much remains to be learned about the role of CHD5 in these processes to clarify these observations.
Further, Chd5 is unique among the family of Chd remodelers in that it provides a biochemical basis for crosstalk between the critical epigenetic marks H3K27me3 and DNA methylation. Chd5 and the closely related remodelers Chd3 and Chd4 are all components of the Mi-2/NuRD histone deacetylase complex that plays a critical role in mediating transcriptional repression in response to DNA methylation in mammals (Allen, Wade, and Kutateladze 2013). Only CHD5 is preferentially expressed in neural tissue, however, and only Chd5 remodelers have biochemical evidence of direct interaction with H3K27me3, which plays a critical role in enabling proper expression of transcriptional programs during neurogenesis (Egan et al. 2013b). Chd5 is thus unique among CHD remodelers in that it is biochemically linked to both DNA methylation and H3K27me3 in addition to being preferentially expressed in neural tissue.
With regards to mechanism, much remains to be learned regarding how Chd5 remodelers contribute to gene expression and tumor suppression. However, the data to date do not show extensive transcript phenotypes and it is not clear how the biochemical action of CHD5 contributes to the neurological phenotypes ascribed to altered expression of CHD5. Therefore, it is critical to determine a suitable context to study the role of CHD5 in these processes. Identification of CHD5-dependent genes in neurons is likely to generate insight into how loss of CHD5 contributes to tumorigenesis, in particular with regards to development of neuroblastoma. Regulatory pathways that drive neurogenesis have been found to be extensively conserved between humans and zebrafish. Therefore, we have turned to the power of the zebrafish model system to characterize how loss of Chd5 alters brain development during embryogenesis.
Importantly zebrafish development, and neurogenesis in particular, occurs largely over the first 5-days of development. Zebrafish are born outside of the mother, which can produce large clutches of several hundred embryos per week, providing us with an accessible context to study the role of chd5, the zebrafish homolog of human CHD5. The central nervous system of the zebrafish develops rapidly, and shares many of the organization features of the mammalian brain (Kalueff, Stewart, and Gerlai 2014). In particular, neuroblastoma arises from a population of cells known as sympathetic ganglion cells that are derived from the neural crest (Pei et al. 2013). These cells are conserved in vertebrates, and several models to study how these cells transform into neuroblastoma exist in zebrafish (Zhu et al. 2017; Morrison et al. 2016; Zhu and Thomas Look 2016). However, our understanding of the mechanisms controlling ganglion cell differentiation is incomplete and requires further investigation to understand how epigenetic and transcriptional mechanisms contribute to development of these cells and how failure of these processes leads to cancer. The neural crest undergoes a series of differentiation steps to form mature sympathetic neurons that are guided by bone morphogenic protein signaling, and transcription changes (Ernsberger and Rohrer 2018). These cells express key enzymes for synthesizing dopamine and norephinephrine to control the sympathetic system throughout the central nervous system (Ernsberger and Rohrer 2018).
To address these questions about Chd5, we have used CRISPR/Cas9 to generate chd5-/- zebrafish that are protein nulls as determined by western blot. These chd5-/- fish are phenotypically indistinguishable from wild-type fish under standard growth conditions as was previously observed for mice lacking CHD5 (Zhuang et al. 2014; Li et al. 2014). By using zebrafish, we are able to perform transcriptome analyses to identify Chd5 target genes at stages much earlier than has previously been performed in mice because we can harvest large amounts of the tissue of interest from the readily accessible embryos. We have therefore undertaken RNA-seq analysis of isolated brains from wild-type and chd5-/- fish to identify chd5-dependent genes in predominantly differentiating (2-day old) and substantially differentiated (5-day old) neural tissue. These data provide a substantively different perspective from previous studies that examine the role of CHD5 in gene expression of differentiated SY-SH5Y cells (Egan et al. 2013a) or in the forebrain of 8-week-old mice (Pisansky et al. 2017). (Jiang, Stanke, and Lahti 2011). One role we identified from this data, is the promotion of development of sympathetic ganglion cells (detailed below), illuminating for the first time a role for chd5 in promoting differentiation of cells directly involved in neuroblatoma.
We observe not only extensive changes in gene expression, but also identify a novel role for Chd5 in enabling proper splicing during this critical window of neurogenesis in the zebrafish brain. We are further exploring the role of CHD5 in these processes by creating comparable cell culture-based models of loss of CHD5 to determine the conservation of molecular phenotypes observed in zebrafish. Furthermore, this model enables us to leverage the extensive biochemical tools available in cell culture to examine alterations to the chromatin that are difficult to interpret from studies of complex tissues such as the brain.
Herein I will describe the research progress we have made to understand the role of Chd5 in gene expression and splicing in zebrafish, as well as ongoing work to engineer mouse embryonic stem cells as an additional model to study the transcriptional consequences of loss of CHD5. Critically, the addition of the cell culture model will greatly enable biochemical characterization of the changes that are leading in particular to the changes in gene expression and splicing and will provide us with a context to test for a direct role of CHD5 in these processes. In addition, this thesis will detail the results from ongoing projects using the zebrafish model system, including: development of models in zebrafish to study the tumor suppressive role of Chd5, phenotypes observed using a targeted chemical-genetic screen, and advancement in developing new tools in zebrafish to engineer specific genomic modifications that will greatly expand the power of this vertebrate model.
Книги з теми "Remodelled genes"
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Yang, Jin, Pei Han, Wei Li, and Ching-Pin Chang. Epigenetics and post-transcriptional regulation of cardiovascular development. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0032.
Повний текст джерелаАнотація:
Cardiac organogenesis requires the control of gene expression at distinct developmental windows in order to organize morphogenetic steps in the correct sequence for heart development. This is facilitated by concerted regulation at three levels: chromatin, transcription, and post-transcriptional modifications. Epigenetic regulation at the chromatin level changes the chromatin scaffold of DNA to regulate accessibility of the DNA sequence to transcription factors for genetic activation or repression. At the genome, long non-coding RNAs work with epigenetic factors to alter the chromatin scaffold or form DNA-RNA complexes at specific genomic loci to control the transcription of genetic information. After RNA transcription, the expression of genetic information can be further modified by microRNAs. Each layer of gene regulation requires the participation of many factors, with their combinatorial interactions providing variations of genetic expression at distinct pathophysiological phases of the heart. The major functions of chromatin remodellers and non-coding RNAs are discussed.
Частини книг з теми "Remodelled genes"
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Cui, Guofei, Qing Dong, Kexin Gai, and Shaohua Qi. "Chromatin Dynamics: Chromatin Remodeler, Epigenetic Modification and Diseases." In Epigenetics - Regulation and New Perspectives [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108385.
Повний текст джерелаАнотація:
The gene transcription patterns are regulated in response to extracellular stimuli and intracellular development programs. Recent studies have shown that chromatin dynamics which include nucleosome dynamics and histone modification play a crucial role in gene expression. Chromatin dynamic is regulated by chromatin modification enzymes including chromatin remodeling complex and histone posttranslational modifications. Multiple studies have shown that chromatin dynamics dysregulation and aberrant and histone modifications resulted in the occurrence of various diseases and cancers. Moreover, frequent mutations and chromosomal aberrations in the genes associated with subunits of the chromatin remodeling complexes have been detected in various cancer types. In this review, we highlight the current understanding of orchestration of nucleosome position, histone modification, and the importance of these properly regulated dynamics. We also discuss the consequences of aberrant chromatin dynamic which results in disease progression and provides insights for potential clinic applications.
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Furet, Francois. "The French Revolution or Pure Democracy." In Rewriting the French Revolution, 33–45. Oxford University PressOxford, 1991. http://dx.doi.org/10.1093/oso/9780198219767.003.0002.
Повний текст джерелаАнотація:
Abstract The repercussions of the French Revolution are universal because it proclaimed itself to be universal. Independent of the particular conditions of its birth and even of the country in which it broke out, it gave itself the mission not of adjusting institutions to the circumstances of national history or to the state of opinion, but rather of remaking the social contract from top to bottom, as though it were an artefact to be completely reworked, remodelled according to the principles of reasoning will. It was thus an event that was inextricably political and philosophical, and contemporary observers immediately saw it as a blend of these two aspects, hailing 1789 as the victory of Enlightenment philosophy in the realm which it had made its speciality — the reorganization of the polis. The unique character of the French Revolution in modem history derives from this combining of genres, by virtue of which 1789 was to be accompanied by a laicized religious annunciation where the promise of democracy was substituted for that of God.
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Pal, Neeraj, Dinesh Kumar Saini, and Sundip Kumar. "Breaking Yield Ceiling in Wheat: Progress and Future Prospects." In Wheat [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102919.
Повний текст джерелаАнотація:
Wheat is one of the most important staple crops that contribute considerably to global food and nutritional security. The future projections of the demand for wheat show significant enhancement owing to the population growth and probable changes in diets. Further, historical yield trends show a reduction in the relative rate of gain for grain yield over time. To maintain future food security, there is a strong need to find ways to further increase the yield potential of wheat. Grain yield is a quantitative trait that is highly influenced by the environment. It is determined by various interlinked yield component traits. Molecular breeding approaches have already proven useful in improving the grain yield of wheat and recent advances in high-throughput genotyping platforms now have remodelled molecular breeding to genomics-assisted breeding. Hence, here in this chapter, we have discussed various advancements in understanding the genetics of grain yield, its major components, and summarised the various powerful strategies, such as gene cloning, mining superior alleles, transgenic technologies, advanced genome editing techniques, genomic selection, genome-wide association studies-assisted genomic selection, haplotype-based breeding (HBB), which may be/being used for grain yield improvement in wheat and as the new breeding strategies they could also be utilised to break the yield ceiling in wheat.
Тези доповідей конференцій з теми "Remodelled genes"
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Dey, Nandini, Jennifer C. Aske, Ethan Thompson, Luis Rojas-Espaillat, David Starks, and Pradip De. "Abstract 1427: Co-alteration of the nucleosome remodeler, ARID1A with the PI3K-pathway genes: A signaling opportunity in ovarian cancers." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1427.
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