Literatura académica sobre el tema "Séquençage de l’ARN"
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Artículos de revistas sobre el tema "Séquençage de l’ARN"
Mathieu, Maxime, Amandine Girousse y Coralie Sengenès. "Et si l’origine des progéniteurs fibro-adipeux contribuait à leur hétérogénéité dans le muscle ?" médecine/sciences 39 (noviembre de 2023): 15–21. http://dx.doi.org/10.1051/medsci/2023129.
Texto completoMontel, Fabien. "Séquençage de l’ADN par nanopores". médecine/sciences 34, n.º 2 (febrero de 2018): 161–65. http://dx.doi.org/10.1051/medsci/20183402014.
Texto completoM., J. M. "Un réseau français de séquençage de l’ADN". Revue Francophone des Laboratoires 2016, n.º 486 (noviembre de 2016): 15. http://dx.doi.org/10.1016/s1773-035x(16)30311-2.
Texto completoDekeuwer, Catherine. "Séquençage de l’ADN à haut débit et relation de soin". Cahiers Droit, Sciences & Technologies, n.º 8 (13 de marzo de 2019): 41–52. http://dx.doi.org/10.4000/cdst.688.
Texto completoBailleul, Quentin, Andria Rakotomalala, Isabelle Ferry, Pierre Leblond, Samuel Meignan y Alessandro Furlan. "L’art de la guerre appliqué aux DIPG". médecine/sciences 37, n.º 2 (febrero de 2021): 159–66. http://dx.doi.org/10.1051/medsci/2020279.
Texto completoLamoril, J., N. Ameziane, J. C. Deybach, P. Bouizegarène y M. Bogard. "Les techniques de séquençage de l’ADN : une révolution en marche. Première partie". Immuno-analyse & Biologie Spécialisée 23, n.º 5 (octubre de 2008): 260–79. http://dx.doi.org/10.1016/j.immbio.2008.07.016.
Texto completoHenry, Jean-Pierre. "Génétique et origine d’Homo sapiens". médecine/sciences 35, n.º 1 (enero de 2019): 39–45. http://dx.doi.org/10.1051/medsci/2018311.
Texto completoOden, Élise. "La génomique équine : tour d’horizon des outils disponibles pour les applications actuelles et à venir". Le Nouveau Praticien Vétérinaire équine 17, n.º 59 (2023): 48–53. http://dx.doi.org/10.1051/npvequi/2024005.
Texto completoVasselon, V., F. Rimet, I. Domaizon, O. Monnier, Y. Reyjol y A. Bouchez. "Évaluer la pollution des milieux aquatiques avec l’ADN des diatomées : où en sommes-nous ?" Techniques Sciences Méthodes, n.º 5 (mayo de 2019): 53–70. http://dx.doi.org/10.1051/tsm/201905053.
Texto completoMattei, Jean-François. "Avis no 124 du CCNE sur l’évolution des tests génétiques liée au séquençage de l’ADN humain à très haut débit". Bulletin de l'Académie Nationale de Médecine 200, n.º 6 (junio de 2016): 1263–68. http://dx.doi.org/10.1016/s0001-4079(19)30646-6.
Texto completoTesis sobre el tema "Séquençage de l’ARN"
Polit, Lélia. "Régulation de l’expression génique par le facteur de transcription SPI1/PU.1 dans l’érythroleucémie : mécanismes de répression des gènes par sa liaison à l’ADN, conséquences de sa liaison à l’ARN". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL064.
Texto completoSPI1/PU.1 is a transcription factor belonging to the ETS family characterized by a highly conserved DNA binding domain (ETS domain) and a common core binding the 5’-GGAA/T-3’ DNA sequence. SPI1 is a key regulator of haematopoiesis, the regulation of SPI1 expression and function depends on lineage. Deregulation of Spi1 expression or activity contributes to hemopathies; SPI1 behaves as an oncogene or a tumor suppressor according to the hematopoietic lineage. SPI1 has been shown to be oncogenic in Waldenström’s macroglobulinemia, pediatric T cell acute lymphoblastic leukemia and erythroleukemia. Acute erythroid leukemia is a rare but high-risk leukaemia of poorly understood genetic basis. In the murine erythroid lineage, SPI1 abnormal unrestrained expression leads to acute leukemia, in part by inhibiting erythroid differentiation and apoptosis of erythroid progenitors.SPI1 is a transcription factor that also affects splicing processes. The ways SPI1 activates gene expression are now mostly established. As a pioneering transcription factor, SPI1 is able to bind closed chromatin and then to recruit many epigenetic and/or lineage specific co- or transcriptional factors. In contrast, Spi1 repressive functions on gene expression remain poorly understood. Whether it acts through its ability to bind DNA and/or RNA is not known. My PhD thesis is dedicated to the characterization of the mechanisms by which SPI1 represses gene expression. In particular, I studied how SPI1 represses gene expression in a model of murine erythroleukemia by investigating the role of SPI1 on epigenetic modifications. I also investigated the consequences of SPI1 binding to RNA. Using pre-leukemic cells issued from Spi1 transgenic mice, cells in which spi1 expression can be controlled (overexpressed or down-regulated), I performed an integrated analysis of several high throughput sequencing data sets to characterize epigenetic histone modifications, chromatin accessibility and gene expression. In order to compare histone modification signals from different conditions, we developed an R package, named ChIP-seq Inter-sample Normalization (CHIPIN). The algorithm of CHIPIN is based on the biological assumption that genes with constant expression across conditions have, on average, similar “true” ChIP-seq binding intensities. Using bioinformatic analysis combined with biological experiments, we demonstrate that SPI1 gene repression activity was based on the coordination of two mechanisms that involved and are controlled by histone deacetylase 1 (HDAC1) and polycomb repressive complex 2 (PRC2). Repressed genes include genes coding for apoptosis and erythroid differentiation. Finally, I studied the landscape of SPI1 binding on RNA using CLIP-seq data and showed that SPI1 binding on RNA was not related to gene expression regulation. Thus, the role of SPI1 when it binds RNA is not fully explain, even if we showed that SPI1 binds mainly in intronic regions on RNA. To sum up, my work highlighted new mechanisms for gene repression regulation by SPI1 in erythroleukemia in cooperation with two epigenetics factors: PRC2 and HDAC1. This work provides new insights in the role of the major hematopoietic regulator SPI1 for gene repression mechanisms. In addition, part of my work was dedicated to develop an R package called CHIPIN allowing for normalization of ChIP-seq signals from several conditions or samples. This method can be also used for ATAC-seq data. The R package is user friendly and can therefore be used by both bioinformaticians and biologists
Mailler, Élodie. "Structural rearrangements of the HIV-1 genomic RNA during maturation of the viral particle". Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ055.
Texto completoThe HIV-1 particle buds from the infected cell as an immature particle and has to undergo a maturation process to become infectious. Proteolytic processing of Pr55Gag triggers morphological rearrangements of the particle whereas the gRNA dimer becomes more stable. Genomic rearrangements remain poorly understood and are facilitated by the RNA chaperone activity of the NCp7 protein. Our goal was to determining the different steps leading to the formation of the mature dimeric gRNA. To this end, the structure of the first 550 nucleotides of the HIV-1 genome was assessed by chemical probing 1. in vitro with Pr55Gag, GagΔp6, NC-containing intermediates and NCp7 proteins and 2. in viro with the hSHAPE-Seq approach we developed. Wild type and mutant viruses mimicking the sequential processing of Pr55Gag were analysed, as well as immature PR- and mature particles treated with the AT-2 zinc ejector, in order to identify the Pr55Gag and NCp7 binding sites and their gRNA destabilising activity
Pradat, Yoann. "Analyses of genomic and transcriptomic profiles of metastatic tumors from precision medicine clinical trials". Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL010.
Texto completoIn the era of extensive data analysis, insights into cancer onset and progression have deepened through molecular analysis of numerous tumors globally. Next-generation sequencing, emerging in the 2000s, transformed cancer cell investigation by enabling exome, transcriptome, and now whole genome profiling. While high-throughput sequencing has not yet entered clinical pratice for all, it is commonly used in trials. The vast data pool thus generated fuels many research areas which contribute to precision oncology advancements. This thesis explores cancer patient cohort analysis and modern oncology tools. The first chapter covers cancer biology fundamentals, emphasizing molecular profiling's evolving role in treatment and research. The second chapter reviews computing tools and databases for sequencing data analysis. These chapters set the stage for the third chapter, focusing on the META-PRISM cohort, comprising 1,031 patients from precision medicine trials at Gustave Roussy. It highlights the molecular specificities of refractory and the promises of predictive modeling based on high-throughput sequencing data. The fourth chapter delves into known and emerging treatment resistance markers in the META-PRISM cohort and two recent clinical studies, revealing target alterations and alternative pathway activations as key resistance factors
Sengenès, Jennifer. "Développement de méthodes de séquençage de seconde génération pour l’analyse des profils de méthylation de l’ADN". Paris 6, 2012. http://www.theses.fr/2012PA066123.
Texto completoThe analysis of DNA methylation patterns has become of great interest as methylome alterations have been found in many diseases. MeDIP (Methylated DNA ImmunoPrecipitation) immunoprecipitates genome-wide methylated sequences many of which are located in the repetitive sequences. Such sequences are difficult to align unambiguously after sequencing (MeDIP-Seq) leading to a large number of sequences that are currently not used for further analysis. We present an innovative method called MeDIP-dep-Seq which depletes a significant part of several classes of these highly repetitive sequences (up to 300-fold decrease), while unique sequences of interest are not affected. After sequencing on a second generation sequencer (GAIIx, Illumina) the alignment rate substantially enhanced increasing thus the amount of usable sequences. We have further developed a pipeline for the analysi of MeDIP-Seq datasets. Potential candidate regions identified in this genome-wide assay can then be validated by the use of selector probes that specifically capture genomic regions of interest. We introduced a bisulfite treatment in the selection protocol and developed a novel multiplex assay. 98 gene loci were enriched in 6 samples and were then sequenced in parallel on a bench sequencer (GS Junior, Roche). The combination of these technologies will permit the establishment of methylome maps and the identification of novel epigenetic biomarkers for cancer and complex diseases diagnostics and prognosis
Gorgé, Olivier. "Diagénèse de l’ADN bactérien et analyses métagénomiques de pathologies bactériennes du passé". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS572/document.
Texto completoThe aim of this study was the identification of pathogenic bacterial DNA traces in ancient animal and human samples, and thus improve knowledge of past diseases that affect humankind over time. In parallel, we studied the DNA degradation phenomena in the soil on the buried corpses of mice after being contaminated by non-pathogenic bacteria. This study of taphonomic processes was spread over three years and has shown a rapid disappearance of simulant bacteria, replaced with the DNA of soil bacteria that colonize the body quickly after burial and degrade both the endogenous DNA (murine) that exogenous (bacteria). This quick degradation can explain the high difficulty to detect and identify bacterial pathogens in old samples, with very few exceptions. Despite the fact in our study we were not able to detect specific pathogens in the samples we have studied, we have shown the interest to analyze certain types of remnants to access preserved and informative genetic data. Dental calculus is a good indicator of the oral flora of the host and calcified cysts ensure good preservation of the endogenous DNA, less subject to contamination and digestion by bacteria from the environment. Cysts generally have an endogenous DNA content higher than all other tissues examined
Kaltenbach, Sophie. "Rôle des facteurs de la réparation de l’ADN dans la dynamique du génome au sein du système immunitaire". Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T038/document.
Texto completoThe immune system is particularly dependent on DNA damage response (DDR) pathways. The development of the adaptive immune system requires certain DDR mechanisms, in particular during the V(D)J recombination and during class switch recombination (CSR), furthermore, the hematopoietic system is very sensitive to spontaneous DNA lesions. Therefore, there are many immune deficiencies in human directly related to a DDR deficiency. The identification of the responsible gene is important for appropriate genetic counseling. Today, we have access to powerful genetic screening tools, in particular next generation sequencing (NGS) and the list of genes responsible for immune deficiency is growing rapidly. The first part of this work focuses on the development of a new screening tool for DDR defects, in particular in the case of immune deficiency, and evaluation of clinical interest. This test is based on the observation of a bias of the TCRα repertoire in circulating T lymphocytes when thymocytes lifespan is diminished and we know that DDR defect causes decreased thymocyte survival. We have developed two techniques, by molecular biology and by flow cytometry, to detect a potential bias of the TCRα repetoire and assess the suitability of this test in some immunodeficiencies linked to a DDR defect. A significant bias was detected in the case of ATM and NHEJ factor deficiency. Furthermore, we have established a cohort of patients suffering from common variable immunodeficiency (CVID) with a clinical presentation highly suggestive of DDR defect, in collaboration with the Clinical Immunology Service of Hôpital Saint-Louis (Paris). Functional test for DDR defect and genetic analysis (CGHarray, whole exome sequencing) were performed in these patients to identify new genes involved in CVID. Among the 18 patients analyzed until now, five cases of cellular sensitivity to genotoxic agents have been detected and a candidate gene was identified in 15 of them. These results are still preliminary and our team will pursue genetic and functional characterization of the identified mutations. Finally, we undertook genetic and functional exploration of two mutations identified in a young patient with combined immunodeficiency (CID) associated with a lymphoproliferative disease and autoimmunity, and in whom a cellular hypersensitivity to mitomycin C, a DNA crosslinking agent, was detected. The first mutation was identified in the ELKS gene, which codes for a factor involved in DNA repair. Functional complementation of this gene demonstrates the involvement of this mutation in the hypersensitivity of patient’s cells to MMC. We have developed a conditional knockout mouse model of this gene in hematopoietic cells that did not show any defect in development of the immune system. The second mutation was identified in BACH2 gene encoding a transcriptional repressor involved in the development of the immune system. Knockout mice for this gene have a similar phenotype to the immune deficiency described in this patient. Investigations on this mutation are ongoing in the patient and among family members that also carry the mutation
Kabalane, Hadi. "Caractérisation pangénomique et analyse comparative du programme de réplication de l'ADN dans 12 lignées cellulaires humaines". Thesis, Lyon, 2019. http://www.theses.fr/2019LYSEN063.
Texto completoThe spatiotemporal program of DNA replication is regulated during development and altered during cancer progression. We propose an original characterization of the plasticity of the DNA replication program based on the profiling of 12 normal or cancerous human cell lines by the Ok-seq method of purification and sequencing of Okazaki fragments which allows to determine the orientation of the progression of replication forks (RFD) at high resolution (10 kilo bases). Comparative analysis of the RFD profiles shows that the replicative changes allow the classification of the cell lines according to their tissue of origin, the cancerous or non-cancerous nature of the cell line type intervening only in second order. There is no hotspot for the accumulation of replicative changes, they are widely dispersed throughout the genome. Nevertheless, the G+C rich and active gene regions, replicated early in the S phase, have the most stable replication program, they present a high density of efficient replication initiation zones (IZ) conserved between cell lines. In contrast, the late replicated, low gene density and low G+C content regions have few efficient IZs, often specific to a tissue or lineage. This leads us to quantify the degree of dissociation between IZ and activation of transcription. This work provides an original overview of replication program changes during normal or pathological differentiation, including a cell line specific control of IZ in late-replication gene deserts
Riaz, Tiayyba. "Approches bioinformatiques pour l'assessment de la biodiversité". Phd thesis, Université de Grenoble, 2011. http://tel.archives-ouvertes.fr/tel-00716330.
Texto completoBenoit, Bouvrette Louis Philip. "Caractérisation systématique des motifs de régulation en cis à l’échelle transcriptomique et liens avec la localisation des ARN". Thesis, 2020. http://hdl.handle.net/1866/24578.
Texto completoThe subcellular localization of RNA allows a rapid and spatially restricted deployment of protein and noncoding RNA activities. The trafficking of RNA is directed by sequence elements (primary subsequences, secondary structures), also called regulatory motifs, present in cis within the RNA molecule. These motifs are recognized by RNA-binding proteins that mediate the transport of transcripts to specific sites in the cell. Recent studies in the Drosophila embryo indicate that the majority of RNAs display an asymmetric subcellular localization, suggesting the existence of a complex "localization code". However, this may represent an exceptional example and the question remained, until now, whether a comparable prevalence of RNA localization is observable in standard cells grown in culture. In addition, readily available information about the topological distribution of pattern instances across full transcriptomes has been hitherto lacking. In order to have a broad overview of the extent and properties involved in RNA localization, we subjected Drosophila (D17) and human (HepG2) cells to biochemical fractionation to isolate the nuclear, cytosolic, membrane and insoluble fractions. We then performed deep sequencing on the extracted RNA and analyzed through mass spectrometry the proteins extracted from these fractions. We named this method CeFra-Seq. Through bioinformatics analyses, I then profiled the enrichment of various RNA biotypes (e.g. messenger RNA, long noncoding RNA, circular RNA) and proteins within the subcellular fractions. This revealed the high prevalence of asymmetric distribution of both coding and noncoding RNA species. An analysis of orthologous genes between fly and human has also shown strong similarities, suggesting that the localization process is evolutionarily conserved. In addition, I have observed distinct attributes (e.g. transcript size) among fraction-specific messenger RNA populations. Finally, I observed specific correlations and anti-correlations between defined groups of messenger RNAs and the proteins they encode. To study motifs topology and their conservation, I created oRNAment, a database of putative RNA-binding protein binding sites instances in coding and noncoding RNAs. Using data from protein binding motifs assessed by RNAcompete and by RNA Bind-n-Seq experiments, I have developed an algorithm allowing their rapid identification in a complete transcriptome. I was able to catalog the instances of 453 motifs from 223 RNA-binding proteins for 525,718 transcripts in five species. The results obtained were validated by comparing them with public data from eCLIP. I then used oRNAment to further analyze the topological aspects of these motifs’ instances and their relative evolutionary conservation. This showed that most motifs are distributed in a similar fashion between species. In addition, I have detected commonalities between the subgroups of proteins linking preferentially distinct biotypes or specific RNA regions. The presence or absence of such pattern between species is likely a reflection of the importance of their functions. Moreover, a more precise analysis of the position of a motif among comparable transcriptomic regions in vertebrates suggests a syntenic conservation, to varying degrees, in all RNA biotypes. The regional topology of certain motifs as repeated instances also appears to be evolutionarily conserved and may be important in order to allow adequate binding of the protein. Finally, the results compiled with oRNAment allowed to postulate on a potential new role for the long noncoding RNA HELLPAR as an RNA-binding protein sponge. The systematic characterization of RNA localization and cis regulatory motifs presented in this thesis demonstrates how the integration of information at a transcriptomic scale enables the assessment of the prevalence of asymmetry, the distinct characteristics and the evolutionary conservation of RNA clusters.
Aid, Malika. "Une nouvelle approche computationnelle pour la découverte des sites de fixation de facteurs de transcription à l’ADN, adaptée aux données de ChIP-chip et de ChIP-séquençage". Thèse, 2012. http://hdl.handle.net/1866/12729.
Texto completoTranscription factors (TF) play important roles in various biological processes such as differentiation, cell cycle progression and tumorigenesis. They regulate gene expression by binding to specific DNA sequences (TFBS). Identifying these cis-regulatory elements is a crucial step to understand gene regulatory networks. Technological developments have enhanced DNA sequencing at genomic scale. On the basis of the resulting sequences, computational biologists now attempt to localize the most important functional regions, starting with genes, but also importantly the whole genome characterization of transcription factor binding sites and allow the development of several computational DNA motif discovery tools. Although these various tools are widely used and have been successful at discovering novel motifs, they are not adapted to ChIP-chip and ChIP-sequencing data. The main drawback of these approaches is that most of the predicted motifs represent artifacts due to an inefficient assessment of their enrichment. This thesis is about transcription factor proteins and statistical analysis of their binding sites in ChIP-chip and ChIP-sequencing data. The first objective was to develop a new do novo DNA motif discovery tool adapted to ChIP-chip and ChIP-sequencing data. SAMD-ChIP combines enumerative and stochastic strategies to predict enriched motifs in the vicinity of the ChIP peak summits. Our approach is an automated pipeline that includes motif discovery, motif clustering, motif optimization and finally motif identification using transcription factor (TF) databases. SAMD-ChIP outperforms state-of-the-art motif discovery tools in term of the number of predicted motifs and the prediction of rare and degenerate motifs. In particular, SAMD-ChIP efficiently identifies gapped motifs such as inverted or direct repeats bound by nuclear receptors and composite motifs resulting from the association of different single TF binding sites. The underlying assumption of the second objective is that in regulatory regions, binding sites of interacting transcription factors co-occur more often than expected by chance in the vicinity of the ChIP-peak summits. We proposed an approach to predict transcription factor binding sites co-localization based on the prediction of single motifs by do novo motif discovery tools or by using TFBS models from TF data bases.
Capítulos de libros sobre el tema "Séquençage de l’ARN"
PIERELLA KARLUSICH, Juan José, Charlotte NEF, Chris BOWLER y Richard G. DORRELL. "Modèles biogéographiques et génomes des photoautotrophes aquatiques". En Planète bleue, photosynthèse rouge et verte, 45–82. ISTE Group, 2023. http://dx.doi.org/10.51926/iste.9082.ch3.
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