Dissertationen zum Thema „Protéine liant les ARNs“
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Majo, Vanessa. „Phosphorylation de la protéine liant les ARNs HuR/ELAVL1 par la tyrosine kinase Abelson : implications sur la fonction de HuR/ELAVL1 dans le carcinome hépatocellulaire“. Thesis, Bordeaux 2, 2010. http://www.theses.fr/2010BOR21803/document.
Der volle Inhalt der QuelleThe RNA binding proteins (RBPs) HuR/ELAVL1 is involved in the stabilization of mRNAs whose 3'UTR contains motifs enriched in A and U (« AU-rich element », ARE). These mRNAs encode mainly proteins whose deregulation promotes the emergence of cancer (oncogenes, cyclins, growth factors...). In particular, HuR is overexpressed in hepatocellular carcinoma (HCC) and in human HCC cell lines in culture and is abnormally found in the cytoplasm of liver tumor cells contributing to their proliferation. Furthermore, the Posttranslational modifications of RNA binding proteins (RBPs) modulate their subcellular localization and their ability to bind and control the fate of their targeted mRNAs. Some sérine/thréonine identified kinase are capable of modulating the function of the AUBP (« AU-binding protein ») HuR. By in vitro studies, we identified Y200 as a target (probably the only one) of the « non-receptor tyrosine kinase » Abelson on HuR. This kinase is also overexpressed in hepatocellular carcinoma (HCC) and in human HCC cell lines in culture (as cells HuH7). The inhibition of Abl by Nilotinib (one inhibitor) influences the acido-basic profile of the protein HuR, on Gel 2D, in cells HuH7, suggesting a role of Abl in the functions of HuR on its targets ARNm
Rekad, Zeinab. „Rôle de la protéine de liaison aux ARNs SAM68 dans l'adhésion des cellules endothéliales et la genèse de leur matrice extracellulaire“. Electronic Thesis or Diss., Université Côte d'Azur, 2023. http://www.theses.fr/2023COAZ6006.
Der volle Inhalt der QuelleAngiogenesis is the process underlying the formation of new blood vessels from pre-existing ones. This process relies on the modification of the adhesive properties of vascular endothelial cells as well as the production and assembly of their specialized extracellular matrix (ECM) known as the basement membrane. Endothelial cell adhesion is mediated by interactions between extracellular matrix (ECM) components and transmembrane receptors (integrins) that, upon engagement, drive the formation of dynamic multimolecular adhesion complexes that regulate cytoskeletal organization and force transmission (mechanotransduction) for cell migration and function. Recent studies suggest that local protein production at adhesion sites contributes to their consolidation and maturation.Proteomics screens performed on adhesion sites have identified the presence of RNA-binding proteins (RBP) with gene expression regulatory functions. SAM68 (Src associated in mitosis, of 68 kDa), a member of the STAR (signal transduction and activation of RNA metabolism) family of RBPs, is one such protein known to regulate both RNA biogenesis and signal transduction by playing a scaffolding role following receptor activation at the cell surface. Indeed, SAM68 has been shown to associate with Src kinase following receptor activation and to participate in alternative splicing of genes encoding ECM and ECM-associated proteins, such tenascin-C and the cell surface glycoprotein CD44 involved in adhesion/migration. In the context of angiogenesis and endothelial cell adhesion, we hypothesized that the RBP SAM68 may constitute a molecular relay during integrin-mediated mechanotransduction at adhesion sites by participating in the formation of focal adhesions and downstream transcriptional/post-transcriptional responses that regulates the angiogenic phenotype.Using 2- and 3-D cultures of primary endothelial cells, we showed that the RBP SAM68 participates in the establishment of focal adhesions through its contribution to the localized supply of mRNAs (including the β-actin transcript) required for adhesion site maturation. Further, we demonstrated that SAM68 regulates the expression of genes encoding basement membrane proteins, in particular via regulation of the promoter of the FN1 gene, thus conditioning the sub-endothelial matrix and angiogenic phenotype of cells. Indeed, in a 3-D context, SAM68-depletion was found to hamper endothelial cell sprouting activity and capillary-like tube formation.This work paves the way to explore the role of other RNA-binding proteins as regulators of adhesion signaling and assessment of their function in physiological and pathological angiogenesis processes
Lefrère, Valérie. „La protéine se liant au poly(A) des ARNm (PABP) de Drosophile : structure du gène et expression au cours du développement“. Toulouse 3, 1991. http://www.theses.fr/1991TOU30263.
Der volle Inhalt der QuelleSanterre, Maryline. „Étude de l'action sur l'épissage de protéines nucléaires se liant à la région de l'ARN du virus VIH-1 contenant le site d'épissage A7 et role de ces protéines sur d'autres sites accepteurs d'épissage de VIH-1“. Thesis, Nancy 1, 2010. http://www.theses.fr/2010NAN10115/document.
Der volle Inhalt der QuelleHIV-1 pre-mRNA splicing depends upon 4 donor and 8 acceptor sites, which are used in combination to produce more than 40 different mRNAs. To further characterize nuclear factors involved in these processes, we purified RNP complexes formed by incubation of SLS2-A7 transcripts in HeLa cell nuclear extracts by affinity chromatography to identify new associated proteins. We showed that, in addition to the well known hnRNP A1 inhibitor of site A7, nucleolin, hnRNP H and hnRNP K interact directly with SLS2-A7 RNA. We demonstrated that hnRNP K has multiple binding sites in the vicinity of site A7 and that binds cooperatively to hnRNP A1 to the A7 RNA region and limits the A7 utilization in vitro. As hnRNP A1 is a negative regulator of several HIV-1 splicing sites (A1, A2, A3), we tested whether hnRNP K may also reinforce hnRNP A1 inhibition at these sites. Surprisingly, hnRNP K activated in vitro splicing of the D1-A1, D1-A2 and D1-A3 introns. Interestingly, hnRNP K was found to reinforce strongly the ASF/SF2 activity at site A2, which indicates that depending on the splicing site hnRNP K can be a splicing activator or inhibitor. To test how hnRNP K influences the relative utilization of HIV-1 splicing sites in cellulo, we used plasmid p PSP containing all the HIV-1 splicing sites and tested the effect of over-expression in HeLa cells on alternative splicing of the PSP RNA. Doubling the amount of hnRNP K in HeLa cells led to a drastic change of the PSP RNA alternative splicing, which confirms the strong influence of hnRNP K on alternative splicing. Moreover, increase of cellular concentration of hnRNP K strongly decrease the viral Nef protein production. hnRNP K protein affects A7 splicing regulation but also regulates the majority of regulated splicing sites of HIV. By extension of the study of hnRNP K effect to other HIV-1 splicing sites, we discovered that hnRNP K is a general regulator of HIV-1 splicing
Lussier, Marc. „Identification et caractérisation de nouveaux partenaires d'intéraction liant le domaine de répétitions similaires à l'ankyrine des TRPCs“. Thèse, Université de Sherbrooke, 2008. http://savoirs.usherbrooke.ca/handle/11143/4261.
Der volle Inhalt der QuelleBoy, Sébastien. „Etude de facteurs transcriptionnels et post-transcriptionnels impliqués dans la spécification des cellules rétiniennes chez Xenopus laevis“. Paris 11, 2004. http://www.theses.fr/2004PA112246.
Der volle Inhalt der QuelleRetina is an interesting model to study vertebrate neurogenesis because it is simply organised in three layers and contains only few cell types. Numerous transcription factors are involved in retinogenesis. Among them, bHLH factors play important roles. BHLH activators promote neural differentiation, neurons formation and specification. BHLH repressors tend to limit neuroblasts differentiation and promote gliogenesis. During my thesis, I aimed to isolate post-transcriptionnal factors involved in retinogenesis since genetic regulators so far known to be involved in this process are all transcription factors. I have focused my studies on one of them, a new putative RNA binding protein called XSEB4R. Using overexpression and loss of function experiments, I have shown that Xseb4R is involved in retinogenesis and has a function related to bHLH activators function. I have also shown that some of these factors are upstream Xseb4R. During my thesis, I have also been interested in another novel gene, Xhes2 (Hairy Enhancer of Split). I highlighted that, in addition to promote gliogenesis, as other genes of this family, it also controls neuronal specificity. I have also participated to the determination of the function of the Hedgehog cascade in the development of retinal pigmented epithelium, which is adjacent to neural retina
Thériault, Jimmy. „Clonage et caractérisation de hGMEB1, une nouvelle protéine liant l'élément modulateur des glucocorticoïdes“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0019/MQ49050.pdf.
Der volle Inhalt der QuelleMazzocco, Claire. „Caractérisation pharmacologique, biochimique et moléculaire d'une protéine liant la proctoline : récepteur ou enzyme ?“ Bordeaux 1, 2001. http://www.theses.fr/2001BOR12436.
Der volle Inhalt der QuelleMorigny, Pauline. „Etude des mécanismes liant l'inhibition de la lipase hormono-sensible et l'amélioration de la sensibilité à l'insuline“. Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30267.
Der volle Inhalt der QuelleInsulin resistance is a feature frequently associated to obesity and an early defect in the development of type 2 diabetes. Improvement of fat cell insulin signaling may favor recovery of whole body systemic insulin sensitivity in pre-diabetic and diabetic states. In this context, inhibition of hormone-sensitive lipase (HSL) in adipocytes (an enzyme responsible for fatty acid release by adipose tissue) was demonstrated to be protective against insulin resistance. However, the mechanisms remained unclear. Consequently, my PhD work aimed at understanding the mechanisms linking HSL inhibition and improvement of insulin sensitivity. In human adipocytes, HSL gene silencing increased glucose transport, de novo lipogenesis and insulin signaling. Among de novo lipogenesis enzymes, ELOVL6 was preferentially induced in vitro and in vivo during HSL partial deficiency, resulting in enrichment of phospholipids and triglycerides in oleic acid. ELOVL6 gene silencing in human adipocytes provided the direct demonstration of the role of the enzyme in the beneficial effect of HSL inhibition. Fat cell insulin signaling was also impaired in adipose tissue of Elovl6 null mice. In clinical studies, ELOVL6 expression was blunted in insulin resistant states and restored after bariatric surgery. ELOVL6-mediated oleic acid enrichment of phospholipids was responsible for the positive effect of HSL inhibition on insulin signaling. FRAP studies revealed an increase in plasma membrane fluidity and insulin signaling in adipocytes overexpressing ELOVL6. In the liver, ELOVL6 is a target of ChREBP. Adipose ChREBP, notably the constitutively active isoform ChREBPß, recently emerged as a major determinant of systemic insulin action on glucose metabolism. In humans, we observed in several in vitro models and in vivo studies a strong positive association between adipose ChREBPß and ELOVL6. Dual HSL-ChREBP inhibition blunted adipose ELOVL6 expression in vivo and in vitro and mirrored ELOVL6 gene silencing on fatty acid profile and insulin signaling. Importantly, we found that physical interaction between HSL and ChREBP impairs ChREBP translocation into the nucleus and its transcriptional activity. A naturally short form of HSL devoid of catalytic activity retained the capacity to bind ChREBP. We also demonstrated that ChREBP-HSL interaction was specific of the lipase and restricted to adipocyte. To conclude, our work identifies a novel pathway critical for optimal insulin signaling in fat cells which links the neutral lipase HSL to the glucose-responsive transcription factor ChREBP and its target gene, the fatty acid elongase, ELOVL6. ELOVL6-mediated oleate enrichment in phospholipids increases membrane fluidity and improves insulin signaling. Inhibition of HSL/ChREBP interaction in adipose tissue may be beneficial in the treatment of obesity-associated insulin resistance
Bruckert, Hélène. „Caractérisation d'Hrp48, une protéine de liaison aux ARNs, lors de la morphogenèse axonale chez la drosophile“. Nice, 2012. http://www.theses.fr/2012NICE4063.
Der volle Inhalt der QuelleRecent studies have shown that post-transcriptional regulatory mechanisms play essential roles in axon growth and guidance, processes involved in the establishment of neuronal circuits during development. To study these mechanisms in vivo, my project aimed at characterizing the role of the RNA-binding protein Hrp48, which belongs to the conserved hnRNP A/B family. I showed that inactivating hrp48 function leads to strong and specific axon migration defects, including axon misguidance and overextension. Notably, I have observed that the frequency of hrp48 mutant phenotypes is much higher in females than in males. Moreover, I showed that the female-specific Sex-lethal protein ectopically accumulates in the nucleus of mutant cells. This abnormal nuclear accumulation could explain the sex-specific defects observed in axonal migration. In parallel, I could show that inactivation of sema-1α, an Hrp48 putative mRNA target, causes defects similar to those observed in hrp48 mutants, and that hrp48 and sema-1 α genetically interact. Moreover, the overall levels of sema-1 α transcripts are much lower in females than in males. These results suggest that sema-1 α misregulation may induce the sex-specific defects in axonal growth observe upon hrp48 downregulation. Tis work has allowed us to propose a preliminary in vivo model for a post-transcriptional regulatory mechanism controlled by a member of the hnRNP A/B family. Furthermore, it has revealed cryptic differences between females and males in the context of recent studies revealing sex-specific differences in the control of gene expression
Guitard, Estelle. „Etude du rôle de deux protéines bifonctionnelles apparentées aux protéines de liaison aux ARNs, Sam68 et G3BP, dans la prolifération cellulaire“. Paris 11, 2000. http://www.theses.fr/2000PA11T014.
Der volle Inhalt der QuelleBorsu, Laetitia. „Découverte du gène AROM, "Antisense RNA Overlapping MCH gene" : caractérisation d'une nouvelle famille de protéines liant les acides nucléiques“. Nice, 2000. http://www.theses.fr/2000NICE5477.
Der volle Inhalt der QuelleSpielewoy, Nathalie. „Etude d'AtCCME, une protéine mitochondriale liant l'hème au cours de la maturation des cytochromes de type c“. Université Louis Pasteur (Strasbourg) (1971-2008), 2001. http://www.theses.fr/2001STR13145.
Der volle Inhalt der QuelleForne, Thierry. „Les modifications post-transcriptionnelles du snRNA U6 chez les mammifères : implications dans l'épissage des ARNs pré-messagers“. Montpellier 2, 1995. http://www.theses.fr/1995MON20076.
Der volle Inhalt der QuelleRoussel-Gervais, Audrey. „La protéine liant l'ADN méthylé ZBTB4 localise aux péri-centromères et contrôle la réponse au point de contrôle mitotique“. Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC137.
Der volle Inhalt der QuelleZBTB4 is a mammalian transcription factor with Zinc fingers and a BTB/POZ domains, which can bind methylated CpGs, as well as certain unmethylated consensus sequences. ZBTB4 is frequently downregulated in human cancers, for reasons that are unclear. To address the potential role of ZBTB4 we depleted it from human cells in culture, this led to heightened chromosome missegregation, as evidenced by increases in lagging chromosomes, micronuclei, and binucleation. We could detect a defect in the mitotic checkpoint, which was weakened in cells lacking ZBTB4, maybe as a direct consequence of decreased checkpoint protein abundance. To validate our findings in a more physiological setting, we generated mice. Primary Zbtb4⁻/⁻cells show the satine signs of genome instability seen in human cells in culture. The Zbtb4⁻/⁻ animals are viable and fertile, but smaller than their littermates and with reduced organ size. In addition, we report that mice lacking ZBTB4 are more susceptible to DMBA/TPA-induced skin carcinogenesis. Our results show that the epigenetic regulator ZBTB4 is essential for genome stability in mammals. Its loss in cancer cells may be under positive selection because it promotes faster genome evolution in the tumour cells
Poisot, Emilie. „Recrutement des complexes des groupes Polycomb et trithorax sur la chromatine : Dissection fonctionnelle des complexes liant les séquences d(GA)n des éléments de mémoire épigénétique“. Versailles-St Quentin en Yvelines, 2010. http://www.theses.fr/2010VERS0022.
Der volle Inhalt der QuelleAt least three important mechanisms are known to maintain gene expression patterns: the chromatine state, the epigenetic modifications due to the Polycomb ( PcG) and Trithorax ( TrxG ) groups proteins, and non coding RNAs (ncRNAs). The PcG and trxG genes maintain cell identity through epigenetic modifications of chromatin, thereby maintaining a predefined transcriptional state that establishes "cell memory". Three proteins, i. E. Batman (BAN), Trithorax-like (GAF) and Pipsqueak (PSQ) are components of a DNA-binding cell memory complex. The first goal of my thesis was to refine the description of complexes containing BAN, GAF and PSQ bound to their targets. I showed the existence of several complexes, suggesting a combinatory composition of these complexes depending on the target. Using dsRNA-driven extinction of each of the three proteins, I determined the hierarchy of their recruitment. The extension of this approach to other PcG and trxG proteins lead us to propose a new model for the recruitment of several of the memory complexes. I also studied the link between heterochromatin formation and ncRNAs. By using mutants affecting pathways of ncRNAs production, I showed that they participate in the localization of the heterochromatin protein HP1 on polytene chromosomes and thus in the formation of heterochromatin. All these studies allowed us to characterize the complexity of relations between BAN, GAF and PSQ and to define their respective contribution in the differential recruitment of PcG or TrxG complexes, but also to contribute to establishing the link between the ncRNAs and heterochromatin
Floriot, Océane. „Virus de l’Hépatite B et transcription cellulaire : impact de la protéine HBx et de ses interactions avec les ARNs non-codants“. Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1319/document.
Der volle Inhalt der QuelleHepatitis B virus (HBV) remains a major health problem worldwide despite the availability of the vaccine. No cure is available for the 240 million peoples chronically infected with HBV that are at risk to develop liver cirrhosis and hepatocellular carcinoma (HCC). Viral suppression, achieved by long term treatment with nucleotides analogues (NUCs), impacts on liver fibrosis and prevents liver decompensation but HCC risk is not reduced in the first 5 years of treatment. HBV is a small hepatotropic virus with a partially double strand DNA (rcDNA) genome. After hepatocyte infection the rcDNA is converted into the cccDNA episome that is then organized into a viral minichromosome that is the template for all viral transcripts and initiates replication. The hepatitis B x protein (HBx) is recruited on the cccDNA and is required to launch and maintain cccDNA transcription. HBx has also been shown to directly target cellular genes and this has been related to HCC development.We used a ChIP-Seq approach to determine the full repertoire of HBx genomic targets in HBV replicating cells. HBx targets include both protein coding genes and ncRNA (75 miRNAs and 34 lncRNAs). We showed that HBx represses a subset of miRNAs that would negatively regulate viral replication (i.e. miR-24) and miRNAs involved in HCC development (i.e. miR-21). Among the HBx targeted lncRNAs we focused DLEU2, which is strongly upregulated in HBV infection and HCC. We further showed that DLEU2 binds both HBx the Ezh2 histone methyltransferase, the catalytic subunit of the repressive PRC2 complex. The interaction with DLEU2 and HBx re-wires Ezh2/PRC2 functions leading to the constitutive activation of a subset of Ezh2 target genes that are normally kept in a repressed state. We also showed that HBx interaction with DLEU2 occurs on the cccDNA minichromosome where it boosts HBV transcription/replication. Finally, we characterized by ATAC-Seq HBV imposed changes of chromatin accessibility in primary human hepatocytes
Lefort, Anne. „Clonage, séquençage et purification d'une protéine thyroïdienne liant le calcium et phosphorylée par un processus dépendant de l'AMP cyclique: LA CALCYPHOSINE“. Doctoral thesis, Universite Libre de Bruxelles, 1991. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213024.
Der volle Inhalt der QuelleAliprandi, Pascale. „Etude fonctionnelle et structurale, par RMN, de la région C-terminale de la protéine ribosomique S1 d'Escherichia coli : caractérisation d'un mécanisme unique de reconnaissance des ARNs“. Paris 11, 2007. http://www.theses.fr/2007PA112312.
Der volle Inhalt der QuelleSI protein is the largest ribosomal protein of Escherichia coli. This modular protein is. Composed of six identical motifs. SI plays a key role in the translation initiation of prokaryote messengers when the Shine-Dalgamo sequence is degenerated or lacks. SI is used by several phages. This protein is able to accelerate the endoribonuclease RegB activity which function is to inactivate sorne of the phage messengers by cleaving them at the rniddle of their SD sequences. One SI region (F345) presents SI functions of translation and RegB activation, it corresponds to the same molecular mechanism but its role remains unknown. Our aim is to study, by NMR, the organisation of SI region and analyse the interactions with several RNA to suggest a molecular mechanism. 1 characterized, by NMR, interactions surfaces between domains 3, 4 and 5 in the F345 fragment, which allows us to suggest an organisation model of this region. Data found in the bibliography associated to the results of SI interaction studies with different RNA show that SI is able to bind any RNA and to induce a deformation that promotes the interaction with a third partner (Ribosome in the case of translation or RegB ribonuclease)
Frei, Dit Frey Nicolas. „Mécanismes moléculaires de tolérance au stress : étude fonctionnelle chez arabidopsis de Tudor-SN, une protéine conservée dans l’évolution impliquée dans le métabolisme des ARNs“. Paris 11, 2007. http://www.theses.fr/2007PA112340.
Der volle Inhalt der QuelleTo adapt to their environmental conditions, plants are continuously modulating their growth and differentiation. At the root system level, root apices are ideal to dissect these mechanisms because they host most of cell expansion and cell division activities. In a strategy to identify abundant mRNAs in stress-adapted root tips, a transcript encoding an evolutionary conserved protein, Tudor- SN (TSN), was isolated. TSN is composed of four calcium-dependant Staphylococcus Nuclease domains, and by a protein-protein interaction domain, the TUDOR domain. In animals, TSN was copurified with the RNA Induced Silencing Complex (RISC) and more recently proposed to degrade double stranded RNAs able to act as miRNAs precusors. Nevertheless, no TSN mutant phenotype has been described yet to test these hypotheses. IN this PhD work, we detected TSN protein in all organs of Arabidopsis plants, accumulating preferentially in elongating roots cells. Using immunolocalization and GFP fusions, we localized TSN in the cytosol as a granular signal. To determine TSN functions, a tsn null mutant was generated by crossing T-DNA insertion lines mutated in either TSN1 or TSN2. In vitro, the TSN-1 TSN2-1 double mutant has a root growth-retardation phenotype associated with a defect in cell elongation and a hypersensitivity to salt stress. Stress-sensitivity was also present in soil-grown mature plants. These observations were validated by complementation with the TSN1 or TSN2 genomic loci. Moreover, no morphological nor molecular phenotypes related to RISC dysfunction were observed in tsn1-1 tsn 2-1. Finally, a transcriptomic approach revealed an under-representation of mRNAs encoding almost exclusively for secreted proteins. We have begun studying the stability and the regulation of these transcripts which represent new tools to study the role TSN in RNA metabolism in eukaryotes
Séry, Quentin. „Résistance au témozolomide dans le glioblastome multiforme : rôle de l'induction du HBEGF“. Nantes, 2014. http://archive.bu.univ-nantes.fr/pollux/show.action?id=362effa8-bfad-466c-a23f-cca177c08184.
Der volle Inhalt der QuelleGlioblastoma multiforme (GBM) is a cerebral tumor highly refractory to treatment. Over the past years the akylating agent temozolomide (TMZ) associated with radiotherapy has improved the survival of patients but overall survival is still inferior to one year. During this thesis, we first examine the role of pro-apoptotic proteins Bax and Bak in TMZ-induced apoptosis and highlighted the major role of Mcl-1/Bak axis in TMZ mediated apoptosis. The tyrosine kinase receptor EGFR is implicated in primary GBMs oncogenesis (35-45% of amplification) and in resistance to treatment. Then we analyzed expression of EGFR ligands and founded an up-regulation of HBEGF in response to TMZ in two cell lines without expression of the repair enzyme MGMT the main resistance factor to TMZ. Counter-intuitively HBEGF is not involved in resistance but in TMZ-induced Mcl-1 degradation. This role is independent of EGFR activity. Implication of HBEGF in Mcl-1 degradation has no effect on caspases activity after TMZ treatment. Among the few known intracellular partners of HBEGF the chaperone protein BAG-1 is implicated in Mcl-1 expression maintenance. Indeed BAG-1 regulates Mcl-1 through its deubiquitinase USP9X. TMZ enable HBEGF/BAG-1 interactions and disable USP9X/Mcl-1 interactions. Our results then identify Bak as the main apoptosis inducer in response to TMZ, propose a new mechanism for the induced degradation of Mcl-1 and highlight a new role of HBEGF independently of its receptor EGFR. Moreover they identify BAG-1 as a favored partner of HBEGF and implicate it in Mcl-1 regulation via its deubiquitinase USP9X
Renou, Laurent. „Etude des relations entre le facteur de transcription HOX11L2/TLX3 et les micro-ARNs dans le développement des leucémies aiguës lymphoblastiques T humaines“. Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC311.
Der volle Inhalt der QuelleT cell acute lymphoblastic leukemia (T-ALL) result from the accumulation of genetic lesions leading to aberra proliferation and developmental arrest of T-cell progenitors. Deregulation of expression of microRNAs (miRs) has be( linked to the initiation and progression of human malignancies. The results of a miRnome analysis on a panel of T-AL allowed us to identify a cluster of miRs (125b/99a/100) significantly overexpressed in a group of leukemia characteriz( by inappropriate expression of transcription factor TLX3. We challenged on this to study the functional relationshi] between TLX3, the miRs and their contributions in the development of T-ALL. By the experience of loss and gain function , we highlight: 1) a correlation between TLX3 and miR-125b expression; (2) a similar role of TLX3 and mil 125b in the differentiation blockage of notmal T-cells progenitors that phenocopies the differentiation arrest observed TLX3+ T-ALL patients ; (3) a T-cell growth promotion by both TLX3 and miR-125b. Using ChIP-seq approach, also found TLX3 binding sites in the locus coding a long non-coding RNA LINC00478 that probably functions as pi miR for miR-99a/Let-7c/125b-2 cluster. Transcriptional activation of miR-125b contribute to the differentiation arrest I the downregulation of putative targets: ETS1 and CBFf3 which play an important role in the regulation of TC rearrangements. Our results reveal for the first time new functional link between the TLX3 oncogene, miRl25b and ' ALL development
Billard, Lise-Marie. „Expression des gènes codant les protéines liant l'ADN méthylé (MBD) dans les cancers du sein : implication des MBD dans la répression transcriptionnelle de gènes suppresseurs de tumeurs BRCA1 et CDX1“. Lyon 1, 2003. http://www.theses.fr/2003LYO1T083.
Der volle Inhalt der QuelleNoël, Jean-François. „Identification de rétropseudogènes dérivés des ARNs hY et étude de leur fonction dans l'épissage alternatif chez l'humain et recherche d'un homologue de la protéine RoBP1 chez la levure Saccharomyces cerevisiae“. Mémoire, Université de Sherbrooke, 2006. http://savoirs.usherbrooke.ca/handle/11143/3825.
Der volle Inhalt der QuellePoulet, Anaïs. „Mise en évidence de nouvelles propriétés de TRF1 et de TRF2 impliquées dans la stabilité de l'ADN télomérique humain“. Lyon, Ecole normale supérieure, 2010. http://www.theses.fr/2010ENSL0566.
Der volle Inhalt der QuelleTelomeres are nucleoproteic structures that cap the end of eukaryotic chromosomes. TRF2 is a key protein in the dynamic of telomere. Telomeres can fold into t-loops that were proposed to result from the invasion of the 3' overhang of telomeres into duplex DNA. A model for the formation of the t-loop implicates TRF2 : it could facilitate the invasion of the telomeric single strand into the upstream double strand DNA after the telomere folding. Indeed a previous study shows that TRF2 stimulates the telomeric invasion by modifying DNA topology. We reveal here thet TRF2, with its N-terminal basic domain, stabilizes and protects telomeric Holliday junction, a structure that could be formed at the foot of the t-loop. This result could explain the protective role of TRF2 at telomeres. We also demonstrate that TRF1 owns the same intrinsic properties than TRF2, but these properties are modulated by the N-terminal acidic domain of TRF1. The last part of this thesis reports the fact that there is a balance between quantities of TRF2-Apollo and topoisomerase IIα during the replication of telomeric sequences to resolve topological constraints. The results presented here give fresh insight in new TRF2 functions which are not only implicated in the t-loop formation, but also in the resolution of topological problems at telomeres
Guéguéniat, Julia. „Étude fonctionnelle des sous-domaines de Pcf11 : rôle du 2nd NTD dans la terminaison de transcription des snoRNAs et des motifs liant le zinc dans les activités de maturation de l’extrémité 3’ des ARN messagers“. Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0236/document.
Der volle Inhalt der QuelleIn eukaryotes, poly (A) tails are added to nuclear pre-mRNA 3'-ends in the two steps of cleavage and polyadenylation. This co-transcriptional processing requires the activity of a large protein complex comprising at least 20 different polypeptides in yeast organized primarily into the two factors CF IA and CPF. We are interested in the functional characterization of Pcf11, a CF IA subunit. The Pcf11 protein is organized into seven different domains, but here is still a large portion of the polypeptide that has not yet been characterized. For example the region from the end of the CTD interaction domain (CID) to an uninterrupted stretch of 20 glutamine residues has no known function. Recently, the structure of this region, called the 2nd NTD have been characterized. To gain insight into the function of the 2nd NTD and the two zinc fingers motif surrounding the Clp1 interaction domain, we have employed a systematic strategy of mutagenesis, either by deletion or via point mutations. The 2nd NTD is a folded domain composed of three α-helices. The deletion of this domain induced a severe defect of growth in yeast and impaired transcription termination of snoRNAs. Despite its similarity in structure and function with the CID, the 2nd NTD seems to act like an independent RNA binding domain. We don’t know yet the real function of the two zinc fingers motif at the C-terminal region of Pcf11, but the mutation of Cystein residues into serine of one of the two motifs impaired cleavage and polyadenylation. The mutation of the first motif is less harmful than the mutation of the second motif. The simultaneous mutation is lethal in yeast
Assrir, Nadine. „Analyse des intéractions moléculaires entre deux protéines liant des histones, HIRA et HIRIP3 (HIRA-interacting protein 3) et leur partenaires respectifs, la protéine chaperon d'histones Asf1 et la sérine-thréonine kinase CK2“. Paris 11, 2004. http://www.theses.fr/2004PA11T048.
Der volle Inhalt der QuelleOdye, Gweltas. „Caractérisation fonctionnelle de la protéine ANKS3 impliquée dans les ciliopathies rénales et étude de son rôle dans la régulation des ARNs ANKS3 is a master regulator of BICC1/Argonaute mediated degradation of ciliopathy-gene transcripts“. Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2148&f=12660.
Der volle Inhalt der QuelleNephronophtisis (NPH) is an autosomal recessive tubulo-interstitial nephropathy characterized by the a massive interstitial fibrosis and cyst formation. NPH is the major reason for end-stage renal disease in childhood. It can be isolated or syndromic, associated with extrarenal manifestations. NPH belongs to the ciliopathies, a group of multisystemic diseases, caused by mutations in genes encoding proteins of the primary cilia. The primary cilia acts on the surface of most cells as a mechano and chemosensor controlling signaling pathways essential for tissue development and homeostasis (Shh, Wnt, PC2 / Ca2+ signaling). To date twenty-three causatives genes have been identified for NPH (including 14 in our laboratory). These codes for ciliary proteins implicated in the control of cilia protein composition and ciliary signaling, at the base of the cilium (transition zone (TZ)), at the level of the Inversin compartment (IC), or during intraflagellar transport. We identified a homozygous missense mutation in a new gene responsible for NPH associated with liver fibrosis. ANKS3 code a protein known to interact with several NPH proteins such as NPHP1 (TZ), ANKS6 and NEK8 (IC) as well as BICC1, a ribonucleoprotein mutated in renal cystic dysplasia. My thesis project has been focused on the characterization of ANKS3 function and the impact of human mutation in cellular processes relevant for renal ciliopathies. These studies were performed from different cellular models: patient fibroblasts, renal tubular cells IMCD3 depleted for Anks3 (ANKS3_KD) re-expressing the wild-type or mutated form. My work demonstrated that ANSK3 mutation decreases its interaction with the TZ component, NPHP1 and IC one, NEK8. In addition, the absence or expression of the mutated form of ANKS3 affects the cilia length and the IC biogenesis. Indeed, the IC components are abnormally relocated all along the primary cilia. Moreover, a disruption of the ciliary signaling Shh pathway and the localization of the PC2 protein at the primary cilia were observed in the ANKS3_KD or mutant cells. This last observation is confirmed by zebrafish mutated for anks3 (TALEN) model, which exhibits a decrease in ciliary motility associated with calcium signaling defetcs in the Kupffer vesicle, leading to laterality defects (situs inversus). In addition to these ciliary defects, the loss or mutation of ANKS3 causes apico-basal polarity defects in IMCD cells, with a decrease in cell height and delay in tight junction formation, a phenotype reminiscent of NPHP1 mutated models. Consistent with these results we observed a decrease in the stability of Nphp1 transcripts in ANKS3_KD and mutant cells. The re-expression of NPHP1 in these cells rescues the polarity and cilia length defects demonstrating the ANKS3 implication in the Nphp1 transcripts regulation in these phenotypes. To elucidate the mechanism by which ANKS3 regulates the Nphp1 and possibly other ciliary RNAs stability, we investigated the implication of its partner BICC1, which is known to bind and regulate RNAs. Transcriptomic analyzes notably RNAseq and RIPseq on ANKS3-KD and mutated cells in the presence or absence of BICC1, demonstrate that the absence of ANKS3 or a mutant form triggers BICC1 interaction with the targeted mRNA and the RISC-associated protein AGO2, thus addressing ciliary gene transcripts to degradation. This finding allows us to place ANKS3/BICC1 complex as a key regulator of ciliopathy-related transcripts that orchestrates the biogenesis and function of primary cilia
Rana-Poussine, Vanessa. „Régulation du gène MyoD au cours de la myogenèse post-natale et du développement : et implication du modulateur d'Akt : CTMP dans la prolifération et la différenciation cellulaires“. Montpellier 2, 2008. http://www.theses.fr/2008MON20007.
Der volle Inhalt der QuelleCambuli, Francesca Maria. „Study of Musashi1-Expressing cells and of Musashi1 function in mouse intestinal physiopathology“. Thesis, Lyon, École normale supérieure, 2012. http://www.theses.fr/2012ENSL0794.
Der volle Inhalt der QuelleThe intestinal epithelium is a monolayer of cells surrounding the intestinal lumen. It consists of a differentiated compartment, the villi in the small intestine and a flat surface in the colon, and a proliferative compartment, the crypts of Lieberkühn. This tissue self-renews rapidly and continuously throughout life, due to the presence of adult stem cells in the bottom of the crypts. These cells are capable of self-renewing and give rise to proliferating progenitors (capable of generating all the different epithelial cytotypes) that differentiate and migrate toward the differentiated compartment. My thesis focused on the study of the intestinal epithelial stem cells marker Musashi1 (Msi1).In this context, the first part of my thesis work focused on the isolation and characterization of the intestinal epithelial stem cells that express Msi1 in the mouse. For this, we generated transgenic mice expressing the fluorescent protein GFP under the control of the promoter of Msi1. The intestinal stem cells of these mice co-express Msi1 and GFP. This model has been validated and allowed us to isolate GFP+/Msi-expressing cells in the intestine. By using different cellular and molecular approches, we confirmed their nature of stem cells and provided new data on the composition of the proliferative zone in the murine intestinal epithelium.The second part of my thesis has focused on the study of the function of Msi1 in the intestinal epithelium homeostasis in the mouse, by its over- and ectopic expression all along the epithelium. We have shown that the over-expression of this protein, which is a regulator of the Wnt and Notch pathways, perturbs the intestinal architecture, has pro-proliferative properties and tumorigenic potential
Mallet, Pierre-Luc. „Élucidation chez S. pombe du mécanisme d'import de la protéine nucléaire liant les queues poly(A), Pab2 : ainsi que de son implication en collaboration avec Abp1, une CENP-B homologue, dans la répression d'expression d'éléments génétiques mobiles“. Thèse, Université de Sherbrooke, 2014. http://hdl.handle.net/11143/6660.
Der volle Inhalt der QuelleNaville, Danielle. „Purification et caractérisation partielles d'une protéine liant IGF1 et appartenant au complexe de 145K circulant dans le plasma humain : étude de son activité biologique sur les cellules de Leydig de porc immature en culture en présence de IGF1“. Lyon 1, 1988. http://www.theses.fr/1988LYO1T120.
Der volle Inhalt der QuelleLaugier, Laurie. „Identification de marqueurs de susceptibilité dans les formes chroniques de la maladie de Chagas“. Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0226.
Der volle Inhalt der QuelleChagas disease is a parasitic disease caused by the protozoan Trypanosoma cruzi and transmitted by the hematophagous insects. The disease is composed by acute and chronic phases. Among the infected individuals, 30 % develop chronic form. They suffer from heart, digestive (esophagus, colon) and cardiodigestives injury. Our study was focused on patients with dilated chagasic cardiomyopathy (CCC). Our goal is to identify susceptibility genes that may be involved in the development of chronic forms. Our study revealed a variation in the expression of certain genes between CCC group and controls. We are also interested in epigenetic processes that can regulate the expression of genes. A study of the DNA methylation crossed with the transcriptome allowed us to identify genes presenting both variations in expression and methylation. For some of these genes we demonstrated that methylation is responsible for the expression variation observed. Finally, we studied a long non-coding RNA called MIAT. Our study demonstrated that it is overexpressed in CCC compared to controls and in a murine model infected by T. cruzi. Furthermore, the analysis of the expression of micro-RNAs crossed with transcriptome analysis allowed us to identify several micro-RNAs whose functions are essential in the regulation of gene expression. Finally, a proteomic study allowed us to demonstrate an increase in the production of protein for certain genes, correlated with the increase in expression levels observed
Stuhl-Gourmand, Laetitia. „Role de Naca et de ses partenaires moléculaires dans la différenciation érythroïde normale et pathologique des syndromes myélodysplasiques“. Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20661/document.
Der volle Inhalt der QuelleThe erythropoiesis is a complex process that leads to the formation of 100 billion red cells per day. It is finely regulated to adjust the production of red blood cells according to oxygen needs of peripheral tissues. To understand the complex processes involve in the regulation of erythropoiesis, it requires the study of molecular actors such as the NACA protein (the alpha chain of the nascent polypeptide-associated complex), highlighted as a positive regulator of erythroid human differentiation. We have identified ERGIC-53 as a novel interactor of NACA. ERGIC-53 is a lectin mannose-specific membrane involved in the transport of glycoproteins from the Endoplasmic Reticulum (ER) to the ERGIC compartment (Golgi Endoplasmic Reticulum Compartment Intermediate). We have shown that ERGIC-53 and NACA are involved in the regulation of trafficking of EPO-R. NACA may be also a negative regulator of apoptosis mediated by FADD. We investigated the role of NACA in early stages of myelodysplastic syndromes (ES-MDS) which have ineffective erythropoiesis due to apoptosis of erythroid progenitors. We have demonstrated that transduction of NACA in CD34 + progenitor cells from ES-MDS restores erythroid differentiation and increased survival of erythroid progenitors. Moreover, this study suggests that the level of mRNA NACA may be a new predictive marker of response to rhEPO treatment. In conclusion, our work highlighted that a molecule of the cellular machinery is involved in erythroid differentiation of both normal and ES-MDS CD34+ cells
Deye, Nicolas. „Cardiac Arrest-Induced Brain Injury : Diagnostic And Prognostic Values of Circulating Biomarkers“. Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC150.
Der volle Inhalt der QuelleOutcome of cardiac arrest (CA) remains dramatic. To quickly diagnose the cause of CA and establish a reliable outcome prediction (prognostication) as early as possible could help to guide initial treatments. It could avoid futile treatments in patients with low chance of survival or of good neurological recovery, or conversely allow treatment optimization in patients expected to have a high likelihood of good neurological outcome. Usefulness of biomarkers to guide clinicians in finding the CA diagnosis and helping prognostication is debated. Biomarkers are considered as not sensitive and accurate enough, especially within the first hours after return of spontaneous circulation (ROSC). Their use is only recommended in prognostication for Neuron Specific Enolase (NSE) as a second line tool and after the third day from CA. Our first study confirmed that biomarkers “specific” of brain injury (S100B protein: S100 and moreover NSE) cannot sufficiently discriminate the neurological cause of CA on ICU admission. If early coronary angiogram is the standard for diagnosing a probable cardiac cause of CA, biomarkers cannot replace brain computed-tomography (CT) in CA from a neurological cause. The second study evaluated, during the 1st day after ROSC, the link between biomarkers (S100 and NSE) and 2 surrogates of brain oedema recently proposed as outcome predictors: echography of the optic nerve sheath diameter (ONSD), and grey to white matter attenuation ratio (GWR) on brain CT-scan. Even though we cannot conclude on a definitive relationship between these parameters, ONSD enlargement at day 1 was associated with specific brain damage after CA, such as brain oedema and mostly axonal injuries, as reflected by increases in NSE (on admission and at day 1) and low GWR measurements. Whereas NSE, GWR and ONSD at day 1 were correlated, S100, which is more specific of glial injuries, did not reach significance. NSE and S100 on admission, at days 1 and 2 after ROSC, as well as ONSD at day 1, were associated with survival at hospital discharge. The third study evaluated the prognostic value of several biomarkers in the early phase after CA (NSE and S100 being sampled at median 220 min after ROSC). S100, blinded to physicians, was the biomarker with the best accuracy after ICU admission to correctly predict unfavourable outcome at hospital discharge and at 3 months after CA, compared with all other biomarkers such as lactate, pH, creatinine, and especially NSE. S100 variations during the first day after admission refined prognostication. Initial S100 was an early independent predictive factor associated with unfavourable outcome at hospital discharge, with the no-flow duration, initial lactate value, initial non-shockable rhythm, and the presence of clinical seizure. According to guidelines, prognostication theoretically needs to be delayed and multimodal, biomarkers alone not being recommended especially in the early phase after CA. Biomarkers cannot seem to be an alternative option compared to imaging to precisely diagnose the CA cause. By contrast, some biomarkers, such as S100 after admission, could easily and specifically discriminate CA patients with certainty of unfavourable outcome. Associated with other predictive tools (clinical or using imaging), biomarkers could interestingly be incorporated in early decisional algorithms to optimally guide initial therapies. This correct patient classification could help to avoid unuseful treatments versus to maximize aggressive therapies. The choice of recommended servo-controlled targeted temperature management devices, very efficient but invasive and expensive, or the indication -or not- of a cardio-circulatory assist device implementation should be guided in the early stage after ROSC using this simple strategy of patient selection
Le, Treut Guillaume. „Models of chromosome architecture and connection with the regulation of genetic expression“. Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS411/document.
Der volle Inhalt der QuelleIncreasing evidences suggest that chromosome folding and genetic expression are intimately connected. For example, the co-expression of a large number of genes can benefit from their spatial co-localization in the cellular space. Furthermore, functional structures can result from the particular folding of the chromosome. These can be rather compact bundle-like aggregates that prevent the access to DNA, or in contrast, open coil configurations with several (presumably) globular clusters like transcription factories. Such phenomena have in common to result from the binding of divalent proteins that can bridge regions sometimes far away on the DNA sequence. The physical system consisting of the chromosome interacting with divalent proteins can be very complex. As such, most of the mechanisms responsible for chromosome folding and for the formation of functional structures have remained elusive.Using methods from statistical physics, we investigated models of chromosome architecture. A common denominator of our approach has been to represent the chromosome as a polymer with bending rigidity and consider its interaction with a solution of DNA-binding proteins. Structures entailed by the binding of such proteins were then characterized at the thermodynamical equilibrium. Furthermore, we complemented theoretical results with Brownian dynamics simulations, allowing to reproduce more of the biological complexity.The main contributions of this thesis have been: (i) to provide a model for the existence of transcrip- tion factories characterized in vivo with fluorescence microscopy; (ii) to propose a physical basis for a conjectured regulatory mechanism of the transcription involving the formation of DNA hairpin loops by the H-NS protein as characterized with atomic-force microscopy experiments; (iii) to propose a physical model of the chromosome that reproduces contacts measured in chromosome conformation capture (CCC) experiments. Consequences on the regulation of transcription are discussed in each of these studies
Martel, Catherine. „Caractérisation du transport nucléocytoplasmique de la protéine Staufen chez les mammifères“. Thèse, 2003. http://hdl.handle.net/1866/14646.
Der volle Inhalt der QuelleHecheima, Michel. „Identification et caractérisation moléculaire des protéines liant l'ARN lors de l'acclimatation au froid chez le blé (Triticum Aestivum L.)“. Mémoire, 2006. http://www.archipel.uqam.ca/1650/1/M9180.pdf.
Der volle Inhalt der QuelleCampbell-Valois, François-Xavier. „Application des librairies de codons dégénérés à l'étude du mécanisme de repliement et de la stabilisation de la structure du domaine liant ras de Raf“. Thèse, 2005. http://hdl.handle.net/1866/6799.
Der volle Inhalt der QuelleBenoit, 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.
Der volle Inhalt der QuelleThe 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.
Furic, Luc. „Identification des ARNm liés par les protéines Staufen de mammifères et caractérisation des déterminants structuraux à la base de l'interaction“. Thèse, 2006. http://hdl.handle.net/1866/15238.
Der volle Inhalt der QuelleCroisetière, Christian. „HCaRG "Hypertension-related Calcium Regulated Gene", un gène candidat de la réparation rénale : caractérisation de son interaction avec le cytosquelette et son expression génique“. Thèse, 2007. http://hdl.handle.net/1866/7586.
Der volle Inhalt der QuelleDésormeaux, Anik. „Répercussions paracrines de l'apoptose endothéliale sur l'homéostasie des cellules musculaires lisses vasculaires“. Thèse, 2003. http://hdl.handle.net/1866/14662.
Der volle Inhalt der QuelleKerhoas, Maud. „Un nouveau clone et une nouvelle méthode pour la production et la purification de l’entérotoxine STb d’Escherichia coli“. Thèse, 2016. http://hdl.handle.net/1866/18649.
Der volle Inhalt der QuelleThe heat-stable enterotoxin b gene (estB) of Escherichia coli was fused to the gene for maltose-binding protein (malE) into the pMAL-p vector using PCR. Afterward, two plasmid constructs were realized from this new vector, named pMAL-STb. Firstly, a hexahistidine tag (His6) was added between malE and estB and secondly, a decahistidine tag (His10) was placed upstream of malE. The signal sequence of maltose-binding protein (MBP) directs the export of the fusion protein from the cytoplasm to the periplasm, where the enterotoxin STb acquires its active conformation. MBP is also known to improve the yield and solubility of the passenger protein while the histidine tag, viewed as the best affinity tag for protein purification, facilitates its purification to homogeneity. Furthermore, the fused genes are controlled by the tac promoter (Ptac), a strong inducible promoter. Following IPTG induction, the recombinant strain expressed a protein of approximately 48 kDa, which is easily identified from osmotic shock fluid following electrophoresis. A sequence encoding a factor Xa cleavage site is present in the plasmid to separate MBP and histidine tags from STb. The cleavage of the fusion protein with factor Xa generates the maltose-binding protein (42 kDa) attached to the histidine tag and a polypeptide of 5.2 kDa, corresponding to the molecular mass of mature STb. With this method, we aim at obtaining a more efficient way to produce and purify STb.