Auswahl der wissenschaftlichen Literatur zum Thema „Protéine liant les ARNs“
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Zeitschriftenartikel zum Thema "Protéine liant les ARNs"
Naciri, Ikrame, Audrey Roussel-Gervais, Pierre-Antoine Defossez und Olivier Kirsh. „Nouvelles fonctions d’une protéine liant l’ADN méthylé dans le cancer“. médecine/sciences 33, Nr. 8-9 (August 2017): 714–16. http://dx.doi.org/10.1051/medsci/20173308009.
Der volle Inhalt der QuelleTomavo, S., M. A. Ouaissi, J. F. Dubremetz, A. Capron und A. Vernes. „Identification chezPlasmodium falciparumd’une protéine se liant spécifiquement à la fibronectine humaine“. Annales de Parasitologie Humaine et Comparée 63, Nr. 1 (1988): 22–27. http://dx.doi.org/10.1051/parasite/198863122.
Der volle Inhalt der QuelleReboud-Ravaux, Michèle. „Dégradation induite des protéines par des molécules PROTAC et stratégies apparentées : développements à visée thérapeutique“. Biologie Aujourd’hui 215, Nr. 1-2 (2021): 25–43. http://dx.doi.org/10.1051/jbio/2021007.
Der volle Inhalt der QuelleOTSMANE, B., G. DOSSET, J.-P. LEBEAU und H. WATIER. „LES ANTICORPS MONOCLONAUX ANTI-SARS-COV-2 ET LE ROLE ESSENTIEL DES MEDECINS GENERALISTES DANS CETTE NOUVELLE APPROCHE THERAPEUTIQUE“. EXERCER 32, Nr. 172 (01.04.2021): 166–72. http://dx.doi.org/10.56746/exercer.2021.172.166.
Der volle Inhalt der QuelleFrançois, H., I. Annesi-Maesano, C. Maesano, K. Horo, Y. Toloba, T. Dupré und D. Caillaud. „Impact du taux de la vitamine D et de la protéine liant la vitamine D sur la santé respiratoire chez les fermiers d’Auvergne“. Revue des Maladies Respiratoires 33 (Januar 2016): A40. http://dx.doi.org/10.1016/j.rmr.2015.10.661.
Der volle Inhalt der QuelleNader, N., C. Grenot, A. Emptoz-Bonneton, H. Déchaud und M. Pugeat. „P170 - Mécanismes de régulation hormonale du gène de la SHBG in vitro. Purification d’une protéine de 46 KDa liant le motif (TAAAA)n du promoteur SHBG“. Annales d'Endocrinologie 65, Nr. 4 (September 2004): 372–73. http://dx.doi.org/10.1016/s0003-4266(04)95881-7.
Der volle Inhalt der QuelleDissertationen zum Thema "Protéine liant les ARNs"
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