Rozprawy doktorskie na temat „Immunophilins”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 27 najlepszych rozpraw doktorskich naukowych na temat „Immunophilins”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj rozprawy doktorskie z różnych dziedzin i twórz odpowiednie bibliografie.
Dornan, Jacqueline. "Immunophilins : an investigation into function and structure". Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/22159.
Pełny tekst źródłaMorgan, Gloria Yvonne. "The expression of immunophilins in cells and organelles". Thesis, University of Sussex, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282145.
Pełny tekst źródłaMcKenzie, Neil Iain. "The immunophilins as drug targets : development of novel fluorescence assays". Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/17961.
Pełny tekst źródłaMcCann, Fiona Elizabeth. "Studies on novel immunophilins and the effects of immunosuppressant drugs on neurons". Thesis, University of Kent, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246593.
Pełny tekst źródłaDavies, Todd Howard. "Regulation of glucocorticoid receptor function by associated TPR-domain proteins". Connect to full-text via OhioLINK ETD Center, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1098292002.
Pełny tekst źródła"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences." Major advisor: Edwin Sanchez. Includes abstract. Document formatted into pages: iv, 126 p. Title from title page of PDF document. Includes bibliographical references (p. 100-124).
Davies, Todd Howard. "Regulation of Glucocorticoid Receptor Function by TPR-domain Proteins". University of Toledo Health Science Campus / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=mco1098292002.
Pełny tekst źródłaCluning, Carmel. "Steroid receptor-associated immunophilins : influence of targeted knockdown and altered expression on receptor signalling". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0215.
Pełny tekst źródłaWarrier, Manya. "Role of FKBP51 and FKBP52 in Glucocorticoid Receptor Regulated Metabolism". University of Toledo Health Science Campus / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=mco1223923687.
Pełny tekst źródłaSandhu, Khushwant Singh. "Identification and molecular characterization of the putative immunophilins (IMMs) in the oilseed rape pathogens Leptosphaeria maculans, Leptosphaeria biglobosa, and Plasmodiophora brassicae". Doctoral thesis, Česká zemědělská univerzita v Praze, 2016. http://www.nusl.cz/ntk/nusl-259691.
Pełny tekst źródłaSomarelli, Jason Andrew. "The Role of Splicing Factors and Small Nuclear RNAS in Spliceosomal Formation". FIU Digital Commons, 2009. http://digitalcommons.fiu.edu/etd/83.
Pełny tekst źródłaKontopidis, George A. "Immunophilin ligand design". Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/22386.
Pełny tekst źródłaYuande, Y. "Structural studies of immunophilin-ligand complexes". Thesis, University of Edinburgh, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664185.
Pełny tekst źródłaPatterson, Alan F. "Biophysical and crystallographic studies of immunophilin-ligand complexes". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/15599.
Pełny tekst źródłaLane-Guermonprez, Lydie. "Stress nitro-oxydatif et immunophilines dans le contrôle du métabolisme cholinergique". Paris 11, 2002. http://www.theses.fr/2002PA112112.
Pełny tekst źródłaNitric oxide is a physiological modulator of neuronal functions, which can combine with superoxide to form peroxynitrite. Peroxynitrite is a powerful, short-lived oxidizing and nitrating agent. Calcineurin is the only known calcium-dependent phosphatase. It is enriched in neurons and particularly sensitive to oxidative stress. It plays important roles in synaptic plasticity and axonal regeneration. Available inhibitors of calcineurin are the immunosuppressors cyclosporin A (CsA) and FK506. When clinically administered, these drugs display bath neurotoxic and neurotrophic effects, that are not fully understood. To be able to inhibit calcineurin activity, they first have to complex with intracellular enzymes named immunophilins. Immunophilins are ubiquitously expressed chaperones endowed with cis-trans prolyl isomerase activity. By modifying praline conformation, they can regulate the function, export and oligomerization of numerous proteins, notably transporters and channels. Unfortunately, it is quite uneasy to separate the effects of immunosuppressors linked to calcineurin inhibition from their effects on immunophilins. The goal of this work was to determine, on a simple model of nerve endings, whether peroxynitrite or immunosuppressors could modify acetylcholine metabolism. These questions were assessed by two complementary approaches on the same model, ie purely cholinergic synaptosomes isolated from Torpedo electric organ. First, we studied the short-term effects of peroxynitrite and immunosuppressors on synaptosomal ACh synthesis and/or release. We identified ChAT as a major target of peroxynitrite and the high affinity choline transporter as a target of calcineurin. In a second approach, we searched for cyclophilin ligands in synaptosomes, and found that synapsin can interact with cyclophilin B in a CsA and calcium dependent way. This suggests an important role of cyclophilin B in mid- or long-term regulation of neuromediator storage and release
Guimiot, Fabien. "Etude fonctionnelle de deux immunophilines, Fkbp25 et Fkbp36 dans le développement neuronal". Paris 7, 2003. http://www.theses.fr/2003PA077217.
Pełny tekst źródłaChopard, Christophe. "Régulations de la sécrétion et de l’activité biologique de la protéine Tat du VIH-1 : rôles de la palmitoylation et de Gag". Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20089/document.
Pełny tekst źródłaHIV-1 Tat is a small protein that is required for viral transcription and multiplication. It thus has a crucial role in the infected cell. It was known that Tat can be secreted despite its lack of signal sequence. In fact 2/3 of cellular Tat are exported by infected primary T-cells. The unconventional secretion of Tat relies on its interaction with phosphatidylinositol(4,5)-biphosphate or PI(4,5)P2, a lipid that is concentrated within the inner leaflet of the plasma membrane and is strictly required for Tat secretion. Exogenous Tat has deleterious effects on several cell types, indicating that extracellular Tat is involved in evolution to AIDS. Consistent with this secretion efficiency, Tat is mainly localized at the plasma membrane of primary T-cells infected by HIV-1. A large fraction of Tat is resident at the membrane and we looked for a mechanism that could explain this retention and discovered that Tat is palmitoylated. Our studies show that Tat is palmitoylated, both in T-cells and also in ‘target' cells such as neurons and macrophages. Tat palmitoylation inhibits its secretion and is performed on Tat cysteine 31 (Tat has seven cyteines) by the enzyme DHHC20 using immunophilins (prolyl ismerases), Cyclophilin A (CypA) and FKPB12, as cofactors. Our results also indicate that the presence of Gag inhibits Tat palmitoylation. We believe that the export of CypA due to its encapsidation will make less CypA available for Tat, thereby inhibiting Tat palmitoylation. Indeed, HIV-1 encapsidates 250 copies of CypA/virion and the amount of CypA regulates the virulence of produced virions. In target cells, Tat is strongly palmitoylated and this modification induces its almost irreversible binding to PI(4,5)P2, preventing its secretion and allowing cumulative effect of minute Tat doses.Tat palmitoylation enables Tat to severely inhibit various PI(4,5)P2-dependent processes such as phagocytosis and neurosecretion. These effects of extracellular Tat likely contribute to the development of opportunistic infections and neurological disorders observed during AIDS
Rivière, Sylvie. "Caracterisations biochimiques et fonctionnelles d'une immunophiline, la fkbp25, et d'une cytokine, le mif". Paris 11, 1995. http://www.theses.fr/1995PA112133.
Pełny tekst źródłaLe, Bihan Stéphane. "Role des immunophilines dans le mecanisme d'action des recepteurs des glucocorticosteroides et des progestagenes". Paris 11, 1996. http://www.theses.fr/1996PA11T025.
Pełny tekst źródłaGuimiot-Maloum, Ismahane. "Analyse fonctionnelle de deux gènes nouveaux, C61 et FKbp25, identifiés par comparaison de transcriptomes : leur implications dans le développement cortical". Paris 6, 2005. http://www.theses.fr/2005PA066309.
Pełny tekst źródłaKamah, Amina. "Identification et caractérisation des modifications post-traductionnelles de la protéine TAU : implication dans le processus d'agrégation". Thesis, Lille 1, 2015. http://www.theses.fr/2015LIL10049.
Pełny tekst źródłaSenile dementia are characterized by protein aggregation such as α-synuclein in Parkinsondisease or β-amyloid peptide and Tau protein in Alzheimer disease. Protein misfolding has beenevoked in the pathological processes even though these proteins do not adopt a stable threedimensionalstructure in solution. Tau protein belongs to the MAP (Microtubule-AssociatedProtein) family. It stimulates tubulin polymerization into microtubule allowing for cytoplasmictransport in cell. Tau and its mutated forms are found in neurodegenerative diseases,collectively referred to as tauopathy, the most famous being Alzheimer’s disease. Thesepathologies are characterized by fibrillary aggregates of hyperphosphorylated Tau namedPaired Helical Filaments (PHF) that invades gradually throughout the brain. These observationsare correlated with imbalance between phosphorylation and dephosphorylation in AD brains.Despites extensive studies, the aggregation mechanism is still not understood and severalpathways were considered, especially posttranslational modifications other thanphosphorylation. We have investigated the modifications of Tau protein by NMR spectroscopyand studied effect of these modifications on aggregation process by spectrophotometry. Amongcovalent modifications, we have studied lysine acetylation and Ser/Thr O-β-Nacétylglucosaminylation.The third investigated modification is the conformational switch ofproline residues catalyzed by a peptidyl prolyl cis trans isomerase
Blackburn, Elizabeth Anne. "Biophysical studies of protein-ligand interactions and the discovery of FKBP12 inhibitors". Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/6504.
Pełny tekst źródłaMoore, Stephen. "Characterisation of a novel immunophilin-like gene, repressed by low doses of ionising radiation; identification of interacting proteins". Thesis, University of Ulster, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272344.
Pełny tekst źródłaStrunz, Patrick-Pascal Holger [Verfasser], Petra [Gutachter] Eder-Negrin, Erhard [Gutachter] Wischmeyer i Brenda [Gutachter] Gerull. "Interaktion von TRPC-Ionenkanälen mit dem Immunophilin FKBP52 / Patrick-Pascal Holger Strunz ; Gutachter: Petra Eder-Negrin, Erhard Wischmeyer, Brenda Gerull". Würzburg : Universität Würzburg, 2020. http://d-nb.info/1210862336/34.
Pełny tekst źródłaEdvardsson, Anna. "Peptidyl-prolyl cis-trans Isomerases in the Chloroplast Thylakoid Lumen". Doctoral thesis, Linköping : Univ, 2007. http://www.bibl.liu.se/liupubl/disp/disp2007/med983s.pdf.
Pełny tekst źródłaStrunz, Patrick-Pascal Holger. "Interaktion von TRPC-Ionenkanälen mit dem Immunophilin FKBP52". Doctoral thesis, 2020. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-204298.
Pełny tekst źródłaBackground: TRPC channels play an important role in the pathology of heart failure and cardiac hypertrophy. These effects are partly mediated by the calcineurin-NFAT signaling pathway. An important binding partner and regulator of TRPC channels is the protein FKBP52. Using a Yeast Two-Hybrid System in a cardiac cDNA library, we have recently found an interaction between a C-terminal fragment of TRPC3 (aa 742-848) without the known FKBP binding site (aa 703-714) and FKBP52 indicating a new binding domain. After creation of a FKBP52 fragment – called FKBP52s -, lacking the functional relevant PPIase domain with the known binding site, a first immunoprecipitation between this fragment and TRPC3 was successful. Aim: To analyze whether the presence of the truncated FKBP52 in vivo suppresses complex formation between TRPC3 or TRPC4 and the wild-type FKBP52. In addition, whether FKBP52s interrupts assembling between TRPC3 or TRPC4 and calcineurin in vivo and so activation of the calcineurin-NFAT pathway. Methods: Co-immunoprecipitation (Co-IP) experiments were performed in HEK 293 cells which were transfected with cDNAs encoding TRPC3, TRPC4, calcineurin A and FKBP52s. For detecting the translocation of NFATc1 into the nucleus by fluorescence microscopy, HEK 293 cells were transfected with TRPC3, TRPC4, GFP-NFATc1 ± FKBP52s. Statistical analysis was performed by one-way ANOVA. Results: In this study it was demonstrated for the first time that FKBP52 interacts not only with TRPC4 but also with TRPC3. Additionally, it was shown that a protein fragment of FKBP52 without its PPIase I domain also binds TRPC3 and TRPC4. This PPIase-deficient FKBP52 protein takes part in complex formation between TPRC3 and TRPC4, respectively, and calcineurin. Furthermore, it was shown for TRPC3 that in presence of this FKBP52 fragment, the activation of calcineurin and nuclear translocation of NFAT was significantly reduced after stimulation with c arbachol (GPCR-agonist). Conclusion: Thus, FKBP52 is important in this signaling cascade by assembling calcineurin to the TRPC channel complex and thus also in the activation of the calcineurin-NFAT signaling pathway
Germain, Marie-Anne. "Découverte de nouvelles interactions entre le virus de l'Hépatite C et l'hôte par une approche combinée de Spectrométrie de Masse et de Génomique Fonctionnelle". Thèse, 2012. http://hdl.handle.net/1866/10026.
Pełny tekst źródłaHepatitis C virus (HCV) replication and assembly are tightly regulated in time and space within the cell, most likely due to protein interactions between virus and host. In order to better understand HCV biology and its pathogenesis, there is a need to unravel virus/host interaction network. We extended our knowledge of virus/host interactions by the identification of cellular proteins associated to HCV proteins using an immunoprecipitation (IP) technique coupled to mass spectrometry (MS), and further evaluate the role of retrieved interactors using gene knockdown. FLAG-tagged viral proteins Core, NS2, NS3/4A, NS4B, NS5A and NS5B have been expressed individually in 293T human cells, and immunoprecipitated protein complexes have been submitted to MS analysis for identification of host proteins. In this study, 98 proteins were significantly enriched and showed specific interaction to a viral protein. Retrieval of previously characterized interacting proteins proved the strength of the method. Six newly identified interactors by MS were individually confirmed using IP of viral proteins. We evaluated the role of identified interactors in HCV replication by performing a functional lentivirus-based RNA interference (RNAi) screen. Two reporter systems were used: the sub- genomic replicon (Huh7-Con1-Fluc) and a full length infectious clone (J6/JFH-1/p7Rluc2a), as well as the cellular toxicity assay Alamar blue. Of the identified host interactors, 28 proteins showed a significant effect on HCV replication upon gene knockdown and without cellular toxicity. Overall, the study led to the identification of novel virus/host interactions essential in HCV life cycle and provides novel potential drug targets.
Hui, Kelvin Kai-Wan. "Analysis of Mitochondrial Signaling in the Regulation of Programmed Cell Death". Thesis, 2011. http://hdl.handle.net/1807/29750.
Pełny tekst źródła