Tesis sobre el tema "Protein mechanism"
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Fang, Lin. "Mechanism of client protein binding by heat shock protein 90 /". view abstract or download file of text, 2006. http://proquest.umi.com/pqdweb?did=1251819301&sid=2&Fmt=2&clientId=11238&RQT=309&VName=PQD.
Texto completoTypescript. Includes vita and abstract. Includes bibliographical references (leaves 115-121). Also available for download via the World Wide Web; free to University of Oregon users.
Smart, Nicola. "Studies on the mechanism of protein kinase C down-regulation". Thesis, Royal Veterinary College (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391675.
Texto completoLai, Chun Wan Jeffrey. "Mechanism of G Protein Beta-Gamma Assembly Mediated by Phosducin-Like Protein 1". BYU ScholarsArchive, 2011. https://scholarsarchive.byu.edu/etd/3190.
Texto completoXiao, Ruoyu. "Protein disulfide isomerase : function and mechanism in oxidative protein folding /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-238-1/.
Texto completoBruell, Christian M. "Mechanism of protein synthesis in Mycobacterium smegmatis /". Zürich : ETH, 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17733.
Texto completoStaniforth, Rosemary A. "The mechanism of chaperonin-assisted protein folding". Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238915.
Texto completoHoffman, Mary M. "Mechanism of MDR protein mediated multidrug resistance /". Access full-text from WCMC, 1997. http://proquest.umi.com/pqdweb?did=733008491&sid=6&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Texto completoHill, Donna Monique. "Mechanism of centaurin-alpha-1 control of neuronal differentiation". Birmingham, Ala. : University of Alabama at Birmingham, 2010. https://www.mhsl.uab.edu/dt/2010m/hill.pdf.
Texto completoTitle from PDF t.p. (viewed June 30, 2010). Additional advisors: Lori McMahon, Stephen Watts. Includes bibliographical references (p. 31-35).
Lindgren, Matteus. "On the mechanism of Urea-induced protein denaturation". Doctoral thesis, Umeå universitet, Kemiska institutionen, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-33151.
Texto completoHanazono, Yuya. "Structural studies on the mechanism of protein folding". 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/188506.
Texto completoStingele, Julian. "A dedicated mechanism for DNA-protein crosslink repair". Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-178719.
Texto completoGraham, Deborah Louise. "The catalytic mechanism of Rho-GTPase-activating protein". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322212.
Texto completoVos, Jan. "Understanding the formation mechanism of protein coated microcrystals". Thesis, University of Strathclyde, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431781.
Texto completoQi, Xianghong. "Influence of Cooperativity on the Protein Folding Mechanism". Kent State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=kent1219247325.
Texto completoShrestha, Pooja. "Mechanism of substrate protein remodeling by molecular chaperones". University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1378113185.
Texto completoLorite, M. J. "Mechanism of muscle protein degradation in Cancer Cachexia". Thesis, Aston University, 1997. http://publications.aston.ac.uk/15707/.
Texto completoKimura, Tetsunari. "Contributions of specific intraprotein and protein-water interactions to the protein folding mechanism". 京都大学 (Kyoto University), 2005. http://hdl.handle.net/2433/144930.
Texto completoTonddast-Navaei, Sam M. S. "Mechanism of Substrate Protein Remodeling by Allosteric Motions of AAA+ Nanomachines". University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1384869946.
Texto completoLackner, Laura L. "Investigating the mechanism of E̲s̲c̲h̲e̲r̲i̲c̲h̲i̲a̲ c̲o̲l̲i̲ Min protein dynamics". Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1124832205.
Texto completo[School of Medicine] Department of Molecular Biology and Microbiology. Includes bibliographical references. Available online via OhioLINK's ETD Center.
Matsusaki, Motonori. "Molecular Mechanism of Oxidative Protein Folding by Soybean Protein Thiol Disulfide Oxidoreductases/ERO1 Pathway". Doctoral thesis, Kyoto University, 2016. http://hdl.handle.net/2433/217183.
Texto completo0048
新制・課程博士
博士(農学)
甲第20008号
農博第2192号
新制||農||1045(附属図書館)
学位論文||H28||N5017(農学部図書室)
33104
京都大学大学院農学研究科農学専攻
(主査)教授 裏出 令子, 教授 松村 康生, 教授 三上 文三
学位規則第4条第1項該当
Doctor of Agricultural Science
Kyoto University
DFAM
Matsusaki, Motonori. "Molecular Mechanism of Oxidative Protein Folding by Soybean Protein Thiol Disulfide Oxidoreductases / ERO1 Pathway". Kyoto University, 2009. http://hdl.handle.net/2433/217183.
Texto completo0048
新制・課程博士
博士(農学)
甲第20008号
農博第2192号
新制||農||1045(附属図書館)
学位論文||H28||N5017(農学部図書室)
33104
京都大学大学院農学研究科農学専攻
(主査)教授 裏出 令子, 教授 松村 康生, 教授 三上 文三
学位規則第4条第1項該当
Mouton, Jacoba Martina. "The role of novel protein-protein interactions in the function and mechanism of the sarcomeric protein, myosin binding protein H (MyBPH)". Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86751.
Texto completoENGLISH ABSTRACT: Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity and mortality, and is a feature of common diseases, such as hypertension and diabetes. It is therefore vital to understand the underlying mechanisms influencing its development. However, investigating the mechanisms underlying LVH in such complex disorders can be challenging. For this reason, many researchers have focused their attention on the autosomal dominant cardiac muscle disorder, hypertrophic cardiomyopathy (HCM), since it is considered a model disease in which to study the causal molecular factors underlying isolated cardiac hypertrophy. HCM is a heterogeneous disease that manifests with various phenotypes and clinical symptoms, even in families with the same genetic defects, suggesting that additional factors contribute to the disease phenotype. Despite the identification of several HCM-causing genes, the genetic factors that modify the extent of hypertrophy in HCM patients remain relatively unknown. The gene encoding the sarcomeric protein, cardiac myosin binding protein C, cMyBPC (MyBPC3) is one of the most frequently implicated genes in HCM. Identification of proteins that interact with cMyBPC has led to improved insights into the function of this protein and its role in cardiac hypertrophy. However, very little is known about another member of the myosin binding protein family, myosin binding protein H (MyBPH). Given the sequence homology and similarity in structure between cMyBPC and MyBPH, we propose that MyBPH, like cMyBPC, may play a critical role in the structure and functionality of the cardiac sarcomere and could therefore be involved in HCM pathogenesis. The present study aimed to identify MyBPH-interacting proteins by using yeast two-hybrid (Y2H) analysis and to verify these interactions using three-dimensional (3D) co-localisation and co-immunoprecipitation (Co-IP) analyses. We further hypothesized that both MyBPH and cMyBPC may be involved in autophagy. To test this hypothesis, both MyBPH and cMyBPC were analysed for co-localisation with a marker for autophagy, LC3b-II. The role of MyBPH and cMyBPC in cardiac cell contractility were analysed by measuring the planar cell surface area of differentiated H9c2 rat cardiomyocytes in response to β-adrenergic stress after individual and concurrent siRNA-mediated knockdown of MyBPH and cMyBPC. In the present study we employed a family-based genetic association analysis approach to investigate the contribution of genes encoding the novel MyBPH-interacting proteins in modifying the hypertrophy phenotype. This study investigated the hypertrophy modifying effects of 38 SNPs and haplotypes in four candidate HCM modifier genes, in 388 individuals from 27 HCM families, in which three unique South African HCM-causing founder mutations segregate. Yeast two-hybrid analysis identified three putative MyBPH-interacting proteins namely, cardiac β-myosin heavy chain (MYH7), cardiac α-actin (ACTC1) and the SUMO-conjugating enzyme UBC9 (UBC9). These interactions were verified using both 3D co-localisation and Co-IP analyses. Furthermore, MyBPH and cMyBPC were implicated in autophagy, since both these proteins were being recruited to the membrane of autophagosomes. In addition, a cardiac contractility assay demonstrated that the concurrent siRNA-mediated knockdown of MyBPH and cMyBPC resulted in a significant reduction in cardiomyocyte contractility, compared to individual protein and control knockdowns under conditions of β-adrenergic stress. These results indicated that MyBPH could compensate for cMyBPC, and vice versa, further confirming that both these proteins are required for efficient sarcomere contraction. Results from genetic association analyses found a number of SNPs and haplotypes that had a significant effect on HCM hypertrophy. Single SNP and haplotype analyses identified SNPs and haplotypes within genes encoding MyBPH, MYH7, ACTC1 and UBC9, which contribute to the extent of hypertrophy in HCM. In addition, we found that several variants and haplotypes had markedly different statistical significant effects in the presence of each of the three HCM founder mutations. The results of this study ascribe novel functions to MyBPH. Cardiac MyBPC and MyBPH play a critical role in sarcomere contraction and have been implicated in autophagy. This has further implications for understanding the patho-etiology of HCM-causing mutations in the gene encoding MyBPH and its interacting proteins. This is to our knowledge the first genetic association analysis to investigate the modifying effect of interactors of MyBPH, as indication of the risk for developing LVH in the context of HCM. Our findings suggest that the hypertrophic phenotype of HCM is modulated by the compound effect of a number of variants and haplotypes in MyBPH, and genes encoding protein interactors of MyBPH. These results provide a basis for future studies to investigate the risk profile of hypertrophy development in the context of HCM, which could consequently lead to improved risk stratification and patient management.
AFRIKAANSE OPSOMMING: Linker ventrikulêre hipertrofie (LVH) is 'n primêre risikofaktor vir kardiovaskulêre morbiditeit en mortaliteit asook 'n kenmerk van algemene siektes soos hipertensie en diabetes. Daarom is dit van kardinale belang om te verstaan wat die onderliggende meganismes is wat die ontwikkeling van LVH beïnvloed. Die ondersoek na die onderliggende meganismes wat lei tot LVH in sulke komplekse siektes is ‟n uitdaging. Om hierdie rede fokus baie navorsers hul aandag op die autosomaal dominante hartspier siekte, hipertrofiese kardiomiopatie (HKM), wat beskou word as 'n model siekte om die molekulêre oorsake onderliggend tot geïsoleerde kardiovaskulêre hipertrofie te ondersoek. HKM is 'n heterogene siekte wat manifesteer met verskeie fenotipes en kliniese simptome, selfs in families met dieselfde genetiese defekte, wat impliseer dat addisionele faktore bydra tot die modifisering van die siekte fenotipe. Ten spyte van die identifisering van verskeie HKM-versoorsakende gene, bly die genetiese faktore wat die mate van hipertrofie in HKM pasiente modifiseer relatief onbekend. Die geen wat kodeer vir die sarkomeriese proteïen, kardiale miosien-bindingsproteïen C (kMyBPC) is die algemeenste betrokke in HKM. Die identifisering van proteïene wat bind met kMyBPC het gelei tot verbeterde insigte tot die funksie van hierdie proteïen en die rol wat hierdie proteïen in hipertrofie speel. Ten spyte hiervan, is daar baie min inligting beskikbaar oor 'n ander lid van die miosien-bindingsproteïen families, miosien-bindingsproteïen H (MyBPH). Gegewe die ooreenstemming tussen die DNA basispaar-volgorde en struktuur tussen hierdie twee proteïene, stel ons voor dat MyBPH, net soos kMyBPC, 'n kritiese rol in die struktuur en funksie van die kardiale sarkomeer speel en kan daarom betrokke wees in die patogenese van HKM. Die huidige studie het beoog om proteïene wat met MyBPH bind te identifiseer deur die gebruik van gis-twee-hibried (G2H) kardiale biblioteek sifting en om hierdie interaksies te verifieer met behulp van drie-dimensionele (3D) ko-lokalisering en ko-immunopresipitasie eksperimente. Ons het verder gehipotiseer dat beide MyBPH and kMyBPC betrokke kan wees in outofagie. Om hierdie hipotese te toets is beide MyBPH en kMyBPC geanaliseer vir ko-lokalisering met 'n merker vir outofagie, LC3b-II. Verder het ons beplan om die rol van MyBPH en kMyBPC in kardiale spiersel-sametrekking te ondersoek deur die oppervlak van gedifferensieerde H9c2 rot kardiomiosiete in reaksie op β-adrenergiese stres te meet, na individuele en gesamentlike siRNA-bemiddelde uitklopping van MyBPH en kMyBPC. In hierdie studie het ons 'n familie-gebaseerde genetiese assosiasie analise benadering gevolg om vas te stel of MyBPH en gene wat kodeer vir die geverifieerde bindingsgenote van MyBPH bydra tot die modifisering van die hipertrofiese fenotipe. Die doel van hierdie studie was om die hipertrofiese effek van 38 enkel nukleotied polimorfismes (SNPs) en haplotipes in vier kandidaat HKM modifiserende gene in 388 individue van 27 HCM families te toets, waarin drie unieke Suid-Afrikaanse HKM-stigters mutasies segregeer. G2H analise het drie verneemde MyBPH bindingsgenote geidentifiseer, naamlik miosien (MYH7), alfa kardiale aktien (ACTC1) en die SUMO-konjugerende ensiem UBC9 (UBC9). Hierdie interaksies is geverifieer deur middel van 3D ko-lokalisering en ko-immunopresipitasie analises. Verder is bewys dat MyBPH en kMyBPC betrokke is in outofagie, siende dat beide proteïene gewerf is tot die membraan van die outofagosoom. 'n Kardiale sametrekkings eksperiment het gevind dat die gesamentlike siRNA-bemiddelde uitklopping van MyBPH en kMyBPC 'n merkwaardige vermindering in die kardiomiosiet sametrekking veroorsaak het in reaksie op β-adrenergiese stres kondisies, in vergelyking met die individuele proteïen en kontrole uitkloppings eksperimente. Hierdie resultate bevestig dat MyBPH vir kMyBPC kan instaan en ook andersom, wat verder bevestig dat beide proteïene benodig word vir effektiewe sarkomeer sametrekking. Resultate van die genetiese assosiasie studie het gevind dat 'n aantal SNPs en haplotipes 'n beduidende effek of HKM hipertrofie het. Enkel SNP en haplotipe analises in gene wat kodeer vir MyBPH, MYH7, ACTC1 en UBC9 het SNPs en haplotipes geidentifiseer wat bydra tot die omvang van hipertrofie in HKM. Verder het ons gevind dat sekere SNPs en haplotipes kenmerkend verskillende statisties beduidende effekte in die teenwoordigheid van elk van die drie HKM-stigter mutasies gehad het. Die resultate van hierdie studie skryf twee nuwe funksies aan MyBPH toe. Kardiale MyBPC en MyBPH speel 'n kritiese rol in sarkomeer sametrekking en is betrokke in outofagie. Hierdie resultate het verdere implikasies vir die verstaan van die pato-etiologie van die HKM-veroorsakende mutasies in die MyBPH, MYH7, ACTC1 en UBC9 gene. So vêr dit ons kennis strek is dit die eerste genetiese assosiasie studie wat die modifiserende effek van bindingsgenote van MyBPH ondersoek as risiko aanduiding vir die ontwikkeling van LVH in die konteks van HKM. Ons bevindinge bewys dat die hipertrofiese fenotipe van HKM gemoduleer word deur die komplekse effekte van SNPs en haplotipes in die MyBPH geen en gene wat MyBPH proteïen-bindingsgenote enkodeer. Hierdie resultate verskaf dus 'n basis vir toekomstige studies om die risiko profiel van hipertrofie ontwikkeling met betrekking tot HKM te ondersoek, wat gevolglik kan bydra tot die verbeterde risiko stratifikasie en pasiënte bestuur.
McIntosh, Nicola. "Mechanism and function of complement factor H". Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/8914.
Texto completoMontanier, Cedric Y. G. "The mechanism and functional importance of protein carbohydrate recognition". Thesis, University of Newcastle upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489748.
Texto completoWong, Tse Yuan. "Host protein manipulation as a mechanism in viral cardiomyopathy". Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43095.
Texto completoGruninger, Robert J. y University of Lethbridge Faculty of Arts and Science. "Structure and mechanism of protein tyrosine phosphatase-like phytases". Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Chemistry and Biochemistry, c2009, 2009. http://hdl.handle.net/10133/2473.
Texto completoxix, 148 leaves : ill. (some col.) ; 29 cm
Gladwin, Sharon T. "Studies on the kinetics and mechanism of protein folding". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388718.
Texto completoShibata, Hiroyuki. "Molecular Mechanism of Lipase Activator Protein from Pseudomonas aeruginosa". Kyoto University, 1998. http://hdl.handle.net/2433/157112.
Texto completoKyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第7067号
農博第954号
新制||農||754(附属図書館)
学位論文||H10||N3109(農学部図書室)
UT51-98-C180
京都大学大学院農学研究科農芸化学専攻
(主査)教授 小田 順一, 教授 清水 昌, 教授 江﨑 信芳
学位規則第4条第1項該当
Rodon, Fores Jennifer. "Localized protein-assisted self-assembly : from mechanism to applications". Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAE017.
Texto completoThe cell is a complex chemical system that has benefited from billions of years of evolution to perfect itself, and represents a very well organized machinery leaving nothing to chance. To ensure its role, it controls a set of self-assembly processes where isolated components interact spontaneously with each other to lead to the formation of organized and functional structures such as microtubules, collagen or actin fibers. Inspired by cellular organization, my doctoral project involves the design of artificial chemical systems based on the self-assembly of original peptides. These buildings give rise to supramolecular hydrogels of interest in the field of biomaterials. I am interested at the same time in fundamental aspects concerning the comprehension of the initiation of the processes of self-assembly in the presence of biomacromolecules, but also with more applied problems of elaborating strategies to control the place but also the moment where these self-assembled molecular structures originate. Finally, I am interested in the emergence of the different properties appearing during the formation of certain self-assemblies such as catalysis and auto-catalysis
Lackner, Laura L. "Investigating the Mechanism of Escherichia coli Min Protein Dynamics". Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1124832205.
Texto completoFranzmann, Titus Marcellus. "Chaperone mechanism of the small heat shock protein Hsp26". kostenfrei, 2008. http://mediatum2.ub.tum.de/doc/652224/652224.pdf.
Texto completoTsai, Yu-Cheng. "Mechanism of homologous recombination mediated by human Rad51 protein". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 155 p, 2009. http://proquest.umi.com/pqdweb?did=1654492221&sid=2&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Texto completoCheng, Enzhi (Michael). "Adhesion mechanism of soybean protein adhesives with cellulosic materials /". Search for this dissertation online, 2004. http://wwwlib.umi.com/cr/ksu/main.
Texto completoHui, Daniel Jason. "The Mechanism of Protein Synthesis Inhibition by the P56 Family of Viral Stress Inducible Proteins". Connect to text online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1104848977.
Texto completoZavialov, Andrey. "The Protein Traffic on the Ribosome : The Mechanism and Regulation of Protein Synthesis in Prokaryotes". Doctoral thesis, Uppsala University, Department of Cell and Molecular Biology, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4569.
Texto completoThe aim of this work was to understand the molecular mechanism of translation and the mechanism of translation termination, in particular. Cleavage of peptidyl-tRNA and peptide release terminates translation of mRNA on the ribosome. In prokaryotes, three release factors (RFs) are involved in this process. RF1 and RF2 recognise the three stop codons on mRNA and induce hydrolysis of the ester bond in peptidyl-tRNA. RF3 accelerates the rate of RF1 and RF2 recycling between ribosome in a GTP-dependent manner. We have clarified the mechanism of action of peptide release factor RF3. In the cell, free RF3 is in the GDP conformation. When RF3∙GDP binds to ribosome in complex with RF1 or RF2, these ribosome complexes act as guanine exchange factors for RF3 by inducing rapid dissociation of GDP. If, and only if, the peptide has been removed from tRNA, GDP is quickly replaced by GTP. Binding of GTP to RF3 induces a conformation of the factor with high affinity for the ribosome, which forces RF1 or RF2 to rapidly dissociate. Subsequent hydrolysis of GTP on RF3 induces a factor conformation with low affinity for the ribosome and rapid release of RF3∙GDP. It was further shown how the position of peptidyl-tRNA on the ribosome and the presence or absence of its peptide regulates the binding and GTPase activity of translation factors IF2, EF-G and EF-Tu. The result explains how idling GTPase hydrolysis and negative interference between different translation factors are minimized in living cells. The present biochemical observations, in conjunction with cryo-EM results, lead to new proposals for the role of hybrid sites in translocation of tRNAs, recycling of RF1 and RF2 by RF3 and recycling of post-termination ribosomes back to a new round of initiation.
Scotney, Pierre David. "The catalytic mechanism of Bacillus stearothermophilus pyruvate kinase". Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266959.
Texto completoGrantcharova, Viara. "Folding mechanism of the src SH3 domain /". Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/9231.
Texto completoYamaguchi, Takahiro. "Physicochemical studies on aggregation mechanism of Alzheimer's amyloid β-protein". 京都大学 (Kyoto University), 2012. http://hdl.handle.net/2433/157895.
Texto completoAntoun, Ayman. "Mechanism and Regulation of Initiation of Protein Synthesis in Eubacteria". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5907.
Texto completoFeng, You. "Kinetic Mechanism and Inhibitory Study of Protein Arginine Methyltransferase 1". Digital Archive @ GSU, 2012. http://digitalarchive.gsu.edu/chemistry_diss/68.
Texto completoGómez, de la Cuesta Ramón. "Mechanism of regulation of the Ras-GTPase activating protein CAPRI". Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611173.
Texto completoRobertson, Andrea Marie. "The mechanism of neuropathy in peripheral myelin protein 22 mice". Thesis, University College London (University of London), 1999. http://discovery.ucl.ac.uk/1348752/.
Texto completoOsbourn, Jane Katharine. "An investigation into the mechanism of coat protein-mediated resistance". Thesis, University of East Anglia, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278119.
Texto completoTzortzopoulos, Athanasios. "Activation mechanism of a-Ca²+/calmodulin-dependent protein kinase II". Thesis, St George's, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252397.
Texto completoCosta, Helena. "Mechanism of interleukin-8 induction by human cytomegalovirus UL76 protein". Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2012. http://hdl.handle.net/10362/8500.
Texto completoHuman cytomegalovirus (HCMV) is a -herpesvirus that infects healthy individuals, usually asymptomatically, but can cause severe or fatal disease in immunocompromised individuals such as transplant recipients or AIDS patients. Primary HCMV infection, as with other herpesviruses, is followed by establishment of lifelong latency and periodic reactivation. To ensure its survival and propagation within the host, HCMV has evolved many strategies to subvert both innate and adaptive host immunity. It is known that HCMV infection induces production of interleukin-8 (IL-8), a proinflammatory chemokine with neutrophil chemotatic activity. Significantly, neutrophils are a major carrier of HCMV during viremia and they are able to transmit infectious virus to other cells, playing a key role in virus dissemination through their contact with endothelial cells. In addition, IL-8 enhances HCMV virion production. This work has identified an HCMV gene (UL76), with the relevant property of inducing IL-8 expression at both transcriptional and protein levels. Interestingly, the murine homologue, MHV-68 ORF20, has no significant effect in the expression of IL-8. The main objective of this work was to characterize the mechanism of IL-8 induction by UL76 and the impact of its expression during the viral infection. The UL76-mediated enhancement of luciferase activity was abolished when the NF-kB binding element was mutated in the IL-8 promoter luciferase reporter, thereby demonstrating that activation of NF-kB is essential for the UL76-mediated induction of IL-8. Consistent with the requirement for NF-kB pathway activation, IKK- and degradation of Ik were essential for IL-8 induction by UL76. In addition, and as might be predicted, expression of UL76 resulted in the translocation of p65 to the nucleus.(...)
Leo, Vincenzo Carlo. "The mechanism of action of a mutant mitochondrial fission protein". Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/5052/.
Texto completoLegrand, Anthony. "Anchoring mechanism of the plant protein remorin to membrane nanodomains". Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0285.
Texto completoGroup 1 isoform 3 remorin from Solanum tuberosum (StREM1.3) is a membrane protein belonging to the multigenic family of plant proteins called remorins (REMs), involved in plant immunity, symbiosis, abiotic stress resistance and hormone signalling. REMs’ most well known feature is their ability to segregate into nanodomains at the plasma membrane’s (PM) inner leaflet. For StREM1.3, this is achieved by an interaction between two lysines of the remorin C-terminal anchor (RemCA) and negatively charged phosphatidylinositol 4-phosphate (PI4P). Thus, RemCA undergoes conformational changes and partially buries itself in the PM, resulting in an intrinsic membrane anchoring. Capitalising on pre-existing structural data about this isoform, we investigate StREM1.3’s membrane-interacting properties further, using a wide array of techniques, ranging from fluorescence microscopy and solid-state nuclear magnetic resonance (ssNMR) to atomic force microscopy (AFM), cryo-electron microscopy (cryoEM) and computational modelling. We aim to discover the impact of StREM1.3’s oligomerisation and phosphorylation on its membrane interactions and biological activity, and to assess its influence on lipid dynamics as well as its lipid requirements for membrane binding and nanoclustering. Finally, based on all available structural data, we will undertake the in vitro reconstruction and characterisation of minimal nanodomains of StREM1.3
Wang, Lei. "Molecular Mechanism of Rho GTPase-Activating Protein Function and Application". University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1122910093.
Texto completoKong, Cheng-Te. "Mechanism of the Adenosine 3',5'-Monophosphate Dependent Protein Kinase". Thesis, North Texas State University, 1988. https://digital.library.unt.edu/ark:/67531/metadc330934/.
Texto completoKhal, Jwan. "Mechanism of protein catabolism in skeletal muscle during cancer cachexia". Thesis, Aston University, 2002. http://publications.aston.ac.uk/12620/.
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