Dissertations / Theses on the topic 'Protein 1'
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Stylianou, Julianna. "Protein-protein interaction of HSV-1 tegument proteins." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24663.
Full textTse, Muk-hei. "Investigations on recombinant Arabidopsis acyl-coenzyme A binding protein 1." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B36427664.
Full textLam, Wai Kwan. "Investigation of interaction between solube adenylyl cyclase and p34SEI-1 /." View abstract or full-text, 2010. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202010%20LAM.
Full textTse, Muk-hei, and 謝牧熙. "Investigations on recombinant Arabidopsis acyl-coenzyme A binding protein 1." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36427664.
Full textBennett, D. H. "Protein phosphatase type 1 binding proteins in Drosophila melanogaster." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365689.
Full textHetti, Arachchilage Madara Dilhani. "Coevolution of epitopes in HIV-1 pre-integration complex proteins: protein-protein interaction insights." Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent1530646538935895.
Full textNiessen, Sherry. "p120e4f-1 : a novel Bmi-1 interacting protein." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80343.
Full textLawrence, Charlotte. "Towards a small molecule inhibitor of the HIF-1/HIF-1 protein-protein interaction." Thesis, University of Southampton, 2015. https://eprints.soton.ac.uk/374783/.
Full textLubeseder-Martellato, Clara. "The guanylate binding protein-1." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-11959.
Full textSarkar, Mohosin M. "Engineering Proteins with GFP: Study of Protein-Protein Interactions In vivo, Protein Expression and Solubility." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1261418776.
Full textLai, 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.
Full textLi, Chun-bong. "Mechanisms of HIV-1 Tat induced immune response." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31537169.
Full textLi, Chun-bong, and 李振邦. "Mechanisms of HIV-1 Tat induced immune response." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31537169.
Full textSmith, Stephanie Kathryn Fiona. "Structure/function of presenilin 1 in relation to Alzheimer's disease." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267017.
Full textStriebinger, Hannah. "Membran-assoziierte Protein-Protein-Interaktionen des Herpes simplex-Virus 1." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-146882.
Full textDouglas, Chanel Catherine. "A study into the protein/protein interactions involved in HIV-1 capsid assembly." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/douglas.pdf.
Full textHellborg, Fredrik. "Identification, cloning and characterization of the p53 induced gene human wig-1 /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-190-3/.
Full textGibson, Rosemary M. "Protein engineering of #Beta#-lactamase 1." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.256768.
Full textPaxton, Camille Whitney. "Kelch related protein 1 in myogenesis." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611690.
Full textKoscky, Paier Carlos Roberto 1983. "Caracterização estrutural do complexo protéico Calsarcina 1 : Calcineurina A." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314411.
Full textTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-26T03:49:49Z (GMT). No. of bitstreams: 1 KosckyPaier_CarlosRoberto_D.pdf: 7798282 bytes, checksum: 043e551d51c3a8309982d9ff59835b10 (MD5) Previous issue date: 2014
Resumo: A via de sinalização da Calcineurina (Cn), uma fosfatase dependente de cálcio, desempenha papel chave no desenvolvimento, na hipertrofia e no remodelamento patológico do coração. A Calcineurina é negativamente regulada pelas Calsarcinas (CS), uma família de proteínas específicas do músculo estriado, que interagem diretamente com Cn. No entanto, os mecanismos moleculares de inibição de Cn por CS permanecem obscuros. Compreender a estrutura do complexo Cn:CS é fundamental para desvendar esse mecanismo de regulação. Neste trabalho foram combinados ensaios bioquímicos, crosslinking químico acoplado à Espectrometria de Massas (experimentos de MS / MS), análise mutacional e uma estratégia de modelagem computacional para a caracterização estrutural do complexo CnA:CS1 (isto é, constituído pela subunidade A de Cn e a isoforma 1 de CS, ambas murinas). O complexo recombinante foi submetido a crosslinking químico, tripsinizado e analisado por LC-MS/MS. Os dados obtidos foram utilizados em um docking in silico dos modelos de ambos os polipeptídeos, gerando várias poses para o complexo. As poses de menor energia de ligação foram agrupadas de acordo com semelhança estrutural e submetidas à simulação de dinâmica molecular. A superfície de interação identificada em CnA abrangeu as ?-hélices 1, 3 e loops vizinhos, enquanto a superfície correspondente de CS1 compreendeu os loops carboxiterminais das regiões Leu179-Phe185, Phe195-Ser199 e Thr250-Leu264. Notavelmente, a superfície de interação de CnA situa-se muito próxima à folha-? 14, o principal sítio de ligação do motivo PxIxIT do fator de transcrição NFAT, importante efetor da Calcineurina. Experimentos realizados com vários mutantes de CnA (FLAG- CnA) e CS1 (myc -CS1 ) foram utilizados para validar o modelo estrutural do complexo CnA:CS1. Os resíduos Lys40 (CnA) e Glu254 (CS1) foram identificados como críticos para a estabilidade do complexo. O modelo gerado neste estudo apoia a hipótese de que CS1 interage com um sítio alostérico para inibir a atividade de CnA
Abstract: Signaling by the calcium-dependent phosphatase calcineurin (Cn) plays key roles in regulating cardiac development, hypertrophy, and pathological remodeling. Cn binds to and is negatively regulated by calsarcins (CS), a family of muscle-specific proteins. However, the molecular mechanisms involved in the inhibition of Cn by CS remain unclear. Understanding the architecture and structure of Cn-CS complex is critical to unravel the regulation of Cn by CS. Here we combined biochemical assays, chemical crosslinking coupled to mass spectrometry experiments (MS/MS), mutational analysis and a modeling strategy for structural characterization of CnA-CS1 assembly. The MS/MS data obtained from the cross-linked peptides of both proteins were used to guide an in silico docking of their polypeptide models. The protein complex models with the smallest estimated binding energy were clustered according to structural similarity and submitted to molecular dynamics simulation. The interacting surface of CnA was mapped in a pocket between the 1st and 3rd ?-helixes and surrounding loops, while the corresponding surface of CS1 was mapped to the carboxyterminal loops within the Leu179-Phe185, Phe195-Ser199 and Thr250-Leu264 regions. Notably, the region of CnA that interacts with CS1 was found to be located in close proximity, but not coincident, to the ?-sheet 14, the main binding site for the PVIVIT sequence of NFAT. Experiments performed with several CnA (FLAG-CnA) and CS1 (myc-CS1) mutants were used to validate the structural model of the CnA-CS1 assembly. The Lys40 (CnA) and Glu254 (CS1) residues were identified as critical for the complex stability. The model that emerges from this study supports the notion that CS1 interacts with an allosteric site to inhibit the activity of CnA
Doutorado
Bioquimica
Doutor em Biologia Funcional e Molecular
Laudon, Hanna. "Functional domains in the Alzheimer's disease-associated presenilin 1 protein /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-085-0/.
Full textChan, Man Kid. "The interaction between Y box binding protein 1 and DNA replication proteins." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66802.
Full textUne réponse coordonnée lors de dommages à l'ADN est vitale pour le maintien de la viabilité cellulaire et pour éviter l'installation de maladies. Dans les cellules de mammifères, le point de contrôle de la phase S, la protéine kinase ATR (Ataxia-telangiectasia mutated and RAD3-related), coordonne la réponse aux dommages de l'ADN afin d'assurer une réplication complète et fidèle du génome avant l'entrée en mitose. La protéine YB-1 (Y box Binding Protein 1), un facteur de transcription et de traduction, est impliqué dans la prolifération cellulaire et la résistance aux chimiothérapies. YB-1 est également lié à une large variété de stress cellulaires but aucune donnée n'est disponible quant à son rôle dans la réplication de l'ADN. Lors de mon travail de Master, j'ai pu montrer qu'YB-1 s'associe à la fois à l'origine de réplication de la β-globine et dans les régions contrôles de l'ADN. Ce résultat suggère qu'YB-1 pourrait être impliqué dans la phase d'élongation de la réplication de l'ADN plutôt que dans celui de l'initiation. Par immunoprécipitation, j'ai identifié PCNA et MCM7 comme interacteurs préférentiels d'YB-1 en phase S. Par contre, en immunofluorescence, je n'observe pas de colocalisation nucléaire entre ces protéines. Lors du blocage de la fourche de réplication par un traitement à l'hydroxyurée, l'interaction entre YB-1 et MCM7 a été réexaminée et j'ai mis en évidence que 8h après le traitement, ces deux protéines présentent une co-localisation diffuse dans le noyau. Ces données indiquent qu'YB-1 pourrait être impliqué dans une réponse tardive suite à un arrêt prolongé de la fourche de réplication soit directement au point d'arrêt soit au niveau d'origines « dormantes » liées aux complexes MCM. YB-1 peut donc avoir plusieurs rôles tels que l'aide à la reprise de la réplication de l'ADN ou l'activation d'origines de réplicatio
Begum, Rumena. "Kindlin-1 protein-protein interactions and functional relevance to Kindler syndrome." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/kindlin1-proteinprotein-interactions-and-functional-relevance-to-kindler-syndrome(6c122016-c55d-4cbe-b4c3-99be4def7e9e).html.
Full textBain, Sharon Joanne Macnab. "Analysis of protein-protein interactions in the shell of herpes simplex virus type 1 (HSV-1) capsids." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301830.
Full textMéndez, Vidal Cristina. "Molecular studies of WIG-1, A P53-induced zinc finger protein /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-732-0.
Full textTopping, Ryan. "Quantitative methods for reconstructing protein-protein interaction histories." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14618.
Full textBane, Steven Edward. "Expression and characterization of the human neurokinin 1 receptor from Escherichia coli." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 99 p, 2007. http://proquest.umi.com/pqdweb?did=1342742951&sid=1&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Full textBoutell, Christopher John. "Characterisation of the herpes simplex virus type 1 (HSV-1) triplex proteins." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326428.
Full textChernov, Konstantin Grigorievich. "Interplay of YB-1 between tubulin and mRNA." Thesis, Evry-Val d'Essonne, 2008. http://www.theses.fr/2008EVRY0040/document.
Full textYB-1 is a major regulator of gene expression in eukaryotic cells. In addition to its role in transcription, YB-1 plays a key role in translation and stabilization of mRNAs. We identify several novels YB-1 protein partners by affinity chromatography of different tissue extracts. We observed that YB-1 interacts with tubulin and microtubules and stimulates microtubule assembly in vitro. Microtubules assembled in the presence of YB-1 exhibited a normal single wall ultrastructure where YB-1 probably coats the outer microtubule wall. Furthermore, we found that YB-1 also promotes the assembly of MAPs-tubulin and subtilisin-treated tubulin. Additionally, we demonstrated that tubulin interferes with mRNA:YB-1 complexes. These results suggest that YB-1 may regulate microtubule assembly in vivo and that its interaction with tubulin may contribute to the control of mRNA translation. The translational status of mRNPs in vivo depends on amount of YB-1 associated with mRNA. We show here that at low YB-1:mRNA ratios mRNP complexes possess an incompact structures, whereas saturated mRNPs are compact. This structural change corresponds to translation inhibition when mRNA moves from polysomal (translatable) to free (untranslatable) mRNPs. Saturated mRNPs bind to microtubules via protein:protein interactions and tend to self-aggregate on microtubule surface. This property could contribute to stress granule formation, mRNPs traffic and localization of translation apparatus within cytoplasm. Finally, the facilitated diffusion model was developed to explain enhancement of microtubule assembly by positively charged natural polyamines in living cells. Altogether our data contribute to the understanding of fundamental biological processes
Aviat, Florence. "Étude d'une protéine de leptospires : Hemolysis Associated Protein 1 : Hap 1." Nantes, 2006. http://www.theses.fr/2006NANT2012.
Full textLeptospirosis is a zoonosis with a worldwide distribution concerning most Mammalians among which humans. Hap1 was purified from an antigenic zone with an apparent molecular mass of 32 kDa extracted from leptospires, bacteria responsible for leptospirosis. Immunization with Hap1 expressed by adenovirus or plasmid induced in gerbils a protection against leptospirosis. Then hap1 gene was expressed by E. Coli to product the recombinant protein rHap. This present work confirms these previous data: Hap1 is secreted during the multiplication of only pathogenic leptospires. Very immunogenic and protective in the natural conditions, this protein in the recombinant form doesn't permit to reproduce protective activity in the natural conditions. So, the purpose of this work was to purify one or many Hap1 naturally forms in order to determine the structural difference to understand this contradiction
McCready, Tara Lyn. "Inhibition of protein phosphatase-1 by endogenous inhibitor proteins and natural product toxins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0032/NQ46885.pdf.
Full textLOBO, DENISE DA SILVEIRA. "PROTEIN-PROTEIN INTERACTION ANALYSIS OF THE DEFENSIN PSD1 FROM PISUM SATIVUM WITH NEUROSPORA CRASSA PROTEINS." PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO, 2006. http://www.maxwell.vrac.puc-rio.br/Busca_etds.php?strSecao=resultado&nrSeq=9447@1.
Full textDefensinas de planta, componentes inatos do sistema imune das plantas, são peptídeos antifúngicos, catiônicos, com estrutura primária rica em cisteína. Evidência dada pela literatura demonstrou que trechos de esfingolipídios complexos na membrana dos fungos, contendo manosildiinositolfosforilceramida e glicosilceramida, são sítios de ligação seletivos para as defensinas de planta isoladas de Dahlia merckii e Raphanus sativus, respectivamente. Entretanto, desconhece-se se as defensinas de planta interagem direta ou indiretamente com alvos intracelulares dos fungos. A fim de identificar interações físicas e diretas do tipo proteína- proteína, um sistema de duplo-híbrido, em levedura, baseado no fator de transcrição GAL4, foi construído utilizando-se como isca, a defensina da planta Pisum sativum, Psd1 (Pisum sativum defensin 1). Proteínas alvos, capazes de interagirem com o peptídeo Psd1, foram detectadas através do rastreamento de uma biblioteca de cDNA do fungo Neurospora crassa. Do resultado deste rastreamento, nove dentre quinze candidatos, selecionados pelo método do duplo-híbrido, foram identificados como proteínas nucleares da N. crassa. Um clone, detectado com alta freqüência neste rastreamento, apresentou homologia de seqüência com a proteína ciclina F, relacionada com o controle do ciclo celular. O ensaio de co-purificação utilizando a proteína conjugada a glutationa S-transferase (GST) validou in vitro o resultado obtido pelo sistema duplohíbrido. Análise por microscopia de fluorescência da Psd1, conjugada a FITC, e, dos núcleos do fungo Fusarium solani, marcados com DAPI, demonstrou in vivo a co-localização da defensina de planta Psd1 com os núcleos do fungo. Para pesquisar o modo de ação da Psd1 ao nível do ciclo celular, utilizou-se o modelo multicelular da retina de ratos neonatais, em desenvolvimento. Neste modelo, a migração nuclear intercinética, correlacionada com as transições de fase de S para M do ciclo celular, foi observada na presença da Psd1. Verificouse que Psd1 impediu a migração nuclear em neuroblastos, parando o ciclo celular na transição de S para G2. Estes resultados revelaram modos de ação da defensina de planta Psd1 sobre a fisiologia nuclear.
Plant defensins, innate components of the plant immune system, are cationic, antifungal peptides, with a cysteine- rich primary structure. Evidence from the literature demonstrated that fungus membrane patches containing complex sphingolipids, mannosyldiinositolphosphorylceramide and glucosylceramides, are selective binding sites for the plant defensins isolated from Dahlia merckii and Raphanus sativus, respectively. However, whether the plant defensins interact directly or indirectly with fungus intracellular targets is unknown. To identify direct physical protein-protein interactions, a GAL4-based yeast two-hybrid system was constructed, using the plant peptide, Pisum sativum defensin 1 (Psd1), as the bait protein. Target proteins, capable of interacting with the bait Psd1, were detected by screening a Neurospora crassa cDNA library. In this screening, nine out of fifteen two-hybrid candidates were identified as N. crassa nuclear proteins. One clone, detected with high frequency in the screening, presented sequence similarity to a N. crassa cyclin F, related to the cell cycle control. The GST pull- down co purification assay corroborated this two-hybrid result in vitro. Fluorescence microscopy analysis of FITC- conjugated Psd1 and DAPI-stained Fusarium solani nuclei demonstrated in vivo the co-localization of the plant peptide Psd1 and the fungus nuclei. We used the developing retina of neonatal rats as a multicellular model to study Psd1 mode of action at the cell cycle level. In this model, we observed in vivo the interkinetic nuclear migration, correlated to the transitions from S to M-phase of the cell cycle, in the presence of the Psd1 peptide. It was shown that Psd1 impaired nuclear migration of neuroblasts by arresting the cell cycle at the S to G2- phase transition. These results revealed modes of action of the plant defensin Psd1 upon the nuclear physiology.
McLaren, Lorna J. "The mouse protein phosphatase inhibitor-1 gene." Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/24958.
Full textJesus, João André Fernandes de. "Aß effects in protein phosphatase 1 complexes." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/21535.
Full textThe brain is a complex structure, which is comprised by neurons capable of communication through synapses. These usually occur between an axon terminal and a dendritic spine of different neurons. The dendritic spines are dynamic structures that allow for a rapid adaptation to different stimuli. PP1 is a phosphatase protein that catalyses the majority of dephosphorylation reactions in the human body. It has different functions that vary, from glycogen metabolism to synaptic regulation. Neurabins (1 and 2) are two PP1 regulator subunits that are structurally and functionally similar to each other. They are highly enriched in the dendritic spines, interacting with several proteins, including PP1, and targeting them to receptors, cytoskeleton or other cellular compartments. Thus, regulating neuronal morphology and synaptic transmission and plasticity. Phactr3 belongs to the actin regulatory protein family, which comprises four members. Phactr3 is involved in cell migration and regulates cytoskeleton dynamics. It interacts with PP1 forming a complex that is controlled by changes in cytoplasmic G-actin concentration, thus, regulating actin cytoskeleton dynamics. Neurodegenerative diseases are usually characterised by the loss of synapses, neural death, gradual loss of cognitive functions and memory. It is believed that Aβ is the major culprit in these changes. Aβ results from an abnormal cleavage of APP, via the amyloidogenic pathway, resulting in the overproduction of toxic peptides. The main aim of this thesis was to evaluate the effects of Aβ on Neurabins and Phactr3 expression, and in PP1 complexes. The results show a slight decrease in neurabins’ expression, and a slight increase in Phactr3 expression. The results also show a decrease in interaction between PP1 and Neurabin-1, possibly due to direct effect of Aβ on Neurabin-1 or the imbalance of phosphatases and kinases, and between PP1 and Phactr3, possibly due to variations of G-actin levels which competes with PP1 to binding with Phactr3. The same changes were not observed in Neurabin-2/PP1 complexes. A possible explanation is that both are differently regulated by several kinases. The results allow us to conclude that Aβ interferes in the expression of all three proteins and in the interaction of Neurabin-1/PP1. However, additional studies are required in order to better understand the physiological relevance of these complexes.
O cérebro é uma estrutura complexa, que é composta por neurónios capazes de comunicar através de sinapses. Estas normalmente ocorrem entre um terminal axónico e espinha dendritica de neurónios diferentes. As espinhas dendriticas são estruturas dinâmicas que permitem uma rápida adaptação a diferentes estímulos. A PP1 é uma proteína fosfatase que catalisa a maioria das desfosforilações que ocorrem no corpo humano. Tem diversas funções, que variam desde metabolismo de glicogénio a regulação sináptica. As neurorabinas (1 e 2) são duas subunidades reguladores da PP1 que são estruturalmente e funcionalmente idênticas entre si. São muito enriquecidas nas espinhas dendriticas e interagem com diversas proteínas, incluindo a PP1, e guiam as proteínas para receptores, citoesqueleto ou outros compartimentos celulares, regulando assim a morfologia neuronal e transmissão e plasticidade sináptica. A Phactr3 pertence à família de proteínas reguladoras de actina, á qual pertencem quatro membros. A Phactr3 está envolvida na migração celular e regula a dinâmica do citoesqueleto. Interage com a PP1, formando um complexo que é controlado por alterações na concentração de G-actina citoplasmática, regulando assim a dinâmica do citoesqueleto. Doenças neurodegenerativas, são normalmente caracterizadas pela perda de sinapses, morte neuronal, e perda gradual de funções cognitivas e memória. Acredita-se que o principal fator responsável por essas anomalias seja o péptido Aβ. Este resulta de uma clivagem anormal de APP, pela via amiloidogénica, resultando numa sobreprodução do péptido tóxico. O objectivo desta tese era avaliar os efeitos de Aβ nos níveis de expressão das neurorabinas e Phactr3, assim como os complexos formados com a PP1. Os resultados mostram uma ligeira diminuição nos níveis de expressão das neurorabinas, e num ligeiro aumento na expressão de Phactr3. Os resultados também mostram uma diminuição na interação do complexo Neurorabina-1/PP1, provavelmente devido a um efeito direto de Aβ sobre Neurorabina-1 ou um desequilíbrio nas fosfatases e cinases, e Phactr3/PP1, provavelmente devido a variação nos níveis de G-actina, que compete com a PP1 para interagir com Phactr3. As mesmas alterações não foram verificadas no complexo Neurorabina-2/PP1. Uma explicação possível é que ambas as proteínas são reguladas de forma diferente por diversas cinases. Estes resultados permitem concluir que Aβ interfere na expressão das três proteínas e nos níveis de interação de Neurabina-1/PP1 e Phactr3/PP1. No entanto são necessários mais estudos para obter uma melhor compreensão da relevância fisiológica destes complexos.
Wallach, Thomas. "A dynamic circadian protein-protein interaction network." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16604.
Full textEssentially all biological processes depend on protein-protein interactions (PPIs). Timing of such interactions is crucial for regulatory function. Although circadian (~24 hrs) clocks constitute fundamental cellular timing mechanisms regulating important physiological processes PPI dynamics on this timescale are largely unknown. To elucidate so far unknown regulatory mechanisms within the circadian clockwork, I have systematically mapped PPIs among 46 circadian components using high-throughput yeast-two-hybrid (Y2H) interaction experiments. I have identified 109 so far uncharacterized interactions and successfully validated a sub-fraction via co-immunoprecipitation experiments in human cells. Among the novel PPIs, I have identified modulators of CLOCK/BMAL1 function and further characterized the role of protein phosphatase 1 (PP1) in the dynamic regulation of BMAL1 abundance. Furthermore, to generate a more comprehensive circadian PPI network, the experimental network was enriched and extended with additional interactions and interaction partners from literature, some of which turned out to be essential for normal circadian dynamics. The integration of circadian mRNA expression profiles allowed us to determine the interaction dynamics within our network. Systematic genetic perturbation studies (RNAi and overexpression in oscillating human cells) revealed a crucial role of dynamic regulation (via rhythmic PPIs) for the molecular clockwork. Furthermore, dynamic modular organization as a pervasive circadian network feature likely contributes to time-of-day dependent control of many cellular processes. Global analysis of the proteome regarding circadian regulation of biological processes via rhythmic PPIs revealed time-of-day dependent organization of the human interactome. Circadian PPIs dynamically connect many important cellular processes like signal transduction and cell cycle, which contribute to temporal organization of cellular physiology.
Turner, Kendrick Bruce. "CELL AND PROTEIN-BASED SENSING SYSTEMS FOR THE DETECTION OF ENVIRONMENTALLY AND PHYSIOLOGICALLY RELEVANT MOLECULES." UKnowledge, 2011. http://uknowledge.uky.edu/chemistry_etds/1.
Full textHill, 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.
Full textTitle from PDF t.p. (viewed June 30, 2010). Additional advisors: Lori McMahon, Stephen Watts. Includes bibliographical references (p. 31-35).
Wang, Shu-Zong. "Cloning and characterization of SAPK interacting protein 1 (SIN1), a type 1 IFN receptor subunit 2 (IFNAR2)-interacting protein /." Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3137761.
Full textSmith, Lucy. "Investigating inhibitors of the IgE:high affinity receptor protein-protein interaction." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/44210.
Full textAstanehe, Arezoo. "Role of Y-box binding protein-1 (YB-1) in breast cancer." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/36668.
Full textDawson, John Francis. "The regulation of protein phosphatase-1 by reversible protein phosphorylation and marine toxins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ34753.pdf.
Full textKilisch, Markus. "Quantitative analysis of protein-protein interactions governing TASK-1/TASK-3 intracellular transport." Doctoral thesis, Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://hdl.handle.net/11858/00-1735-0000-0028-87D8-0.
Full textTian, Wang, la Vega Montserrat Rojo de, Cody J. Schmidlin, Aikseng Ooi, and Donna D. Zhang. "Kelch-like ECH-associated protein 1 (KEAP1) differentially regulates nuclear factor erythroid-2–related factors 1 and 2 (NRF1 and NRF2)." AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2018. http://hdl.handle.net/10150/627124.
Full textWadd, Sarah. "Identification of the cellular proteins which interact with the essential HSV-1 protein IE63." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323269.
Full textBradshaw, Richard Thomas. "Predicting structural and energetic effects of mutations at protein-protein interfaces." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/17988.
Full textShurte, Leah A. "Determining Protein-Protein Interactions of ALS-Associated SOD1." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1464283630.
Full textSidiqi, Mahjooba. "The structure and RNA-binding of poly (C) protein 1." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0077.
Full textSchwartz, Christine. "Muscle LIM protein and Nesprin-1 in Mechanotransduction." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066374/document.
Full textI studied three striated muscle proteins that are participating in two different pathways of mechanotransduction, which is the translation of a physical stimulus into a biochemical signal.When isolated cardiomyocytes are stretched in 2D, MLP shuttles to the nucleus. Without shuttling MLP, these cells fail to respond to the stretch stimulus. Human patients with MLP-mutations develop cardiomyopathies, as well as mice with a knock-out of MLP (MLP-/-). By expressing mutated MLP in neonatal cardiomyocytes of MLP-/- mice, I wanted to elucidate the role of mutant MLP. Surprisingly, MLP did shuttle after stretching of 2D but not 3D cell cultures. Although I could not solve this issue, I prepared the setup for subsequent experiments.Nesprins are part of the nuclear envelope (NE) spanning LINC complex, which connects the cytoskeleton with the nucleus. Myoblasts from patients with mutations in Nesprins or LINC-associated Lamins displayed deformed nuclei and had defects in mechanosensitive responses with an elevated level of stress fibers and focal adhesions on soft surfaces. This phenotype could be rescued by knock-down of formin FHOD1, a downstream target of ROCK and SRC, which also were highly active in the mutant cells. While mutations in Nesprins and Lamins are thought to lead to mechanical instability of the NE, these results indicate that signaling pathways through the NE are disturbed as well
Xu, Xiaodong. "Expression and characterization of HIV-1 envelope protein." Thesis, University of Reading, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500515.
Full textNicoli, Francesco. "Immunomodulatory properties of the HIV-1 Tat protein." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-174938.
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