Tesis sobre el tema "Regulation of Cdc42"
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Ravichandran, Yamini. "Cdc42 isoforms : localization, functions and regulation". Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS405.
Texto completoMutations in proteins cause diverse developmental disorders, particularly for individuals with rare diseases or for whom a unifying clinical diagnosis is unknown. Cdc42 is one such protein; vital for establishing cell polarity, a crucial step in many biological processes such as cell migration, division and immune responses. Not surprisingly, mutations in Cdc42 cause a range of diseases such as growth dysregulation, facial dysmorphism and neurodevelopmental, immunological, and hematological abnormalities. In vertebrates there are two isoforms of Cdc42. The first being the ubiquitous isoform, has almost exclusively been studied and the role of the second isoform, being the brain isoform, is largely unknown. We have shown that the two isoforms are localized differently in cells. The ubiquitous isoform is mostly found in the cell cytoplasm and at the plasma membrane, while the Brain isoform localizes at the Golgi apparatus and on intracellular vesicles. We have also shown that the two isoforms carry out different functions during cell migration, suggesting that the differences between these two isoforms which only differs by the last 10 amino acids are responsible for their distinct localisation and function. Interestingly, a mutation in the C-ter sequence of Cdc42 ubiquitous isoform alters Cdc42 localisation and causes a generalized pustular psoriasis disease. Two main objectives have been studied in this project 1) the impact of the last amino acids of the protein in Cdc42 localization; and 2) new regulatory mechanisms of Cdc42 responsible for its intracellular localization. These findings will bring a better understanding of pathologies related to Cdc42 mutations
Lu, Ruifeng y Jean M. Wilson. "Rab14 specifies the apical membrane through Arf6-mediated regulation of lipid domains and Cdc42". NATURE PUBLISHING GROUP, 2016. http://hdl.handle.net/10150/622499.
Texto completoMurali, Arun [Verfasser]. "Role of XIAP in ubiquitin mediated regulation of Cdc42 and other Rho GTPases / Arun Murali". Mainz : Universitätsbibliothek Mainz, 2019. http://d-nb.info/1191286649/34.
Texto completoFrancis, Monika K. "Regulation of GRAF1 membrane sculpting function during cell movement". Doctoral thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-111213.
Texto completoMutavchiev, Delyan Rumenov. "Regulation of fission yeast cell polarity by stress-response pathways". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29006.
Texto completoLanger, Torben [Verfasser]. "Der Einfluss des Tumorsuppressorproteins Merlin auf die Regulation der beiden Rho-GTPasen Rac2 und Cdc42 / Torben Langer". Ulm : Universität Ulm. Medizinische Fakultät, 2013. http://d-nb.info/1036215121/34.
Texto completoYe, Xiangcang. "Role of a CDC42 homologous gene in the regulation of cell polarity and morphogenic transitions in Wangiella dermatitidis /". Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.
Texto completoPrimeau, Martin. "Novel mechanisms of regulation of the Cdc42 GTPase- activating protein CdGAP/ARHGAP31, a protein involved in cell migration and adhesion". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96901.
Texto completoLes Rho GTPases forment une famille d'enzymes qui contrôlent de nombreux processus cellulaires, tels que la migration cellulaire et la prolifération, grâce à leurs effets sur le cytosquelette, le trafic membranaire et l'adhésion cellulaire. L'activité de ces interrupteurs moléculaires est modulée par les protéines activatrices de GTPases (GAPs), un groupe de régulateurs négatifs qui inclu CdGAP (Cdc42-GTPase activating protein). Cette protéine régule négativement les Rho GTPases Cdc42 et Rac1 de façon spécifique. Dans la présente étude, nous montrons que CdGAP est régulée par des interactions lipidiques, protéiques et intramoléculaire. Premièrement, nous démontrons qu'une région polybasique (PBR), précédant le domaine GAP et retrouvée dans plusieurs GAP de la famille Rho, est requise pour l'association spécifique de CdGAP avec le phosphatidilinositol-3,4,5-trisphosphate (PI(3,4,5)P3). Nos résultats suggèrent que l'activation des GAP requiert la liaison du PI(3,4,5)P3 à CdGAP dans un contexte in vitro et un PBR intact pour que CdGAP provoque ses effets GAP-dépendants dans un contexte in vivo. Deuxièmement, nous caractérisons le site de liaison du régulateur négatif de CdGAP Intersectin-1. Ce site est localisé dans le domaine riche en résidus basiques (BR) de CdGAP. Nous suggérons que cette interaction, médiée par le domaine SH3D d'Intersectin, requiert de un à trois résidus lysine dans le domaine BR de CdGAP. Troisièmement, nous montrons que CdGAP est régulé de manière négative par son propre domaine C-terminal. Cette observation fait partie d'une étude qui associe deux mutations humaines du gène CdGAP à un syndrôme présentant une combinaison d'aplasie cutis congenita (ACC) et de malformation des doigts et des orteils (TTLD). Les gènes mutants produisent des protéines tronquées qui ont une activité GAP supérieure à la protéine de type sauvage. Nous montrons que ce C-terminal peut lier le domaine GAP de CdGAP, supportant un modèle expliquant comment l'absence du C-terminal induit ce syndrome. En bref, ce travail présente un nouvel aperçu des mécanismes de régulation de CdGAP, une protéine impliquée dans la migration cellulaire et dans l'adhésion des cellules en plus d'être directement impliquée dans une maladie humaine.
Ofo, Enyinnaya. "Flourescent biosensor-based, Cdc42 activity imaging for understanding the regulation of Epidermal Growth Receptor (EGFR) signalling in head and neck cancer". Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/flourescent-biosensorbased-cdc42-activity-imaging-for-understanding-the-regulation-of-epidermal-growth-receptor-egfr-signalling-in-head-and-neck-cancer(32081fef-10f1-4a3e-ac33-67afbbf78376).html.
Texto completoBretou, Marine. "Regulation of the dynamics of the fusion pore : importance of the SNARE protein synaptobrevin 2 and of the Rho GTPase Cdc42". Paris 7, 2010. http://www.theses.fr/2010PA077157.
Texto completoExocytosis ends with the formation of a fusion pore. The initial pore is narrow, only small molecules flow through it. The pore then enlarges, releasing larger secretory products. I studied the role of two proteins on the dilation of the pore: the SNARE protein synaptobrevin 2 (Syb2), and the Rho GTPase Cdc42. Zippering of SNAREs in opposed membranes might give energy to catalyze fusion. Inserting a linker between the SNARE core and the transmembrane domain of Syb2 did not modify the frequency of exocytotic events detected by amperometry at 1|jM free [Ca2+] but prevented the occurrence of an extra component of release at higher [Ca2+]. Analysis of these events led to their classification into two groups, due to the rate and extent of dilation of the pore; lengthening Syb2 reduced the population of fast spikes, leaving the slow one unchanged. Slow fusion events might be due to a partial zippering of the SNAREpin while fast fusion events require a tight one, i. E. A short intermembrane distance to assure rapid dilation of the pore. Cdc42 controls actin dynamics. TIRFM experiments showed that its silencing in BON cells reduced the number of granules undergoing full fusion, with little effect on their recruitment and docking at the membrane. Using amperometry, we showed that this silencing reduced the number of high spikes due to fast and complete dilation of the pore, and increased stand-alone foot signals reflecting pores failing to enlarge. Increasing membrane tension rescued the effects of silencing while decreasing it through actin depolymerization mimicked Cdc42 silencing. Cdc42 might control fusion pore dilation by modulating membrane tension
Meir, Michael [Verfasser] y Nicolas [Akademischer Betreuer] Schlegel. "Bedeutung der desmosomalen Adhäsion und Rolle der Rho-GTPasen RhoA, Rac1 und Cdc42 für die Regulation der Darmbarriere / Michael Meir. Betreuer: Nicolas Schlegel". Würzburg : Universität Würzburg, 2013. http://d-nb.info/1107802563/34.
Texto completoLeung, Daisy W. "Biochemical and biophysical characterization of the allosteric equilibrium of the Wiskott-Aldrich Syndrome protein". Access to abstract only; dissertation is embargoed until after 12/20/2006, 2005. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=131.
Texto completoAnnan, Robert Bruce. "Roles and regulation of «Saccharomyces cerevisiae» Rho-type GTPases Rho5p and Cdc42p". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32262.
Texto completoLa famille eucaryote des GTPases Rho agit à titre de régulateur principal de nombreux processus biologiques, incluant la polarisation de la morphologie cellulaire, le transport membranaire, la transcription et la voie de signalisation MAPK. En tant que GTPases, les protéines Rho jouent un rôle de controlleurs moleculaires qui, sous la forme liée au GTP, transmettent les signaux en amont à une variété d'effecteurs en aval, générant ainsi les réponses cellulaires appropriées. Étant des acteurs principaux de la signalisation, les protéines Rho sont sujettes à une régulation précise. La régulation du cycle GTP-GDP par les membres de la famille Rho a été largement caractérisée. Cependant, les GTPases Rho participent à une variété de mécanismes qui, dans plusieurs cas, sont encore aujourd'hui sous-étudiés. Cette étude examine plus particulièrement les rôles et la régulation de deux GTPases Rho chez la levure Saccharomyces cerevisiae, Rho5p and Cdc42p. Dans un premier temps, nous décrivons la régulation de la signalisation de Rho5p par la phosphorylation et l'ubiquitination, ceci étant le premier exemple de régulation post-traductionnelle d'une GTPase de type Rho chez la levure. Cette régulation est arbitrée par un module impliquant la kinase Npr1p et son inhibiteur MSi1p. Nous démontrons également une interaction génétique entre RHO5 et STE50. En effet, une délétion au niveau de STE50 combinée à l'expression d'un allèle activé de RHO5 résulte en une sensibilité osmotique. De plus, nous identifions Rgd2p comme étant le RhoGAP pour Rho5p in vivo. Dans un deuxième temps, nous décrivons un rôle pour Rho5p dans l'activation d
Aldharee, Hitham Abdulrahman. "Role of ERK3 in Regulating RhoGDI1-PAKs Signaling Axis". Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1498007023965276.
Texto completoBöhm, Stefanie. "The Cdc48 Shp1 complex mediates cell cycle progression by positive regulation of Glc7". Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-154660.
Texto completoRumpf, Sebastian. "Regulation des Abbaus von Cdc48-Substraten durch die antagonistischen Aktivitäten von Ufd2 und Ufd3". Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-54278.
Texto completoJensen, Bryan. "Regulation of the G1 to S-phase transition in S. cerevisiae by CDC4 /". Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/10257.
Texto completoEwert-Krzemieniewska, Katarzyna. "Investigation into the regulation of DNA repair by the S. pombe cell cycle kinase Cdc2-cyclinB". Thesis, Bangor University, 2009. https://research.bangor.ac.uk/portal/en/theses/investigation-into-the-regulation-of-dna-repair-by-the-spombe-cell-cycle-kinase-cdc2cyclinb(71f3241d-b969-4ff1-9b16-47161f91b755).html.
Texto completoKöhler, Tim. "Regulation of growth and development by the small GTPase Cdc42p and the transcription factor Tec1p in Saccharomyces cerevisiae". [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969652704.
Texto completoBöhm, Stefanie [Verfasser] y Stefan [Akademischer Betreuer] Jentsch. "The Cdc48 Shp1 complex mediates cell cycle progression by positive regulation of Glc7 / Stefanie Böhm. Betreuer: Stefan Jentsch". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2011. http://d-nb.info/1032131713/34.
Texto completoMavrakis, Konstantinos J. "Functional analysis of DEF6 and def8 revealed DEF6 as a novel activator of Rac, Cdc42 and Rho GTPases regulating cell morphology". Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404145.
Texto completoGao, Yanzhe. "Regulation of The DNA Unwinding Element Binding Protein DUE-B in The Cell". Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1355250568.
Texto completoBryant, Victoria. "CMG Helicase Assembly and Activation: Regulation by c-Myc through Chromatin Decondensation and Novel Therapeutic Avenues for Cancer Treatment". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6191.
Texto completoQuaresma, Paula Gabriele Fernandes 1987. "Estudo da regulação da proteína CDC2-Like Kinase (Clk2) em hipotálamo e fígado de camundongos controles e obesos = CDC2-Like Kinase (Clk2) hypothalamic and hepatic regulation in lean and obese mice". [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311558.
Texto completoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-21T14:12:45Z (GMT). No. of bitstreams: 1 Quaresma_PaulaGabrieleFernandes_M.pdf: 949361 bytes, checksum: 237d0acc0b5bc5358adba045381b4a92 (MD5) Previous issue date: 2012
Resumo: O hipotálamo é um órgão crucial na regulação do balanço energético por integrar sinais hormonais e nutricionais de órgão periféricos. O hormônio produzido pelo pâncreas - insulina - e o hormônio derivado de células adiposas - leptina- reconhecidamente, agem no SNC controlando a ingestão alimentar e o gasto energético. Recentemente foi demonstrado que a fosforilação em treonina 343 da proteina Cdc2-like kinase 2 (Clk2) é induzida pela sinalização de PI3-q/Akt no fígado. Esta regulação envolve a repressão de genes que controlam a gliconeogênese e produção de glicose hepática, levando a hipoglicemia. Porém, não há informações de que a insulina ou a leptina podem regular a Clk2 no hipotálamo in vivo. Camundongos das linhagens Swiss, db/db e C57/BL6J com oito semanas de idade foram utilizados nos experimentos. Nossos resultados mostraram que a Clk2 é expressa e regulada por insulina e leptina em hipotálamo e também que a inibição da Clk2 causou aumento da adiposidade e ingestão alimentar, diminuição do gasto energético e alterações na expressão de neuropeptídeos e do metabolismo de glicose. Além disso, a fosforilação no sítio treonina 343 da Clk2 está diminuída em animais com obesidade induzida por dieta e geneticamente obesos (db/db). A avaliação da gliconeogênese hepática em animais com a proteína Clk2 inibida via ICV mostrou uma tendência ao aumento da produção hepática de glicose, revelando uma possível participação da proteína Clk2 no controle hipotalâmico da gliconeogênese hepática. Sendo assim, podemos sugerir que a Clk2 hipotalâmica é importante no controle do balanço energético pois sua inibição acarreta obesidade acompanhada por aumento da ingestão alimentar e diminuição do gasto energético, e também podemos sugerir um papel no controle hipotalâmico da produção hepática de glicose
Abstract: The hypothalamus plays an important role in the regulation of whole-body energy balance by integrating nutrients and hormones signals from peripheral inputs. The pancreatic hormone - insulin - and the adipocyte hormone - leptin - are known to act in the CNS controlling food intake and energy expenditure. Leptin and insulin signaling regulate anorexigenic neuropeptide expression. Recently, it was shown that Cdc2-like kinase 2 (Clk2) threonine 343 phosphorylation is induced by PI3K/Akt signaling in the liver. This regulation is involved in the repression of gluconeogenic gene expression and hepatic glucose output leading to hypoglycemia. Thus, it was not shown if insulin or leptin are able to regulate Clk2 threonine 343 phosphorylation in the hypothalamus in vivo. Swiss, db/db and C57/BL6J mice eight-weeks-old were used to proceed the experiments. Our data show that Clk2 is expressed and regulated by insulin and leptin in hypothalamus and hypothalamic Clk2 inhibition increased adiposity and food intake, decreased energy expenditure and disrupted neuropeptides expressions and glucose metabolism. Indeed, Clk2 threonine 343 phosphorylation is impaired in the hypothalamus of DIO and db/db mice. Hepatic gluconeogenesis was evaluated and showed increase in ICV inhibited Clk2 mice, it is plausible that Clk2 participates of hypothalamic control of hepatic gluconeogenesis. We suggest that hypothalamic Clk2 is crucial to control energy balance because its inhibition triggers obesity accompanied by increased food intake, decreased energy expenditure and increased hepatic gluconeogenesis
Mestrado
Clinica Medica
Mestra em Ciências
Winters, Zoe Ellen. "The role of p53 in the regulation of Cdc2 and cyclin B1 in radiation-induced G2 arrest in human cells". Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299469.
Texto completoBirot, Adrien. "Regulation of fission yeast cohesin by the Cyclin Dependent Kinase PeF1". Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0386/document.
Texto completoCohesin is a highly conserved ring-shaped protein complex made of four essential subunits: Psm1, Psm3, Rad21 and Psc3. By its ability to capture DNA molecules within its ring-like structure, cohesion plays a key role in many cellular processes such as chromosome segregation, DNA damage signalling and repair, transcriptional gene regulation and nuclear organization. To ensure all of its biological functions, cohesin must be tightly regulated in space and time. This regulation relies in part on the control of cohesin binding to chromatin (DNA capture). Cohesin recruitment to chromatin requires the action of a “loading complex” made of two conserved and essential proteins named Mis4 and Ssl3 in the fission yeast. How this complex regulates where and when DNA capture by the cohesin ring must occur remains poorly understood. To identify regulators of cohesin binding to chromatin we have performed a genetic screen for suppressors of the thermosensitive mutation mis4-367. This genetic screen has led to the identification of the cyclin-dependent-kinase Pef1 that acts as a negative regulator of sister chromatids cohesion may be bynegatively controlling cohesin binding to chromatin. Strong experimental evidences indicate that Pef1 exerts its function at least in part by directly phosphorylating the Rad21 subunit of the cohesin complex. Interestingly, a genetic screen made in parallel identified the Pph3/Psy2 phosphatase as implicated in the establishment of sister chromatid cohesion by regulating Rad21 dephosphorylation. Strikingly, the control of Rad21 phosphorylation status appears central to the cohesion process in the fission yeast S. pombe
Bhaduri, Samyabrata. "Regulation of CDK1 Activity during the G1/S Transition in S. cerevisiae through Specific Cyclin-Substrate Docking: A Dissertation". eScholarship@UMMS, 2014. http://escholarship.umassmed.edu/gsbs_diss/871.
Texto completoKommajosyula, Naveen. "Regulation of DNA Replication Origins in Fission Yeast: A Dissertation". eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/436.
Texto completoBorgne, Annie. "Etude de la regulation de cdc2/cycline b a la transition prophase/metaphase de l'ovocyte d'etoile de mer. Caracterisation des effets de la roscovitine, un nouvel inhibiteur chimique de cdk". Paris 6, 1998. http://www.theses.fr/1998PA066422.
Texto completoVendrell, Arasa Alexandre. "SCF cdc4 regulates msn2 and msn4 dependent gene expression to counteract hog1 induced lethality". Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7153.
Texto completoTambé hem observat que la mort cel·lular causada per l'activació sostinguda de Hog1 és deguda a una inducció d'apoptosi. L'apoptosi induïda per Hog1 és inhibida per la mutació al complexe SCFCDC4. Per tant, la via d'extensió de la vida és capaç de prevenir l'apoptosi a través d'un mecanisme desconegut.
Sustained Hog1 activation leads to an inhibition of cell growth. In this work, we have observed that the lethal phenotype caused by sustained Hog1 activation is prevented by SCFCDC4 mutants. The prevention of Hog1-induced cell death by SCFCDC4 mutation depends on the lifespan extension pathway. Upon sustained Hog1 activation, SCFCDC4 mutation increases Msn2 and Msn4 dependent gene expression that leads to a PNC1 overexpression and a Sir2 deacetylase hyperactivation. Then, hyperactivation of Sir2 is able to prevent cell death caused by sustained Hog1 activation.
We have also observed that cell death upon sustained Hog1 activation is due to an induction of apoptosis. The apoptosis induced by Hog1 is decreased by SCFCDC4 mutation. Therefore, lifespan extension pathway is able to prevent apoptosis by an unknown mechanism.
Perl, Abbey Leigh. "Leveraging Small Molecule Activators of Protein Phosphatase 2A (PP2A) toElucidate PP2As Role in Regulating DNA Replication and Apoptosis". Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1574418174603893.
Texto completoGrewal, Navneet. "Identification of amino acids involved in Cdc42-calmodulin interaction and regulation of Cdc42 activation". 2015. http://hdl.handle.net/1993/30716.
Texto completoOctober 2015
Elsaraj, Sherif. "Regulation of Rac1 and Cdc42 GTPases through direct interaction with calmodulin". 2006. http://hdl.handle.net/1993/20344.
Texto completoMeir, Michael. "Bedeutung der desmosomalen Adhäsion und Rolle der Rho-GTPasen RhoA, Rac1 und Cdc42 für die Regulation der Darmbarriere". Doctoral thesis, 2013. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-85111.
Texto completoThe integrity of intestinal barrier function is essential. In some diseases intestinal barrier breakdown can lead to contamination by bacteria in the human body. In our research we investigated on the one hand the relevance of desmosomal adhesion and the role of Rho GTPases in regulation of intestinal barrier function. For our research we characterized Caco2 cells. We could reveal, that 14 days after confluence Caco2 cells form the "terminal bar" and show a barrier function similar to rat muccosa. To address the relevance ofdesmosomal adhesion we applied an antibody directed against the extracellular domain (Dsg2 ED) in order to test whether impaired Dsg2-mediated adhesion affects intestinal epithelial barrier functions in vitro. This antibody was capable to specifically block Dsg2 interaction. The application of Dsg2 ED led to a fragmentation in tight junction proteins and an impaired barrier function as revealed by an increase of permeability and a decrease of transepithelial electrical resistance. We could show that Dsg2 mediated adhesion is essential for intestinal barrier function. Second we investigated the role of the Rho-GTPases. We modulated the activity of Rho-GTPases by the application of bacterial toxins like CNF-1, CNF-y, toxin B, C3-TF and LT and mediators like Y27632. We could show that an increase as well as a decrease of RhoA activity led to a fragmentation of tight junction proteins as revealed by immunostaining. These morphologic changes correlated with a significant increase of permeability as well as a decreased transepithelial electrical resistance. Apart from that an increased activation of Rac1 and Cdc42 led to a stabilization of intestinal barrier function with an increase of transepithelial electrical resistance and a decrease in permeability. A destabilization of intestinal barrier function was shown after a reduction of Rac1 and Cdc42 activity. Under these conditions we could observe a fragmentation of tight junction and adherens junction proteins. Furthermore decreased Rac1 and Cdc42 activity led to an increased permeability and a decreased transepithelial electrical resistance. In the final analysis this publication led to new insights in the complex regulation of intestinal barrier functions and therefore can possible lead to new targets in the therapy of impaired intestinal barrier function
Diederich, Wendy-Anneliese [Verfasser]. "Apolipoprotein AI und HDL3 inhibieren die Migration humaner Monozyten durch Induktion der Cholesterinefflux und Regulation von CDC42 / vorgelegt von Wendy-Anneliese Diederich". 2006. http://d-nb.info/980289513/34.
Texto completoKöhler, Tim. "Regulation of Growth and Development by the Small GTPase Cdc42p and the Transcription Factor Tec1p in Saccharomyces cerevisiae". Doctoral thesis, 2003. http://hdl.handle.net/11858/00-1735-0000-0006-AE6F-C.
Texto completoDeplazes, Joëlle [Verfasser]. "Die Rolle der kleinen Rho-GTPasen Rac1, Rho und Cdc42 in der Regulation der Motilität und Invasion von Tumorzellen mit einer Mutation in E-Cadherin / Joëlle Deplazes". 2009. http://d-nb.info/995844062/34.
Texto completoKalwat, Michael Andrew. "F-Actin regulation of SNARE-mediated insulin secretion". Thesis, 2013. http://hdl.handle.net/1805/3624.
Texto completoIn response to glucose, pancreatic islet beta cells secrete insulin in a biphasic manner, and both phases are diminished in type 2 diabetes. In beta cells, cortical F-actin beneath the plasma membrane (PM) prevents insulin granule access to the PM and glucose stimulates remodeling of this cortical F-actin to allow trafficking of insulin granules to the PM. Glucose stimulation activates the small GTPase Cdc42, which then activates p21-activated kinase 1 (PAK1); both Cdc42 and PAK1 are required for insulin secretion. In conjunction with Cdc42-PAK1 signaling, the SNARE protein Syntaxin 4 dissociates from F-actin to allow SNARE complex formation and insulin exocytosis. My central hypothesis is that, in the pancreatic beta cell, glucose signals through a Cdc42-PAK1-mediated pathway to remodel the F-actin cytoskeleton to mobilize insulin granules to SNARE docking sites at the PM to evoke glucose stimulated second phase insulin secretion. To investigate this, PAK1 was inhibited in MIN6 beta cells with IPA3 followed by live-cell imaging of F-actin remodeling using the F-actin probe, Lifeact-GFP. PAK1 inhibition prevented normal glucose-induced F-actin remodeling. PAK1 inhibition also prevented insulin granule accumulation at the PM in response to glucose. The ERK pathway was implicated, as glucose-stimulated ERK activation was decreased under PAK1-depleted conditions. Further study showed that inhibition of ERK impaired insulin secretion and cortical F-actin remodeling. One of the final steps of insulin secretion is the fusion of insulin granules with the PM which is facilitated by the SNARE proteins Syntaxin 4 on the PM and VAMP2 on the insulin granule. PAK1 activation was also found to be critical for Syntaxin 4-F-actin complex dynamics in beta cells, linking the Cdc42-PAK1 signaling pathway to SNARE-mediated exocytosis. Syntaxin 4 interacts with the F-actin severing protein Gelsolin, and in response to glucose Gelsolin dissociates from Syntaxin 4 in a calcium-dependent manner to allow Syntaxin 4 activation. Disrupting the interaction between Syntaxin 4 and Gelsolin aberrantly activates endogenous Syntaxin 4, elevating basal insulin secretion. Taken together, these results illustrate that signaling to F-actin remodeling is important for insulin secretion and that F-actin and its binding proteins can impact the final steps of insulin secretion.
Weidmann, Rolf Günter [Verfasser]. "Endothel und Regulation der Inflammation : Überexpression inaktiver Mutanten der kleinen GTP-bindenden Proteine RhoA/Rac1/Cdc42 inhibiert die LPS-induzierte Expression von Interleukin-8/CXCL8 in humanen mikrovaskulären Endothelzellen / von Rolf Günter Weidmann". 2005. http://d-nb.info/978803736/34.
Texto completoPollok, Sibyll [Verfasser]. "Untersuchungen zur Regulation des humanen Replikationsfaktors Cdc45 / von Sibyll Pollok". 2007. http://d-nb.info/985809736/34.
Texto completoRumpf, Sebastian [Verfasser]. "Regulation des Abbaus von Cdc48-Substraten durch die antagonistischen Aktivitäten von Ufd2 und Ufd3 / vorgelegt von Sebastian Rumpf". 2006. http://d-nb.info/980478286/34.
Texto completoKolawa, Natalie J. "Proteomic Analysis of the Cdc48/Ubx Network Identifies a Role for Ubx2 in the Regulation of Lipid Biosynthesis". Thesis, 2013. https://thesis.library.caltech.edu/7761/1/kolawa_natalie_2013_thesis.pdf.
Texto completoCdc48/p97 is an essential, highly abundant hexameric member of the AAA (ATPase associated with various cellular activities) family. It has been linked to a variety of processes throughout the cell but it is best known for its role in the ubiquitin proteasome pathway. In this system it is believed that Cdc48 behaves as a segregase, transducing the chemical energy of ATP hydrolysis into mechanical force to separate ubiquitin-conjugated proteins from their tightly-bound partners.
Current models posit that Cdc48 is linked to its substrates through a variety of adaptor proteins, including a family of seven proteins (13 in humans) that contain a Cdc48-binding UBX domain. As such, due to the complexity of the network of adaptor proteins for which it serves as the hub, Cdc48/p97 has the potential to exert a profound influence on the ubiquitin proteasome pathway. However, the number of known substrates of Cdc48/p97 remains relatively small, and smaller still is the number of substrates that have been linked to a specific UBX domain protein. As such, the goal of this dissertation research has been to discover new substrates and better understand the functions of the Cdc48 network. With this objective in mind, we established a proteomic screen to assemble a catalog of candidate substrate/targets of the Ubx adaptor system.
Here we describe the implementation and optimization of a cutting-edge quantitative mass spectrometry method to measure relative changes in the Saccharomyces cerevisiae proteome. Utilizing this technology, and in order to better understand the breadth of function of Cdc48 and its adaptors, we then performed a global screen to identify accumulating ubiquitin conjugates in cdc48-3 and ubxΔ mutants. In this screen different ubx mutants exhibited reproducible patterns of conjugate accumulation that differed greatly from each other, pointing to various unexpected functional specializations of the individual Ubx proteins.
As validation of our mass spectrometry findings, we then examined in detail the endoplasmic-reticulum bound transcription factor Spt23, which we identified as a putative Ubx2 substrate. In these studies ubx2Δ cells were deficient in processing of Spt23 to its active p90 form, and in localizing p90 to the nucleus. Additionally, consistent with reduced processing of Spt23, ubx2Δ cells demonstrated a defect in expression of their target gene OLE1, a fatty acid desaturase. Overall, this work demonstrates the power of proteomics as a tool to identify new targets of various pathways and reveals Ubx2 as a key regulator lipid membrane biosynthesis.
Thattikota, Yogitha. "Regulation of chromosome condensation in Saccharomyces cerevisiae during mitosis". Thèse, 2017. http://hdl.handle.net/1866/19316.
Texto completoKöhler, Tim [Verfasser]. "Regulation of growth and development by the small GTPase Cdc42p and the transcription factor Tec1p in Saccharomyces cerevisiae / vorgelegt von Tim Köhler". 2003. http://d-nb.info/969652704/34.
Texto completoVan, Zijl Magdalena Catherina. "In vitro effects of 2-methoxyestradiol, an endogenous estrogen, on MCF-12A and MCF-7 cell cycle progression". Diss., 2006. http://hdl.handle.net/2263/26594.
Texto completoDissertation (MSc (Physiology))--University of Pretoria, 2008.
Physiology
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