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Gopalbhai, Kailesh. "Régulation négative des MAP kinase kinases par phosphorylation /". [Montréal] : Université de Montréal, 2003. http://wwwlib.umi.com/cr/umontreal/fullcit?pNQ92759.
Pełny tekst źródła"Thèse présentée à la Faculté des études supérieures en vue de l'obtention du grade de Philosophiae Doctor en Pharmacologie" Version électronique également disponible sur Internet.
Sengar, Ameet Singh. "Mkh1, a novel MAP kinase kinase kinase in Schizosaccharomyces pombe". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq20852.pdf.
Pełny tekst źródłaGatesman, Ammer Amanda. "PKCalpha direct cSrc activation and podosome formation through the adaptor protein AFAP-110". Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3762.
Pełny tekst źródłaTitle from document title page. Document formatted into pages; contains vii, 350 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 322-346).
Nadeau, Philippe. "Régulation de la MAP3-kinase Ask1 par oxydoréduction". Doctoral thesis, Université Laval, 2009. http://hdl.handle.net/20.500.11794/21223.
Pełny tekst źródłaJean, Steve. "Caractérisation fonctionnelle de nouveaux partenaires protéiques des kinases xPAK1 et xMLK2 chez Xenopus laevis". Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25722/25722.pdf.
Pełny tekst źródłaVaglio, Philippe. "Etude de la relation structure-fonction de la protéine kinase CK2 par mutagenèse dirigée des résidus basiques conservés". Montpellier 1, 1996. http://www.theses.fr/1996MON1T029.
Pełny tekst źródłaWan, Omar Wan Bayani. "Studies into interactions between MAP kinase and MAP kinase kinase proteins of Arabidopsis". Thesis, Heriot-Watt University, 2011. http://hdl.handle.net/10399/2490.
Pełny tekst źródłaMazharian, Alexandra. "Rôle complémentaire des MAP Kinases ERK2, p38 et JNK1 dans l'activation plaquettaire". Paris 7, 2007. http://www.theses.fr/2007PA077217.
Pełny tekst źródłaThe MAP Kinases belong to a serine/threonine kinase family that include the "Extracellular signal-Regulated Kinases" (ERKs), p38MAPKs and the "c-jun N-terminal Kinases" (JNKs). The study of the MAP Kinase in platelets allows identifying new targets and new rôles in particular in the haemostasis and thrombosis. In the first study, we describe complementary roles of ERK2 and p38MAPK in platelet adhésion and spreading over a collagen matrix. The role of ERK2 is dependent of blood flow and vWF/GPIb interaction. In contrast, the role of the p38MAFK in platelet adhesion is independent of blood flow and involved the α2β1 integrin. In the second study, we show the ERK2 and p38MAPK are involved in platelet spreading on a fibrinogen matrix after PAR4 stimulation. Activation of p38MAPK, required for actin polymerization, is dependent of ADP signalling through its receptor P2Y12, In contrast, ERK2, required for Myosin Light Chain phosphorylation, is dependent on integrin αllbβ3 outside-in signalling and the Rho pathway, Both MAP Kinases act on cytoskeleton rearrangement required for platelet spreading, Lastly, we show for the first time a role of JNKl in platelet aggregation and secretion induced by low concentrations of collagen. In addition, JNKl is required for thrombus growth at high shear involving activation of integrin αllbβ3 and vWF/GPIb interaction. Finally, in vivo, JNKl is involved in a mouse model of arterial thrombosis. In conclusions, our works bring us new knowledge as for the roles of MAP Kinases ERK2, p38MAPK and JNKl in the different stages of platelet activation
Beggs, James. "The MAP-kinase interacting kinases (Mnks) as targets in cancer". Thesis, University of Southampton, 2015. https://eprints.soton.ac.uk/390651/.
Pełny tekst źródłaChetoui, Nizar. "Caractérisation du rôle de la protéine kinase MEK1 dans les voies de transduction des MAP kinases". Thesis, Université Laval, 2005. http://www.theses.ulaval.ca/2005/22589/22589.pdf.
Pełny tekst źródłaSamuels, Ivy S. "The roles of ERK₁ and ERK₂ MAP kinase in neural development and disease". Cleveland, Ohio : Case Western Reserve University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1214495630.
Pełny tekst źródłaWaskiewicz, Andrew Jan. "Mitogen-activated protein kinase : evolutionary conservation and activation of downstream kinases /". Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/9216.
Pełny tekst źródłaSimard-Bisson, Carolyne. "Rôles de la "Dual leucine zipper-bearing Kinase" dans la réorganisation des microtubules et la différenciation des kératinocytes humains". Doctoral thesis, Université Laval, 2015. http://hdl.handle.net/20.500.11794/28201.
Pełny tekst źródłaSkin barrier function greatly depends on proper keratinocyte differentiation in the epidermis. During this process, many changes occur within the cell such as decrease in cell proliferation, cytoskeleton reorganization, changes in gene expression, nucleus and organelles elimination as well as cornified envelope formation. Keratinocyte differentiation must be finely orchestrated since misregulation of this process may lead to pathological conditions. The Dual Leucine zipper-bearing Kinase (DLK) is a Mitogen-Activated Protein Kinase Kinase Kinase showing a strong expression in the granular layer, the last layer composed of living cells before reaching the cornified layer. Previous studies revealed DLK capacity to induce keratinocyte terminal differentiation process. However, how DLK promotes such an event remains unknown. The main objective of this thesis is to identify mechanisms and potential effectors of the DLK-induced keratinocyte differentiation. Our hypothesis is that DLK is required for keratinocyte differentiation by promoting microtubule stabilization as well as the expression or the activity of transcription factors involved in this process. In order to test our hypothesis, a tissue-engineered skin (TES) model with a reduced DLK expression was produced using a RNA interference approach. Impaired distribution of cornified envelope proteins such as filaggrin and transglutaminase 1 as well as reduced granular and cornified layers were observed in TES with reduced DLK expression. In those samples, immunofluorescence and electron microscopy analyses pointed out desmosomal and tight junctional defects suggesting a role for DLK in the maintenance of these types of cell junctions. The impact of DLK expression on microtubules was also studied in TES with reduced DLK expression and in keratinocytes in culture overexpressing DLK following gene transduction using adenoviral vectors. These studies led to the conclusion that DLK not only promotes but is also required for microtubules reorganization and stabilization to cell periphery. To explain DLK capacity to induce such a process, effects of DLK depletion or overexpression on microtubule regulators such as LIS1 and HSP27 were investigated by immunofluorescence staining. These analyses revealed that DLK induces and is required for LIS1 and HSP27 relocalization to cell periphery. In additional studies, our results show that DLK expression in normal human keratinocytes in culture not only promotes HSP27 distribution to cell periphery but also induces HSP27 insolubilization and phosphorylation in an ERK-dependent manner. In order to more precisely define the role of microtubules in keratinocyte differentiation process, TES were treated with nocodazole, a microtubule depolymerizing agent. The effect of such a treatment was to reproduce the phenotype of DLK-depleted TES suggesting that microtubules are important effectors of DLK-induced keratinocyte differentiation. In an attempt to describe the impact of DLK on global gene expression, RNA samples of DLK-depleted TES were studied using microarray analyses. This approach revealed a reduction in the expression of many genes coding for cornified envelope proteins. Reductions of c-Jun and C/EBPα immunofluorescence staining were also noted in TES with a reduced DLK expression suggesting this kinase as a c-Jun and C/EBPα regulator in the context of keratinocyte differentiation. Globally, our works show that DLK is required for keratinocyte differentiation since it promotes microtubule reorganization to cell periphery, desmosomes and tight junction consolidation as well as c-Jun and C/EBPα localization to the nucleus.
Klaus, Anna. "Interactomique de kinases clefs du métabolisme énergétique : caractérisation d'interactions de la protéine kinase activée par l'AMP et de la créatine kinase". Grenoble, 2010. http://www.theses.fr/2010GRENV063.
Pełny tekst źródłaUne propriété clé des systèmes biologiques est la présence d'un réseau d'interactions protéiques, crucial pour toute fonction cellulaire comme par exemple la régulation du métabolisme énergétique. Deux enzymes clé impliquées dans cette régulation sont la créatine kinase (CK), dont la fonction consiste dans la gestion du stock et du transfert d'énergie, et la protéine kinase activée par l'AMP (AMPK), qui régule l'homéostasie énergétique au sein de la cellule et de l'organisme entier. Dans un premier temps un crible de double hybride en levure original fut appliqué afin d'identifier de nouveaux partenaires d'interaction de la CK cytosolique du cerveau (BCK) et de l'AMPK dans le cerveau humain. Différents candidats d'interaction furent identifiés, dont des protéines membranaires associées aux vésicules (VAMP) interagissant avec les deux kinases. L'interaction AMPK-VAMP fut confirmée par co-immunoprecipitation à partir de vésicules synaptiques, mais ne menait pas à la phosphorylation de VAMP, suggérant que VAMP recrute AMPK pour la régulation de processus d'endo- et d'exocytose. Une seconde stratégie combinant un essai d'interactions biophysique, basé sur la résonance plasmonique de surface (SPR), avec des essais de phosphorylation in vitro permit la sélection de cibles AMPK isoforme spécifique. Une de ces cibles fut la fumarate hydratase, dont la phosphorylation préférentielle par l'AMPK221 provoque une augmentation de l'efficacité enzymatique in vitro. Finalement, une classe de candidats d'interaction, les glutathion S-transférases GSTM1 et -P1, fut caractérisée en détail par un panel de méthodes d'interactomique (SPR, double hybride, co-immunoprécipitation). Cette étude les identifie comme interacteurs fiables à haute affinité ainsi que nouveaux substrats de l'AMPK. Dans le cas de GSTP1 la phosphorylation par AMPK provoque une augmentation de son activité enzymatique suggérant un rôle direct de la signalisation par AMPK dans la défense contre le stress oxydatif
Wall, Jason A. "Mechanisms of mitogen activated kinase kinase 6 mediated cardioprotection /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3185930.
Pełny tekst źródłaGandhi, Payal. "Characterization of the Parkinson's disease associated protein, leucine-rich repeat kinase 2 (LRRK2), as a Ras-related GTPase". Cleveland, Ohio : Case Western Reserve University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1195574448.
Pełny tekst źródłaCheng, Kwan-wai. "Regulation of equilibrative nucleoside transporter-1 by protein kinase C and mitogen-activating protein kinase /". View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31494912.
Pełny tekst źródłaDennis, Patrick B. (Patrick Brian). "Autophosphorylation and Autoactivation of an S6/H4 Kinase Isolated From Human Placenta". Thesis, University of North Texas, 1994. https://digital.library.unt.edu/ark:/67531/metadc279364/.
Pełny tekst źródłaNurimba, Margaret. "Roles of SR protein kinase Dsk1 and LAMMER kinase Kic1 in mRNA processing in fission yeast, Schizosaccharomyces pombe". Scholarship @ Claremont, 2014. http://scholarship.claremont.edu/scripps_theses/305.
Pełny tekst źródłaNADAL, WOLLBOLD FLORENCE. "Activation et regulation des map kinases extracellular signal-regulated kinase 2 et c-jun nh2-terminal kinase 1 dans les plaquettes humaines". Paris 7, 2000. http://www.theses.fr/2000PA077163.
Pełny tekst źródłaLee, Gui-in. "Structure and dynamics of the receptor kinase interacting FHA domain of kinase associated protein kinase from arabidopsis". Free to MU campus, others may purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3100058.
Pełny tekst źródłaFragoso, Cristina Margarida Gomes Grangeio. "Fosforilação da HsPI3-Kinase-C2? = Phosphorylation of HsPI3-Kinase-C2?" Master's thesis, Universidade de Aveiro, 2002. http://hdl.handle.net/10773/23128.
Pełny tekst źródłaVárias isoformas da enzima fosfoinositide-3-cinase (PI3-Cinase), uma vasta família de cinases lipidicas têm nos últimos anos vindo a ser clonada e caracterizada. P13-Cinases constituem uma família de cinases conservadas durante a evolução que catalisam a adição de uma molécula de fosfato ao fosfatidilinositol e seus derivados, esta adição tem lugar no anel inositol na posição D3. P13-Cinases estão agrupadas em três classes de acordo com as moléculas que preferencialmente utilizam como substrato in vitro e de acordo com as suas características estruturais. Fosfoinositide-3-Cinase-C2a (PI3-Cinase-C2a), pertence à classe I1 de P13- Cinases, esta classe é caracterizada pela utilização de fosfatidilinositol e fosfatidilinositol-4-P como substrato in vitro. Todos os membros da classes I1 possuem no seu C-terminal um domínio C2, característico da classe. Este trabalho permitiu a identificação do local de fosforilação da HsPI3-Cinase- C2a bem como a identificação de duas cinases envolvidas na sua fosforilação. A fosforilação de HsP13-Kinase-C2a ocorre na Ser259 e este resíduo é um alvo comum de fosforilação mitótica e de fosforilação induzida por radiação UV. Durante o ciclo celular HsP13-Cinase-C2a é predominantemente fosforilada na M fase e a cinase envolvida 6 a Cdk1,após radiação UV a fosforilação é mediada pela JNK.
In recent years, a large family of Phosphoinositide-3-Kinases (PI3-Kinase) isozymes has been characterized and cloned. PI3-Kinases constitute a family of evolutionary conserved lipid kinases that catalyse the addition of a phosphate molecule to the D3 position of the inositol ring of phosphatidylinositol and its derivatives. P13-Kinases are grouped into three classes according to the molecules that they preferentially utilize as substrates and their structural characteristics. Phosphoinositide-3-Kinase-C2a (P13-Kinase-C2a) belongs to class II P13- Kinases, which are defined by their in vitro use of phosphatidylinositol and phosphatidylinositol-4-phosphate as substrates. All type II P13-Kinases contain a C2 domain at their C-terminus. This work resulted in the identification of a phosphorylation site on HsP13- Kinase-C2a as well the identification of two kinases involved in mitotic and UVinduced phosphorylation of HsP13-Kinase-C2a. The phosphorylation of HsP13- Kinase-C2a occurs in Ser259 and this serine is a common target in mitotic and UV-induced phosphorylation. We found that during the cell cycle HsP13- Kinase-C2a is predominantly phosphorylated in mitotic phase and the kinase involved is Cdkl and after UV irradiation the phosphorylation of HsPI3-Kinase- C2a is mediated by JNK.
Dutil, Erica M. "Phosphorylation of protein kinase C by the phosphoinositide-dependent kinase /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9961757.
Pełny tekst źródłaFesquet, Didier. "Mécanisme d'activation de la kinase cdc2 : purification de la thréonine 161 kinase activatrice des complexes CDK-cyclines". Montpellier 1, 1993. http://www.theses.fr/1993MON1T026.
Pełny tekst źródłaYoung, Stephen W. "The insulin receptor tyrosine kinase and the activation of the map kinase cascade : interactions with the protein kinase C and protein kinase A signalling pathways". Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238958.
Pełny tekst źródłaDittmann, Linda [Verfasser]. "Expressionsanalyse von Aurora-Kinase A, Aurora-Kinase B, Repp 86, Cyclin-Dependent-Kinase 1 und Cyclin-Dependent-Kinase 2 bei Mamma- und Ovarialkarzinomen / Linda Dittmann". Kiel : Universitätsbibliothek Kiel, 2014. http://d-nb.info/1062536061/34.
Pełny tekst źródłaRojnuckarin, Ponlapat. "Mitogen-activated protein kinase pathways in megakaryocyte development /". Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/9200.
Pełny tekst źródłaKannanayakal, Theresa Joseph. "Casein kinase 1 isoforms in degenerative disorders". Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1094264800.
Pełny tekst źródłaDocument formatted into pages; contains 150 p. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2005 Sept. 7.
Sallam, Hatem. "Pharmacological and analytical studies of the cyclin dependent kinase inhibitors". Stockholm, 2009. http://diss.kib.ki.se/2009/978-91-7409-706-1/.
Pełny tekst źródłaGraham, Heidi C. "Nuclear magnetic resonance studies of a kinase : 3-phosphoglycerate kinase (PGK)". Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334917.
Pełny tekst źródłaHynes, Andrews Mark. "Rx-kinase and protein kinase C in superoxide production from neutrophils". Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267858.
Pełny tekst źródłaFoukas, Lazaros. "Defining the physiological role of phosphatidylinositol 3-kinase protein kinase activity". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397223.
Pełny tekst źródłaDunn, L. M. "Characterisation of leucine-rich repeat kinase-2 regulation and kinase function". Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1322688/.
Pełny tekst źródłaHolland, Pamela M. "Identification, interactions, and specificity of a novel MAP kinase kinase, MKK7 /". Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/9262.
Pełny tekst źródłaBrown, Jacob D. "Liver Kinase B1/AMP-Activated Protein Kinase Signaling in the Diaphragm". BYU ScholarsArchive, 2010. https://scholarsarchive.byu.edu/etd/2543.
Pełny tekst źródłaYoon, Moon-Young. "Studies of the Mechanism of the Catalytic Subunit of cAMP Dependent Protein Kinase". Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc332161/.
Pełny tekst źródłaPenfold, Lucy. "Investigating the roles of AMP-activated protein kinase and calcium/calmodulin-dependent protein kinase kinase β in prostate cancer". Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/54390.
Pełny tekst źródłaWalker, Valerie Glynis. "Pl3-kinase mediates cSrc activation and podosome formation through the adaptor protein, AFAP-110, in response to PKC[alpha] activation". Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5191.
Pełny tekst źródłaTitle from document title page. Document formatted into pages; contains viii, 306 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
Murail, Pauline. "Pyridin-2(1H)one derivatives - a new class of therapeutics for trigeminal pain". Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2024. http://theses.bu.uca.fr/nondiff/2024UCFA0026_MURAIL.
Pełny tekst źródłaChronic pain affects about 10% of the population worldwide. Despite extensive research, the management of chronic pain, particularly trigeminal chronic pain, is still a clinical challenge, requiring new therapeutics. Protein kinases (PK) in the spinal dorsal horn or trigeminal nucleus caudalis (TNC)-extracellular signal-regulated protein kinase, γ isoform of protein kinase C, p38 mitogen-activated protein kinase (p38 MAPK)-contribute to pain hypersensitivity in animals. PKs may represent new molecular targets for chronic pain treatment. We aim to synthesize PK inhibitors with analgesic properties.A 1st series of pyridin-2(1H)-one derivatives was designed, synthesized, and evaluated on a rat inflammatory mechanical hypersensitivity (MH) model. Several compounds strongly inhibited inflammatory MH. The most active, 3-(2-Bromophenyl)-5-(phenylamino)pyridin-2(1H)-one (C69), also reversed neuropathic MH. Evaluated against a panel of 50 PKs, C69 appeared to be a p38α MAPK inhibitor. We synthesized a 2nd series of pyridin-2(1H)-one derivatives, substituting the 2 pyridinones, at the 3-position, with various aryl/heteroaryl moieties, and at the 5-position, with a phenylamino group. The most active, C60 exhibited strong analgesic properties.We have 2 objectives: i) to assess the analgesic efficacy and characterize the mechanism of action of compounds C69 and C60 in various models of trigeminal pain, and ii) to design, synthesize, and evaluate a 3rd series of compounds to improve analgesic potency.Using behavior, in vivo electrophysiology, and c-Fos immunoreactivity in male and female rats, we examined the effect of per os or intracisternally (i.c.) applied compounds on spontaneous and evoked pain-like behavior and TNC neuronal sensitization in several trigeminal pain models: inflammatory [capsaicin, formalin, Complete Freund Adjuvant (CFA)], neuropathic [infraorbital nerve chronic constriction (ION-CCI)] and migraine [isosorbide dinitrate (ISDN)]. We also assessed their cytotoxicity, cardiotoxicity, and effect on motor performance, and for per os C69, its pharmacokinetic.I.c. C69 prevents capsaicin- and formalin-induced rubbing behavior and facial MH and CFA-induced facial MH. It also reverses ION-CCI-induced MH. Per os, C69 inhibits CFA and ISDN-induced facial MH. All these effects are long-lasting in both sexes. In TNC, i.c. C69 prevents CFA-induced c-Fos expression and inhibits the responses of wide dynamic range (WDR) neurons to both innocuous and noxious stimuli, as well as wind-up. Moreover, C69 appears safe: showcasing no evident cytotoxicity and cardiotoxicity, exerting analgesia with no motor impairment, and, persistently applied, does not affect mechanical sensitivity. Finally, its pharmacokinetic is similar to that of established analgesics.The 2nd series produced more potent anti-MH compounds. C60 completely inhibits CFA-, capsaicin- and formalin-induced facial MH. But it has no effect on capsaicin- or formalin-induced rubbing behavior. Per os, C60 reduces CFA-induced facial MH. In TNC, i.c. C60 prevents CFA-induced c-Fos expression and inhibits the responses of WDR neurons to innocuous mechanical stimuli but neither to noxious mechanical ones nor to C-fiber stimulation nor to wind-up. It nevertheless attenuates C-fibers-evoked post-discharges. Finally, C60 displays the same favorable safety profile as C69.We recently synthesized a 3rd series of compounds, comparing their efficacy with that of C60 on the hindpaw capsaicin model. Of 21 compounds synthesized, only 8 compounds efficiently inhibit capsaicin-induced MH, and C10, the most active, is more potent than C60.Pyridin-2(1H)-one derivatives may represent a new class of therapeutics for chronic pain. The p38α MAPK inhibitor C69 seems to have the greatest therapeutic potential with demonstrated analgesic effects on various pain symptoms and etiologies through, at least in part, segmental, pre- and postsynaptic, effects
Weir, Marion. "Novel Mechanisms Governing Autoregulation of the Src Family Kinase Fyn and its Crosstalk with Protein Kinase A". ScholarWorks @ UVM, 2016. http://scholarworks.uvm.edu/graddis/592.
Pełny tekst źródłaLala, Hitesh Nagin. "Subcloning of calcium-dependent protein kinase related kinase homologues in arabidopsis thaliana". Thesis, Georgia Institute of Technology, 1997. http://hdl.handle.net/1853/25343.
Pełny tekst źródłaFox, Gavin Connor. "Structural studies on MAP kinase phosphatases and the receptor tyrosine kinase TrkA". Thesis, Birkbeck (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268768.
Pełny tekst źródłaLachance, Gabriel. "Implication de la MAPK kinase kinase DLK dans la différenciation des kératinocytes". Mémoire, Université de Sherbrooke, 2009. http://savoirs.usherbrooke.ca/handle/11143/4823.
Pełny tekst źródłaMazot, Pierre. "Anaplastic lymphoma kinase un récepteur tyrosine kinase orphelin impliqué dans les neuroblastomes". Paris 6, 2011. http://www.theses.fr/2011PA066161.
Pełny tekst źródłaHmitou, Isabelle. "Rôle et régulation des isoformes de la MAPKinase Kinase Kinase B-Raf". Paris 11, 2006. http://www.theses.fr/2006PA112178.
Pełny tekst źródłaThe B-Raf serine/threonine kinase is involved in many cellular processes in Metazoans. The B-raf gene encodes several isoforms resulting from alternative splicing. The presence of the sequences encoded by exons 8b and 9b, located between the regulation domain and the kinase domain of B-Raf, modulates the biochemical and oncogenic properties of B-Raf: the exon 9b increases the kinase activity and the interaction with MEK, the exon 8b decreases them. My work aimed at the same time to understand the molecular basis of the mechanism of differential regulation of B-Raf isoforms and also to analyze their functional roles. I thus showed that the presence of the sequences encoded by exons 8b and 9b interferes with the autoinhibition of the regulation domain on the kinase domain. These sequences also interfere with phosphorylation of the residues S365 and S429 located in the same hinge region, independently of the intramolecular interactions. Thus, whereas the phosphorylation level of S365 is modulated by the presence of exons, the phosphorylation of S429 is not modulated by the alternative sequences but would have different consequences according to the isoform. In addition, in order to understand the physiological role of the B-Raf isoforms containing the sequences encoded by exons 8b and 9b, we generated mice strain lines in which the conditional deletion of these exons is possible by a Cre/Lox strategy. Obtaining mice invalidated for exons 8b and 9b will render possible to better understand the specific role of B-Raf isoforms, especially during development
Kerkelä, R. (Risto). "Signaling pathways in myocyte hypertrophy:role of GATA4, mitogen-activated protein kinases and protein kinase C". Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514269950.
Pełny tekst źródłaMa, Sheng. "Caractérisation du rôle des protéines phosphatases impliquées dans la déphosphorylation de la protéine kinase Greatwall lors de la sortie de mitose". Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTS007/document.
Pełny tekst źródłaThe establishment of mitosis requires phosphorylaton of several substrates induced by kinases. Cdk1-cyclin B and Greatwall kinases are both necessary for the entry into mitosis. Cdk1-cyclin B complex phosphorylates many substrates and at the same time Greatwall phosphorylates Arpp19 which binds PP2AB55 phosphatase and inhibits it. PP2AB55 has an important role in the dephosphorylation of Cdk1-cyclin B mitotic substrates.In my laboratory, we found that after Greatwall depletion, either in Xenopus egg extracts or in human cells, PP2A is no longer inhibited and cells exit mitosis. Since activation of Greatwall requires its phosphorylation in the c-terminal part and in the T-loop site, we suppose that mitosis exit require dephosphorylation of Greatwall. So these dephosphorylations could be involved for Greatwall inactivation. Several phosphatases are candidates for this process: Fcp1, PP1, PP2A and Calcineurin. My project proposes to determine the involvement of these four phosphatases in Xenopus egg extracts after depletion and overexpression of these four proteins
Walker, Dianne. "Bacillus stearothermophilus pyruvate kinase". Thesis, University of Bristol, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335572.
Pełny tekst źródłaNadeau, Valérie. "Implication de MEK1 et MEK2 dans la morphogenèse du placenta de souris". Doctoral thesis, Université Laval, 2015. http://hdl.handle.net/20.500.11794/25734.
Pełny tekst źródłaThe mammalian genome contains two ERK/MAP kinase kinase genes, Mek1 and Mek2, which encode dual-specificity kinases responsible for ERK/MAP kinase activation. In the mouse, the loss of Mek1 function causes embryonic lethality, whereas Mek2 mutants survive with a normal lifespan, suggesting that Mek1 rescues the lack of Mek2 function. The first objective of my thesis was to clarify potential functions of Mek2 during mouse embryogenesis. To do, I have analyzed the loss of Mek2 function in the presence of Mek1 haploinsufficiency. Most Mek1+/-Mek2+/- embryos die during gestation from placenta defects affecting extra-embryonic tissues. Thus, even though Mek1 plays a predominant role, these results enlightened the function of Mek2 in placenta development. The histological characterization of Mek1+/-Mek2+/- placentas revealed a diminution of the vascularization and an aberrant formation of multinucleated trophoblast giant (MTG) cells. Genetic experiments on the SynT-II cellular lineage in vivo demonstrated that MTG cells derive from the aberrant SynT-II differentiation and that their formation results from a cell-autonomous effect. The second objective of my thesis was to determine in which cell types the ERK/MAPK activation is essential for placenta development. Genetic analyses combined with histological studies revealed that MTG formation resulted from the ectopic fusion between both layers of SynT, which normally participate in an independent way in the blood-placental barrier. The blood-placental barrier is constituted of a double layer of SynT and by the cells derived from the allantois, the endothelial cells and their perycites. The deletion of both Mek1 alleles in allantois-derived tissues in a Mek1+/-Mek2+/- placenta environment increases the penetrance and the expressivity of the MTG phenotype. These results demonstrate the role of the ERK/MAPK pathway in defined embryonic and extraembryonic cell populations for correct placenta formation. Using mouse genetics, we also demonstrated that the normal development of syncytiotrophoblasts type I into a thin layer of multinucleated cells depends on the presence of the syncytiotrophoblasts type II. Finally, the combined mutations of Mek1 and Mek2 genes alter the expression of several genes involved in cell fate specification, cell fusion and cell polarity that likely explain the underdeveloped placenta and the MTG phenotype seen in Mek1Mek2 mutants.
Chen, Xi. "The role of PI3K and ERK/MAPK signal transduction cascades in long-term memory formation /". Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6248.
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