Дисертації з теми "Ser/Thr protein kinases"
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Lee, Guinevere Kwun Wing Queenie. "Serine/threonine phosphorylation in mycobacterium tuberculosis : identification of protein kinase B (PknB) substrates." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/693.
Повний текст джерелаHaj, Slimane Ammar Zeineb. "Dynamique Spatiotemporelle de la protéine kinase AMPc dépendante dans les myocytes cardiaques." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00954406.
Повний текст джерелаGONZALEZ, MAYA LETICIA. "Etude de la transduction du signal impliquant la phospho-proteine pii et des ser/thr-kinases chez les cyanobacteries." Université Louis Pasteur (Strasbourg) (1971-2008), 2000. http://www.theses.fr/2000STR13092.
Повний текст джерелаKobir, Ahasanul. "Physiological roles of Eukaryotic Hanks type Ser/Thr kinase in transition to stationary phase in Bacillus subtilis." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00911812.
Повний текст джерелаWehenkel, Annemarie. "Etude structurale et fonctionnelle de Ser/Thr kinases et phosphates mycobactériennes." Paris 6, 2007. http://www.theses.fr/2007PA066177.
Повний текст джерелаMacaccaro, Paolo. "Immunophenotypic characterization of B-lymphopoiesis in KO mice for oncogenic Ser / Thr kinases by multiparameter flow cytometry." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3422901.
Повний текст джерелаProtein kinase CK2 and CK1 are a pleiotropic and evolutionary conserved serin-threonin kinase that is involved in several cellular processes. A number of studies revealed many mechanisms through which this kinase regulates cell cycle, apoptosis, cell survival and tumorigenesis. CK2 participates in many developmental pathways, of which particularly relevant for hemo-lymphopoiesis are those dependent on Hedgehog, NF-κB and STAT3, which regulate cell differentiation, proliferation, self-renewal as well as lineage choice commitment.. CK1 regulates also molecular pathways which are important for multiple myeloma plasma cells survival, like WNT/β-catenin pathway and PI3K/AKT pathway. However, despite all this data, little is known about the role of CK2 and CK1 in B-lymphopoiesis and lymphomagenesis. To elucidate the physiological and pathogenetic role of CK2 and CK1 in B-lymphocytes, we generated B cell specific conditional KO mice, were we studied the effects of deletion during normal B cell development with multiparameter flow cytometry analysis. In the bone marrow (BM), CK2β KO mice displayed a reduction of B cells, especially of the recirculating population of transitional and follicular (FO) B-cells. In peripheral blood and spleen the number of B-cells was markedly reduced. In the spleen of CK2β KO we observed an imbalance between the amount of FO and marginal zone (MZ) B-cells was found with an absolute reduction of FO B cells by approximately 2-folds and an increase of MZ B-cells and MZB cell precursors by up to three folds.. In vitro class-switch recombination assays demonstrated impairment in IgG1 and IgG3 class-switch and a marked reduction of the generation of antibody-producing cells. In CK1 KO mice we observed the totally absence of mature B cells and the presence of early precursors B cells. CK1 HET mice showed a reduction of B cells in bone marrow and an light imbalance of FO B cells an MZB cells in spleen. In vitro class-switch recombination assays doesn’t showed significant difference between HET and CTRL mice in IgG1 and IgG3 class-switch. Here, we found that the β subunit of protein kinase CK2 is a novel regulator of peripheral B cell differentiation. CK2β has a role in regulation of the GC reaction and in homeostasis of FOB and MZB cells. Furthermore we found that CK1 has a pivotal role in early B cells development. On one side our data enrich the knowledge on the mechanisms regulating B-cell development, on the other side they inform about the potential mechanisms altered by CK2 and CK1 during B-cell tumorigenesis.
石崎, 敏理. "The small GTP-binding protein Rho binds to and activates a 160kDa Ser/Thr protein kinase homologous to myotonic dystrophy kinaseに関する研究(myotonic dystrophy kinaseに相同性を有し,低分子量GTP結合蛋白質Rhoに結合,活性化される160kDaセリン/スレオニンキナーゼ)". Kyoto University, 1997. http://hdl.handle.net/2433/202205.
Повний текст джерела0048
新制・課程博士
博士(医学)
甲第6788号
医博第1888号
新制||医||664(附属図書館)
15860
UT51-97-H172
京都大学大学院医学研究科分子医学系専攻
(主査)教授 月田 承一郎, 教授 永田 和宏, 教授 中西 重忠, 教授 成宮 周
学位規則第4条第1項該当
Deupí, i. Corral Xavier. "Influence of Ser and Thr residues in the geometry of transmembrane helices: implications on the structure and function of G protein-coupled receptors." Doctoral thesis, Universitat Autònoma de Barcelona, 2003. http://hdl.handle.net/10803/4426.
Повний текст джерелаSe sap que determinats residus, com prolina, serina o treonina, provoquen distorsions locals en l'estructura de les hèlices a. L'anàlisi de bases de dades de seqüències de segments transmembrana mostra com certes combinacions d'aquests residus són més comunes que d'altres, i que algunes d'elles estan sobre-representades de manera significativa, mentre que d'altres estan clarament sots-representades. La restricció d'aquesta anàlisi de seqüències a la regió transmembrana dels GPCRs de la Classe A mostra com aquestes combinacions es troben en posicions específiques i, a més, es troben conservades en certes subfamílies de receptors.
L'estructura i la dinàmica de les hèlices transmembrana que contenen aquestes combinacions de prolina i serina o treonina s'han estudiat mitjançant simulacions de dinàmica molecular en un entorn hidrofòbic explícit. Els resultats mostren com algunes d'aquestes combinacions indueixen distorsions importants en l'estructura de l'hèlix a, degut al seu efecte desestabilitzador de la xarxa de ponts d'hidrogen que dóna estabilitat a l'hèlix.
Aquests resultats s'han aplicat a la construcció d'un model tridimensional del receptor de quimiocines CCR5 , utilitzant tècniques de modelització molecular per homologia. En aquest model es proposa que les hèlices transmembrana (TMH) 2 i 3 del receptor CCR5 són estructuralment diferents del patró de rodopsina. TMH2 està més doblegada degut a la presència d'un motiu Thr-X-Pro, que, a més, fa que aquesta hèlix es doblegui cap a TMH3. Així doncs, es proposa que, en aquest receptor, aquestes dues hèlices interaccionen. Aquesta interacció estaria mediada per la presència de residus hidrofòbics conservats i específics en les dues hèlices. Aquestes hipòtesis han estat posades a prova mitjançant experiments de mutagènesi dirigida, gràcies a la col·laboració amb l'Institut de Recherche Interdisciplinaire en Biologie Humaine et Nucléaire (IRIBHN), Université Libre de Bruxelles. Els resultats experimentals permeten establir la hipòtesi que la interfície TMH2-TMH3 participa en l'activació induïda per quimiocines del receptor CCR5.
Com a conclusió, aquesta tesi pretén mostrar com, mitjançant la utilització d'eines bioinformàtiques, és possible traduir les seqüències primàries de proteïnes i les interaccions a nivell atòmic en estructures tridimensionals de proteïnes. A més, aquesta tesi mostra que, encara que l'estructura tridimensional de la rodopsina bovina és un patró útil per la modelització per homologia de GPCRs, s'han de tenir en compte de manera explícita les especificitats de seqüència de cada receptor per tal de construir models de receptors particulars. Aquestes especificitats de seqüència consisteixen en patrons de seqüència conservats en determinades famílies, que es tradueixen en divergències estructurals. Entre aquests patrons de seqüència, es proposa que els residus de serina i treonina, sols o combinats amb residus de prolina propers, poden modular la geometria de les TMHs, degut a la seva capacitat d'interferir amb la xarxa de ponts d'hidrogen que dóna estabilitat a les hèlices a.
Finalment, es proposa que la influència dels motius de serina, treonina i prolina en l'estructura de les TMHs pot estar relacionada amb els processos d'activació dels GPCRs de la Classe A i, possiblement, d'altres proteïnes de membrana. En els GPCRs, aquests motius poden haver evolucionat per tal d'adaptar uns mecanismes d'activació conservats als lligands característics de cada família de receptors.
This thesis is framed in the study of particular biological systems through the use of bioinformatics. In particular, the theoretical study of the influence of certain amino acids on the structure and dynamics of the secondary structure elements of proteins has been applied to homology modelling of G protein-coupled receptors (GPCRs) and to the study of their mechanisms of activation.
Certain residues, as proline, serine or threonine, are known to induce local distortions in the a-helical structure. Analysis of sequence databases of transmembrane segments evidence that certain combinations of these residues are more common than others, and that some of them are significantly over-represented, while others are clearly under-represented. The focusing this sequence analysis on the transmembrane region of Class A GPCRs illustrates that these combinations are located in some specific locations and conserved within certain subfamilies of receptors.
The structure and dynamics of transmembrane a-helices containing these combinations of proline and serine or threonine have been studied using molecular dynamics simulations in an explicit hydrophobic environment. The results show how some of these combinations induce significant distortions in the a-helical structure, due to their effect on the hydrogen bond network that stabilizes the helix.
These results have been applied to the building of a three-dimensional model of the chemokine CCR5 receptor, using homology modelling techniques. In this model, transmembrane helices (TMH) 2 and 3 of CCR5 are proposed to be different from the bovine rhodopsin template. TMH2 is more bent due to the presence of a Thr-X-Pro motif, which, in turn, induces this helix to lean towards TMH3. As a consequence, an interaction between these two helices is proposed for this particular receptor. This interaction would be mediated through the presence of specific and conserved hydrophobic and aromatic residues in both helices. These hypothesis have been tested through site-directed mutagenesis experiments, thanks to a collaboration with the Institut de Recherche Interdisciplinaire en Biologie Humaine et Nucléaire (IRIBHN), Université Libre de Bruxelles. The experimental results let us to hypothesize that the TMH2-TMH3 interface is involved in the chemokine-induced activation of the CCR5 receptor.
As a conclusion, this thesis aims to show how through the use of bioinformatics tools, primary sequences of proteins and interactions at an atomic level can be translated to three-dimensional protein structures. In addition, this thesis illustrates that, even though the three-dimensional structure of bovine rhodopsin is a very useful template for homology modelling of GPCRs, the sequence specificities of each receptor have to be explicitly taken into account in order to build models. These sequence specificities consist in sequence patterns conserved within certain families, which are translated into structural divergences. Among these sequence patterns, we hypothesize that serine and threonine, alone or combined with nearby proline residues, can modulate the geometry of TMHs, due to its capability to interfere with the hydrogen bond network that stabilize a-helices.
Finally, we propose that the influence of serine, threonine and proline motifs in the structure of TMHs may be related to processes of activation in the Class A of GPCRs, and, possibly, other membrane proteins as well. In GPCRs, these motifs may have evolved in order to adapt a conserved mechanism of activation of the G protein to the cognate ligands of each receptor family.
Shor, Audrey Cathryn. "Src kinase inhibitors for the treatment of sarcomas : cellular and molecular mechanisms of action." [Tampa, Fla] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0001906.
Повний текст джерелаUnsworth, Amanda J. "The role of protein kinase C in platelet activation." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:114582b8-185a-41f5-958c-77038fb185df.
Повний текст джерелаHollin, Thomas. "Analyse de l’interactome de la Ser/Thr protéine phosphatase de type 1 (PP1) chez plasmodium falciparum : caractérisation moléculaire et fonctionnelle de Gametocyte EXported Protein 15." Thesis, Lille 2, 2017. http://www.theses.fr/2017LIL2S020/document.
Повний текст джерелаA major obstacle in the development of novel anti-malarials is our limited knowledge of basic parasite biology and the paucity of identified potential intervention targets. Protein-protein interactions are involved and essential in broad range of biological processes including the post-translational modifications. Substrate-kinase or phosphatase interactions are considered as transient binding and play a central and essential role in Plasmodium cell cycle. The Ser/Thr Protein Phosphatase Type 1 (PP1), one of the main contributors of eukaryotic phosphatase activity, is essential to malaria parasite Plasmodium falciparum and is highly regulated by many regulatory subunits. In humans, there are about 200 distinct regulators, however, only 4 have been so far reported in Plasmodium.To explore the P. falciparum PP1 (PfPP1) regulatory network as complete as possible, we carried out three complementary approaches to characterize the PfPP1 interactome. Co-affinity purification followed by Mass Spectrometry-based proteomics identified 6 PfPP1 interacting proteins (PIPs) of which 3 contained the RVxF consensus binding motif, 2 PIPs with a Fxx[RK]x[RK] binding motif, one with both binding motifs. The Yeast Two-Hybrid screening identified 134 proteins of which 30 have the RVxF binding motif and 20 contain the Fxx[RK]x[RK] binding motif. The in silico screen of the P. falciparum genome using a consensus RVxF motif as template revealed the presence of 55 potential PfPP1 interacting proteins. As further demonstration, 35 candidate partners were validated in an independent ELISA-based assay using recombinant proteins. The data reports several conserved PP1 interacting proteins as well as a high number of specific interactors to PfPP1, indicating a high diversity of biological functions for PP1 in Plasmodium. Among these candidates, one partner assigned as Gametocyte EXported Protein 15 (GEXP15) has been confirmed as a direct interactor of PfPP1 by different approaches. In addition, GEXP15 is over-expressed during gametocyte stage, responsible for the transmission of the parasite in the mosquito. These results as well as functional studies will be presented and discussed
Galioot, Amandine. "Contribution à l'étude du rôle des SER/THR protéine-phosphatases PP1/PP2A dans les processus de mort cellulaire et de maturation du précurseur du peptide Beta-Amyloïde." Paris 7, 2013. http://www.theses.fr/2013PA077219.
Повний текст джерелаOuTlabhas previousry proposed a concept denominated "Drug Phosphatase Technology" (DFT) based on the use of cationic penetrating sequences capable of interacting with PP1/PP2A phosphatases in order to deregulate specific intracellular signais Ser/Thr proteins-phosphatases of PP1 and PP2A family are key factors of the cellular signalization and deregulation of their activity through interaction with cellular or viral protein often leads to severe dysfunctions. For exemple, E4orf4 protein of adenoviruses interacts with PP2A1 and leads to apoptotic death in infected or transformed cells while healthy cells remain unaffected. In a first part of this work, we have identified an interacting sequence between PP2A1 and E4orf4 from which we - have characterized the peptide DFT-F4orf44, which provokes the apoptosis of a subset of human tumoral cellswithout affecting healthy cells of fibroblastic type. Protein-phosphatases of PP1 and PP2A family also play a crucial role in the physiological regulation of neuronal substracts Tau and APP (Amylold Peptid Precursor). A diminution of the phosphatase activity in nerve cells leads to a drastically increasjng of phosphorylation state of these proteins for patients affected by Alzheimer's disease. I The second part of this work has allowed the identification of the phosphatase proteins responsible for the regulation of phosphorylation of APP T668 residue, which is an essential modification for APP maturation and processing
Brelle, Solène. "Phosphorylation et interaction hôte/pathogène : analyse de deux facteurs bactériens sécrétés, la kinase CstK de Coxiella burnetii et la phosphatase PtpA de Staphylococcus aureus." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTS094/document.
Повний текст джерелаBacterial pathogens have developed diverse strategies towards host signalling pathways, in order to subvert the immune response and/or create permissive niches for their survival. One such strategy is based on the secretion of bacterial signalling proteins into the target host cells, thereby directly modulating the status of host signalling networks. Because the mechanisms involved are largely intractable to most in vivo analyses, very little is known about the signals, sensors, and effectors mediating these adaptations. Sensing the host environment is a key component to execute appropriate developmental programs, and the eukaryotic-like phosphosignaling systems in prokaryotes are emerging as equally important regulatory systems as the well-known eukaryotic systems, but the study of their functions is still in its infancy. The innovative aspect of this project resides in the study of the emerging role of secreted Ser/Thr kinases and phosphatases in the control of host-pathogen interactions thus modifying the global host response during infection. During my thesis, I first investigated the role of a novel bacterial protein kinase identified in Coxiella burnetii that we named CstK (Coxiella serine threonine Kinase). C. burnetii, the etiological agent of the emerging zoonosis Q fever, subverts host cell defenses, permitting its intracellular replication in specialized vacuoles within host cells. Secretion of a large number of bacterial effectors into host cell is absolutely required for rerouting the Coxiella phagosome. We demonstrated that this putative protein kinase identified by in silico analysis of the C. burnetii genome is able to autophosphorylate and undergoes in vitro phosphorylation. Moreover, we identified specific host cell proteins interacting with CstK, by the use of the model amoeba Dictyostelium discoideum, an eukaryotic professional phagocyte amenable to genetic and biochemical studies. In the second part of my project, I was interested in the role of a putative secreted protein tyrosine phosphatase (PtpA) during Staphylococcus aureus infection. Well-known in hospital-acquired diseases, this bacteria produces multiple virulence factors that lead to various severe diseases, and the increase of multi-resistant strains is a major concern. This pathogen has the ability to invade and persist in a number of different human host cell types, secreting effector proteins to modulate cellular responses. Here we demonstrated that PtpA is secreted during the bacterial growth. We also determined that PtpA presents a tyrosine phosphatase activity that is regulated by the tyrosine protein kinase CapA1B2 of S. aureus. At last, using the D. discoideum model, we identified some host proteins that interact with PtpA, but their link with infection still remain to be studied
Rajagopalan, Krithika. "Characterization of a novel Ser/Thr kinase/phosphatase pair in Escherichia coli." Thesis, 2018. https://doi.org/10.7916/D8ZG893N.
Повний текст джерелаGoldová, Jana. "Studium funkce Ser/Thr proteinkináz a fosfatáz Pseudomonas aeruginosa." Doctoral thesis, 2011. http://www.nusl.cz/ntk/nusl-311410.
Повний текст джерелаKleinová, Simona. "Identifikace nových substrátů Ser/Thr proteinkinázy StkP." Master's thesis, 2019. http://www.nusl.cz/ntk/nusl-397477.
Повний текст джерелаMalíková, Eliška. "Úloha proteinkinázy StkP v regulaci buněčného dělení Streptococcus pneumoniae." Master's thesis, 2011. http://www.nusl.cz/ntk/nusl-312578.
Повний текст джерелаLIN, JANET TING-MEI. "MUTAGENIC STUDIES OF RDOA, A EUKARYOTIC-LIKE SER/THR PROTEIN KINASE IN SALMONELLA ENTERICA SEROVAR TYPHIMURIUM." Thesis, 2010. http://hdl.handle.net/1974/6118.
Повний текст джерелаThesis (Master, Microbiology & Immunology) -- Queen's University, 2010-09-29 21:35:42.815
Janaki, Chintalapati. "Development and application of sequence-based approaches for recognition and functional characterization of protein kinases." Thesis, 2019. https://etd.iisc.ac.in/handle/2005/4393.
Повний текст джерелаHe, Ying. "A conserved Ser/Thr protein kinase, Trc regulates the integrity of epidermal cellular extensions through partially conserved network." 2005. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3168474.
Повний текст джерелаVacková, Zuzana. "Funkční studie potenciální nukleotidázy kódované genem spr1057 Streptococcus pneumoniae, homologa proteinu YjjG E. coli." Master's thesis, 2010. http://www.nusl.cz/ntk/nusl-285203.
Повний текст джерелаPiot, Frédéric. "Pattern of expression of the F8A24.12 gene from Arabidopsis thaliana which encodes a NAK ser/thr protein kinase and functional analysis of the suORF present in its 5'UTR." Thesis, 2003. http://spectrum.library.concordia.ca/1962/1/MQ77949.pdf.
Повний текст джерелаFox, Melanie Joy. "The role of Rtr1 and Rrp6 in RNAPII in transcription termination." 2015. http://hdl.handle.net/1805/7372.
Повний текст джерелаRNA Polymerase II (RNAPII) is responsible for transcription of messenger RNA (mRNA) and many small non-coding RNAs. Progression through the RNAPII transcription cycle is orchestrated by combinatorial posttranslational modifications of the C-terminal domain (CTD) of the largest subunit of RNAPII, Rpb1, consisting of the repetitive sequence (Y1S2P3T4S5P6S7)n. Disruptions of proteins that control CTD phosphorylation, including the phosphatase Rtr1, cause defects in gene expression and transcription termination. There are two described RNAPII termination mechanisms. Most mRNAs are terminated by the polyadenylation-dependent cleavage and polyadenylation complex. Most short noncoding RNAs are terminated by the Nrd1 complex. Nrd1-dependent termination is coupled to RNA 3' end processing and/or degradation by Rrp6, a nuclear specific subunit of the exosome. The Rrp6-containing form a 3'-5' exonuclease complex that regulates diverse aspects of nuclear RNA biology including 3' end processing and degradation of a variety of noncoding RNAs (ncRNAs). It remains unclear whether Rrp6 is directly involved in termination. We discovered that deletion of RRP6 promotes extension of multiple Nrd1-dependent transcripts resulting from improperly processed 3' RNA ends and faulty transcript termination at specific target genes. Defects in RNAPII termination cause transcriptome-wide changes in mRNA expression through transcription interference and/or antisense repression, similar to previously reported effects of Nrd1 depletion from the nucleus. Our data indicate Rrp6 acts with Nrd1 globally to promote transcription termination in addition to RNA processing and/or degradation. Furthermore, we found that deletion of the CTD phosphatase Rtr1 shortens the distance of transcription before Nrd1-dependent termination of specific regulatory antisense transcripts (ASTs), increases Nrd1 occupancy at these sites, and increases the interaction between Nrd1 and RNAPII. The RTR1/RRP6 double deletion phenocopies an RRP6 deletion, indicating that the regulation of ASTs by Rtr1 requires Rrp6 activity and the Nrd1 termination pathway.
Abbineni, Prabhodh S. "Examining phospho-modulation of regulated exocytosis and the release-ready state of native secretory vesicles." Thesis, 2016. http://hdl.handle.net/1959.7/uws:38315.
Повний текст джерела