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Dissertations / Theses on the topic 'Protein kinases'

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Published: 4 June 2021
Last updated: 29 July 2024

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1

Nguyen, Giang Huong. "A functional analysis of the human LPA₁G protein coupled receptor." Thesis, Available online, Georgia Institute of Technology, 2004:, 2004. http://etd.gatech.edu/theses/available/etd-06072004-131304/unrestricted/nguyen%5Fgiang%5Fh%5F200405%5Fms.pdf.

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2

Gatesman, 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.

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Thesis (Ph. D.)--West Virginia University, 2004
Title from document title page. Document formatted into pages; contains vii, 350 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 322-346).
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3

Cowan, Richard H. "Refolding of protein kinases." Thesis, University of Warwick, 2009. http://wrap.warwick.ac.uk/3133/.

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The vast increase in the number of protein structures identified since the first high resolution protein structure was determined has shown that there are relatively few protein folds. The study of the folding of proteins has also expanded significantly since its inception. The contact-order of residues in the native structure has been implicated as important in folding. This has raised the question of whether the common folds observed in protein structures fold via common mechanisms. The protein kinase domain is a large, pharmaceutically important and conserved protein fold, of which many examples fail to fold correctly when overexpressed as recombinant proteins in Escherichia coli. The kinase domain forms an excellent area in which to study the folding of a large conserved domain with varying sequence. To study the refolding of the kinase fold a refolding screen was created, using p38α as a model protein kinase. The results of this screen were compared to the results of refolding a further four protein kinases, AKT2, KIS, PhK and TTK to determine commonalities in the folding of protein kinases. The refolding of the five protein kinases was also examined using a fractional factorial screen which examined combinations of refolding additives. In the screening of the refolding of protein kinases no factors were idenified which were common to the refolding of all five of the tested protein kinases. The equilibrium folding of a single protein kinase, TTK, was also studied. The folding of TTK was determined to proceed via different pathways on folding and unfolding, with a co-operative unfolding pathway through a molten-globule intermediate, and a non-cooperative refolding pathway via an intermediate with different secondary structure content to the unfolding intermediate. The difference between the folding properties of protein kinases determined in the screen and through the analysis of the equilibrium folding of TTK suggest that there may not be a common protein kinase folding mechanism.
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4

Gold, Matthew. "Targeting AGC protein kinases." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504788.

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A-kinase anchoring proteins (AKAPs) restrict the action of the broad-specificity cyclic AMP-dependent protein kinase (PKA) to discrete subcellular locations. The highresolution crystal structure of the docking and dimerisation (D/D) domain of the RIIa regulatory Bubunit of PKA in complex with the high-affinity anchoring peptide AKAP-IS explains the molecular basis of AKAP specificity for PKA regulatory subunits. AKAPIS folds into an amphipathic a-helix that engages an essentially preformed shallow groove on the surface of the RUa dimer D/D domains. Conserved AKAP aiiphatic residues dominate interactions to RUa at the predominantly hydrophobic interface, whereas polar residues are important in conferring regulatory subunit isoform specificity. Structural information for the AKAP family was previously limited to studies of the PKA-AKAP interface. To address this deficiency, a bioinformatic screen of AKAPs was performed to identify domains within AKAPs that might be suitable for structural investigation. A central domain in AKAP18 was identified, and its crystal structure was solved. The domain is structurally similar to 2H phosphoesterase enzymes, which catalyse the hydrolysis of cyclic nucleotides, with a central groove at the base of which two His-x-Thr motifs are positioned. The domain binds specifically to 5' AMP/CMP, with a dissociation constant for AMP in the physiological range, and the molecular basis for nucleotide specificity has been established. No catalytic activity was associated with the domain, so it may function as an AMP sensor. AKAP79 is a prototypical mammalian scaffold protein, which nucleates mUlti-protein kinase-phosphatase complexes, and localises at the cell membrane under the control of calmodulin. A system for expression and purification of AKAP79 has been developed enabling sufficient production of pure AKAP79 complexes for structural and biochemical investigation. Imaging of an AKAP79-PKA-calmodulin complex by negative-staining transmission electron microscopy indicates that the first three-dimen'sional reconstruction of this complex may be possible in the near future.
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5

Ferris, Douglas K. "Protein phosphatases and protein kinases in dictyostelium." Diss., Virginia Polytechnic Institute and State University, 1986. http://hdl.handle.net/10919/50017.

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In the present work, the chromatographic behavior and partial characterization of 5 protein phosphatases, 6 paranitrophenyl phosphate (pnpp) phosphatases and 2 protein kinases from Dictyostelium are described. .Two of the protein phosphatases are shown to have subunit structures. All of the protein phosphatase activities described were able to dephosphorylate sites on proteins that had previously been phosphorylated by the cAMP-dependent protein kinase. Therefore it may be that these phosphatases function in vivo to antagonize the action of the cAMP-dependent protein kinase. Various pnpp phosphatase activities, varying in size, cation requirements and pH optima are described. Since many pnpp phosphatases also function with protein substrates it is possible that these activities represent protein phosphatases that function with phosphoproteins that have not been tested. Evidence for the existence of protein kinase C in Dictyostelium is presented. A histone protein kinase was found in Dictyostelium extracts that eluted from DE52 cellulose at the same salt concentration that rabbit brain protein kinase C did. In addition in one experiment clear dependency on calcium and phospholipids is shown. The purification to homogeneity, and characterization of a low molecular weight autophosphorylating protein kinase, pp20, is described. This protein kinase is a major phosphorylated protein and in addition represents at least 0.03% of the total cellular protein. The autophosphorylation reaction can be inhibited by EDTA but not by EGTA. Following inhibition by EDTA, autophosphorylation can be reactivated by the addition of Mn²⁺, Mg²⁺, or Ca²⁺. Western blotting evidence is presented that shows cross reactivity of pp20 and an 85 KDa protein that may possess casein kinase activity.
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6

Walker, 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.

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Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains viii, 306 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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7

Holland, 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.

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8

Saurin, Adrian Thomas. "Protein kinases in myocardial protection." Thesis, King's College London (University of London), 2001. https://kclpure.kcl.ac.uk/portal/en/theses/protein-kinases-in-myocardial-protection(ba5e7b96-cf59-409a-b290-f18fec8be6b1).html.

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9

Kaser, Matthew R. "Beryllium-sensitive nuclear protein kinases." Thesis, University of Oxford, 1987. http://ora.ox.ac.uk/objects/uuid:746dac6e-9609-42b7-a809-82ebc3dd465d.

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Much effort has been spent over the last decade in producing so called "Machine Vision" systems for use in robotics, automated inspection, assembly and numerous other fields. Because of the large amount of data involved in an image (typically ¼ MByte) and the complexity of many algorithms used, the processing times required have been far in excess of real time on a VAX-class serial processor. We review a number of image understanding algorithms that compute a globally defined "state", and show that they may be computed using simple local operations that are suited to parallel implementation. In recent years, many massively parallel machines have been designed to apply local operations rapidly across an image. We review several vision machines. We develop an algebraic analysis of the performance of a vision machine and show that, contrary to the commonly-held belief, the time taken to relay images between serial streams can exceed by far the time spent processing. We proceed to investigate the roles that a variety of pipelining techniques might play. We then present three pipelined designs for vision, one of which has been built. This is a parallel pipelined bit slice convolution processor, capable of operating at video rates. This design is examined in detail, and its performance analysed in relation to the theoretical framework of the preceeding chapters. The construction and debugging of the device, which is now operational in its hardware is detailed.
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10

Waskiewicz, 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.

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11

Stack, Jeffrey H. Emr Scott. "Protein and phosphatidylinositol kinases in yeast protein sorting /." Diss., Pasadena, Calif. : California Institute of Technology, 1995. http://resolver.caltech.edu/CaltechETD:etd-10262007-081900.

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12

Wang, Huachun. "Protein phosphorylation regulation in Arabidopsis." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/5896.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2006.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on July 18, 2008) Vita. Includes bibliographical references.
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13

Guthrie, Chris Raymond. "Neural specific isoforms of protein kinase A and the role of protein kinases in neural gene expression /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6258.

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14

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.

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Abstract Cardiac myocytes react to increased workload and hypertrophic neurohumoral stimuli by increasing protein synthesis, reinitiating expression of fetal forms of structural genes, α-skeletal actin (α-SkA) and β-myosin heavy chain (β-MHC), and by increasing expression and secretion of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP). Initially, the response is beneficial, but when prolonged, it leads to pathological cardiomyocyte hypertrophy. In this study, cardiomyocyte hypertrophy was initiated by hypertrophic agonists, endothelin-1 (ET-1) and phenylephrine (PE), and by increased stretching of atrial wall. Transcription factor GATA4 was studied to identify the mechanism leading to increased gene expression of BNP. In BNP promoter, GATA4 binds to cis elements mediating hypertrophic response. Eliminating GATA4 binding by using the decoy approach, basal BNP gene expression was reduced. To identify mechanisms regulating GATA4, the roles of mitogen-activated protein kinases (MAPKs) were studied. Activation of p38 MAPK increased GATA4 binding to BNP gene and led to increased GATA4 dependent BNP gene expression. p38 MAPK was required for ET-1 induced GATA4 binding, whereas extracellular signal-regulated kinase (ERK) was required for maintaining basal GATA4 binding activity. PE and ET-1 activated protein kinase C (PKC) signaling in cardiac myocytes. Antisense oligonucleotide inhibition of PKCα markedly reduced PE induced ANP secretion and ET-1 induced BNP secretion, whereas gene expression of natriuretic peptides was not affected. Antisense PKCα treatment inhibited PE induced expression of α-SkA, while increased protein synthesis or β-MHC gene expression were not affected. Sretching of the perfused rat atria increased BNP, c-fos and BNP gene expression via mechanism involving p38 MAP kinase activation of transcription factor Elk-1. In cultured neonatal rat atrial myocytes stretch induced BNP gene expression was dependent upon transcription factor Elk-1 binding sites within the BNP gene promoter. In conclusion, hypertrophic signaling in cardiac myocytes involves multiple signaling cascades. Activation of p38 MAPK is required for the development of ET-1 induced hypertrophic phenotype and GATA4 mediated BNP gene expression in cultured ventricular myocytes, and for stretch induced Elk-1 dependent BNP gene expression in atrial myocytes. PKCα is involved in PE induced hypertrophic response and PE induced switch in gene programming inducing expression of α-SkA, the fetal form of cardiac α-actin.
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15

Megidish, Tamar. "Sphingosine as second messenger, sphingosine dependent protein kinases and their substrates /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/9285.

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16

Chan, Ka-wai. "Characterization of a physiological 62-kDa protein substrate for ganglioside-stimulated protein kinase in central nervous system myelin." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B30595575.

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17

Noble, J. E. "Fluorescent peptide substrates for protein phosphates and protein kinases." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406155.

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18

Samiei, Mitra. "Characterization of protein kinases in platelets." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0025/NQ46416.pdf.

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19

Cheng, Kwan-wai, and 鄭軍偉. "Regulation of equilibrative nucleoside transporter-1 by protein kinaseC and mitogen-activating protein kinase." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45009983.

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20

Song, Hongman. "The roles of the phosducin family proteins in the regulation of heterotrimeric G proteins in vertebrate photoreceptors." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10413.

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Thesis (Ph. D.)--West Virginia University, 2009.
Title from document title page. Document formatted into pages; contains vi, 96 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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21

Lindzen, Eric Crandall. "Cloning, sequencing, molecular characterization and expression of a cDNA encoding CRK, an atypical protein kinase homologous to plant calcium-dependent protein kinases." Diss., Georgia Institute of Technology, 1996. http://hdl.handle.net/1853/25639.

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22

Cheng, 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.

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23

Liu, Heong-fai Michael. "Characterization of the functional role of AMP-activated protein kinase in tumor suppression." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557157.

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24

Liu, Heong-fai Michael, and 呂向暉. "Characterization of the functional role of AMP-activated protein kinase in tumor suppression." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557157.

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25

Salmeen, Annette. "Crystallographic studies on interactions between protein kinases and protein phosphatases." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393269.

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26

Brancho, Deborah Marie. "Regulation and Function of Stress-Activated Protein Kinase Signal Transduction Pathways: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/101.

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The c-Jun NH2-terminal kinase (JNK) group and the p38 group of mitogen-activated protein kinases (MAPK) are stress-activated protein kinases that regulate cell proliferation, differentiation, development, and apoptosis. These protein kinases are involved in a signal transduction cascade that includes a MAP kinase (MAPK), a MAP kinase kinase (MAP2K), and a MAP kinase kinase kinase (MAP3K). MAPK are phosphorylated and activated by the MAP2K, which are phosphorylated and activated by various MAP3K. The work presented in this dissertation focuses on understanding the regulation and function of the JNK and p38 MAPK pathways. Two different strategies were utilized. First, I used molecular and biochemical techniques to examine how MAP2K and MAP3K mediate signaling specificity and to define their role in the MAPK pathway. Second, I used gene targeted disruption studies to determine the in vivo role ofMAP2K and MAP3K in MAPK activation. I specifically used these approaches to examine: (1) docking interactions between p38 MAPK and MAP2K [MKK3 and MKK6 (Chapter II)]; (2) the differential activation of p38 MAPK by MAP2K [MKK3, MKK4, and MKK6 (Chapter III)]; and (3) the selective involvement of the mixed lineage kinase (MLK) group of MAP3K in JNK and p38 MAPK activation (Chapter IV and Appendix). In addition, I analyzed the role of the MKK3 and MKK6 MAP2K in cell proliferation and the role of the MLK MAP3K in adipocyte differentiation (Chapter III and Chapter IV). Together, these data provide insight into the regulation and function of the stress-activated MAPK signal transduction pathways.
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27

Tsui, Marco Man Kin. "Studies on yeast SNARE complex formation /." View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202003%20TSUI.

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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2003.
Includes bibliographical references (leaves 130-138). Also available in electronic version. Access restricted to campus users.
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28

Gruszczyk, Jakub. "Structural analysis of bacterial protein tyrosine kinases (by-kinases) and their substrates." Paris 11, 2010. http://www.theses.fr/2010PA112135.

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Des tyrosine-kinases bactériennes atypiques (appelées BY-kinases) ont été identifiées comme constituant d'un complexe multiprotéique transmembranaire responsable de la synthèse et l'export des polysaccharides de la capsule bactérienne. Les BY-kinases s'autophosphorylent sur un cluster de tyrosine C-terminal et phosphorylent des protéines endogènes de la bactérie comme des UDP-sucres déshydrogénases impliquées dans la synthèse des précurseurs des exopolysaccharides. Les données structurales et fonctionnelles disponibles posaient la question de la conservation du degré d'oligomérisation et du mécanisme d'autophosphorylation entre BY-kinases de firmicutes et de protéobactéries. J'ai donc résolu la structure cristalline du domaine cytoplasmique de la BY-kinase Wzc de la protéobactérie E. Coli. Cette nouvelle structure montre que, comme la BY-kinase CapAB du firmicute S. Aureus, Wzc forme un anneau octamérique expliquant le mécanisme d'autophosphorylation intermoléculaire. Des mesures d'affinité par fluorimétrie m'ont également permis de montrer qu'une tyrosine interne Y569, initialement supposée réguler la trans-autophosphorylation du tyrosine-cluster, est directement impliquée dans la fixation du nucléotide. Nous montrons également qu'une boucle flexible riche en résidus basiques joue un rôle essentiel dans la synthèse de la capsule, probablement en interagissant avec d'autres protéines impliquées dans ce processus. De plus, j'ai résolu la structure cristalline de l'UDP-N-acétylmannosamine déshydrogenase CapO, substrat de la BY-kinase CapAB de S. Aureus. Cette structure révèle la formation d'un pont disulfure entre la cystéine catalytique C258 et le résidu C92 et la présence de potentiels sites de phosphorylation, Y89 et Y264, à proximité de ces deux cystéines. L'analyse de mutants est en cours afin d'élucider le mécanisme de régulation de cette enzyme. La comparaison avec les structures d'autres membres de cette famille de déshydrogénases permet également de mieux comprendre leur spécificité de substrat
Atypical bacterial tyrosine kinases (BY-kinases) have been identified as part of a multiprotein transmembrane complex responsible of the biosynthesis and export of capsular polysaccharides. BY-kinases autophosphorylate on a C-terminal tyrosine cluster and phosphorylate endogenous bacterial proteins like UDP-sugar dehydrogenases involved in the synthesis of exopolysaccharide precursors. Available structural and functional data raised the question of the conservation of the oligomerization state and of the autophosphorylation mechanism between BY-kinases from proteobacteria and firmicutes. I thus solved the crystal structure of the cytoplasmic domain of the BY-kinase Wzc from E. Coli. This new structure shows that, like the BY-kinase CapAB from the firmicute S. Aureus, Wzc forms an octameric ring explaining the intermolecular autophosphorylation mechanism. Fluorimetric affinity measurements further allowed me to show that the internal tyrosine Y569, initially supposed to regulate tyrosine-cluster trans-autophosphorylation, is directly involved in nucleotide binding. We also show that a flexible loop rich in basic residues plays an essential role in capsule synthesis, most probably through interaction with other proteins involved in this process. Moreover, I solved the crystal structure of UDP-N-acetylmannosamine dehydrogenase CapO, the substrate of the BY-kinases CapAB from S. Aureus. The structure reveals the formation of a disulfide bridge between the catalytic cysteine C258 and residue C92 and the presence of potential phosphorylation sites, Y89 and Y264, close to these two cysteines. Mutational analysis is underway in order to elucidate the regulatory mechanism of this enzyme. Comparison with the structures of other members of this family of dehydrogenases also allows us to shed light on their specific substrate recognition
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Dennis, 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/.

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A number of protein kinases have been shown to undergo autophosphorylation, but few have demonstrated a coordinate increase or decrease in enzymatic activity as a result. Described here is a novel S6 kinase isolated from human placenta which autoactivates through autophosphorylation in vitro. This S6/H4 kinase, purified in an inactive state, was shown to be a protein of Mr of 60,000 as estimated by SDS-PAGE and could catalyze the phosphorylation of the synthetic peptide S6-21, the histone H4, and myelin basic protein. Mild digestion of the inactive S6/H4 kinase with trypsin was necessary, but not sufficient, to activate the kinase fully
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30

Yu, Yan. "Functional investigation of the neuronal Cdk5 activator p35 in the regulation of actin dynamics /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20YUY.

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31

Vearing, Christopher John, and chris vearing@med monash edu au. "Structure, function & control of the EphA3 receptor tyrosine kinase." Swinburne University of Technology, 2005. http://adt.lib.swin.edu.au./public/adt-VSWT20051017.094940.

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The implication of the transmembrane signalling Receptor Tyrosine Kinases (RTKs) in cancer has accelerated the pursuit for drugs to target these molecules. In the process our understanding of how these membrane bound molecules are entangled in cell signalling has significantly expanded. There is now evidence that RTKs can facilitate the formation of a lattice-type network of signalling molecules to elicit whole cell responses to external ligand stimuli. Although beginning to be unravelled, knowledge pertaining to the mechanisms of molecular control that initiate these signalling pathways is still in its infancy. In this thesis, a random mutagenesis approach allowed the identification of the crucial interaction surfaces between membrane-bound EphA3 and its preferential binding partner ephrinA5, that are required to induce the formation of higher-order Eph signalling complexes. Modelling and experimental dissection of this co-ordinated receptor aggregation has provided detailed insights into the molecular mechanisms of Eph receptor activation, which in some aspects may also apply to other members of the RTK family. In particular, the importance of certain molecular interfaces in determining preferential and non-preferential Eph/ephrin interactions, suggests their role in the selection of biologically important binding partners. In addition to the assignment of the ephrin-interaction surfaces, the random mutagenesis strategy also identified a continuous conformational epitope as binding site for an anti-EphA3 monoclonal antibody. Fortuitously, antibody binding to this site functionally mimics ephrin stimulation of EphA3 positive cells, and in particular together with divalent ephrinA5, yields synergistically enhanced EphA3 activation. Elucidation of the underlying mechanism has provided opportunities to develop an efficient EphA3 targeting mechanism that is based on increased affinity and accelerated ephrinA5 uptake as consequence of this unique activation mechanism. On a genetic level, novel oligonucleotide analogues known as Peptide Nucleic Acids (PNAs) were analysed for their ability to sterically inhibit EphA3 DNA transcription and suggest a dosedependent downregulation of EphA3 expression, in malignant melanoma cells. Combined, ephrinA5, the anti-EphA3 MAb (IIIA4) and PNA, offer the possibility to investigate the specific machinery involved in Eph receptor expression and signalling for the specific targeting of EphA3 expressing tumour cells.
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32

Murdoch, Fern E. (Fern Elizabeth). "Occurrence and Structure of an Activating Enzyme for an S6 Kinase Determined by Monoclonal Antibody Analysis." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc798366/.

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In this study, the production of monoclonal antibodies directed against the activating enzyme for an S6 kinase is examined and described. Evidence is presented for the association of an Mr. 55,000 abd Mr. 95,000 protein with the s6 kinase. These proteins are phosphorylated in the presence of Activating Enzyme. A sequence of regulatory events for insulin-stimulated phosphorylation of ribosomal protein S6 in cells is postulated as follows: insulin activates the receptor tyrosine kinase, which phosphorylates the Mr 116,000 subunit of Activating Enzyme. The Activating Enzyme then activates the S6 kniase by phosphorylation, and phosphorylation of the ribosomal protein s6 is promoted.
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33

Gushwa, Nathan Ness. "Electrophilic nucleosides: Tools to explore protein kinases." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3378488.

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34

Yates, Alexandra Caroline. "Stress-activated protein kinases and neurodegenerative disease." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287325.

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35

Camacho-Soto, Karla. "Selective Control of Protein Kinases and Phosphatases." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/578903.

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The reversible phosphorylation of proteins plays a key role in nearly every aspect of cell life. This essential post-translational modification controls a myriad of cellular events from cell survival, differentiation, and migration to apoptosis. Two classes of enzymes, kinases and phosphatases, tightly control all phosphorylation events. Perturbation in the activity of any member of these classes of enzymes has been linked to numerous diseases including cancer, metabolic disorders, immune disorders and neurological disorders. Therefore, there is a great interest among the scientific community to develop methods to selectively modulate the activity of kinases and phosphatases not only for therapeutic purposes but also to understand the fundamental role of these enzymes in signaling events. The more than 500 kinases encoded in the human genome share a common catalytic fold and most inhibitors target the ATP binding site. Therefore selective targeting of a single kinase by an inhibitor at the highly conserved ATP binding site is one of the main concerns for designing probes or drugs. Our group has taken advantage of the potency and possible selectivity imparted by bivalent inhibitors and developed an in vitro selection approach to discover bivalent ligands. The strategy involves the use of an ATP-competitive small molecule warhead and a library of cyclic peptides displayed on phage that interact with the kinase of interest in a dynamic selection. The selection for a kinase binding peptide is carried out until consensus peptides are found and bivalent ligands are constructed by linking the selected cyclic peptide with the small molecule warhead through a synthetic linker. Using this approach a potent and selective bivalent inhibitor was found for PKA, a serine/threonine kinase. To interrogate the generality of this approach, a kinase closely related to PKA (PRKX) was used for which a very potent and selective bivalent ligand was found. The same selection strategy was further extended to the two kinases Lyn and Brk, which belong to the tyrosine kinase family. Though peptides were isolated that bound the desired kinase, potent bivalent inhibitors were not discovered. More generally, these experiments in sum are building a library of information regarding how to best design selections of potent and selective bivalent inhibitors. We further explored modulation of the activity of kinases and phosphatases by employing a ligand-gated split-protein approach. The small molecule gated spatial and temporal control of these enzymes should allow the study of signaling events in a controlled manner. The strategy employed consists in the identification of possible fragmentation sites within the catalytic domain of kinases and phosphatases by a sequence dissimilarity approach. Loop insertion mutants at the selected sites were tested for catalytic activity. Successful insertion mutants were further split into two catalytically inactive fragments, which were appended to two conditionally interacting protein domains. Upon addition of a small molecule, the two conditionally interacting domains reassemble the catalytic domain of the enzyme and restore catalytic activity. Using this approach we were able to modulate the activity of the tyrosine kinases Lyn, Fak and Src and the AGC kinase PKA. We also extended the approach to gate the activity of tyrosine phosphatases PTP1B, SHP1 and PTPH1. Finally, these ligand-gated split-kinases and phosphatases were validated in-cellulo. Thus, this work resulted in a new method for designing split-proteins and provided a palette of kinases and phosphatases that can be turned-on by small molecules. In total, these efforts describe two alternative routes that can be used to modulate phosphorylation events in a selective and controlled manner.
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36

Burns, Christopher John. "Tyrosine kinases and mitogen-activated protein kinases : roles in pancreatic β-cell function." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313990.

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37

Yoon, 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/.

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The kinetic mechanism of the cAMP-dependent protein kinase has been determined to be random in the direction of MgADP phosphorylation by using initial velocity studies in the absence and presence of the product, phospho-Serpeptide (Leu-Arg-Arg-Ala-Ser[P]-Leu-Gly) , and dead-end inhibitors. In contrast to the kinetic parameters obtained in the direction of Serpeptide phosphorylation, the only kinetic parameters affected by Mg^2+ are the dissociation constants for E:phospho-Serpeptide and E:MgADP, which are decreased by about 4-fold. The dead-end analog MgAMPCP binds with an affinity equal to that of MgADP in contrast to MgAMPPCP, which binds weaker than MgATP. The ratio of the maximum velocities in the forward and reverse reactions is about 200, and the Haldane relationship gives a K-eq of (7.2 ± 2) x 10^2. The latter can be compared to the K-eq obtained by direct measurement of reactant concentrations (2.2 ± 0.4) x 10^3 and 31-P NMR (1 ± 0.5) x 10^3. Data for the pH dependence of kinetic parameters and inhibitor dissociation constants for the cAMP dependent protein kinase are consistent with a mechanism in which reactants selectively bind to an enzyme with the catalytic base unprotonated and an enzyme group required protonated for Ser-peptide binding. Preferentially MgATP binds fully ionized and requires an enzyme residue (probably lysine) to be protonated. The maximum velocity and V/K-MgATP are pH independent. The V/K for Serpeptide is bell-shaped with estimated pK values of 6.2 and 8.5. The dependence of 1/K-i for Leu-Arg-Arg-Ala-Ala-Leu-Gly is also bell-shaped, giving pK values identical with those obtained for V/K-Serpeptide, while the K-i for MgAMPPCP increases from a constant value of 650 μM above pH 8 to a constant value of 4 mM below pH 5.5. The K-i for uncomplexed Mg^2+ obtained from the Mg^2+ dependence of V and V/K-MgATP is apparently pH independent.
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38

Wan, Yong. "Role of tyrosine kinases in G-protein signaling /." Access full-text from WCMC, 1997. http://proquest.umi.com/pqdweb?did=733008261&sid=12&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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39

Taylor, Allison Antoinette. "Regulation of an S6/H4 Kinase in Crude Lymphosarcoma P1798 Preparations." Thesis, University of North Texas, 1998. https://digital.library.unt.edu/ark:/67531/metadc501281/.

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Purified S6/H4 kinase (Mr 60,000) requires autophosphorylation for activation. A rabbit anti-S6/H4 kinase peptide (SVIDPVPAPVGDSHVDGAAK) antibody recognized both the S6/H4 kinase holoenzyme and catalytic domain. Immunoreactivity with p60 kinase protein, and S6/H4 kinase activity were precisely correlated in fractions obtained from ion exchange chromatography of P1798 lymphosarcoma extracts. An enzyme which catalyzed the MgATP-dependent phosphorylation and activation of S6/H4 kinase coeluted with immunoreactivity from Mono 5, but not Mono Q chromatography. Since S6/H4 kinase is homologous with rac-activated PAK65, the observation that phosphorylation is also required for activation suggests a complex mechanism for in vivo activation of the S6/H4 kinase.
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40

Pinsky, Benjamin Alan. "Characterization of the Ipl1/Aurora protein kinase in chromosome segregation and the spindle checkpoint /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/5028.

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41

Nemeth, Joseph. "Design and synthesis of chemical probes for the protein kinase B PH domain." Thesis, St Andrews, 2008. http://hdl.handle.net/10023/572.

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42

Goodman, Alan Gabriel. "P58IPK, the cellular eIF2alpha kinase inhibitor, promotes viral mRNA translation and limits host death during influenza virus infection /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8082.

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43

Grabbe, Caroline. "Protein tyrosine kinases and the regulation of signalling and adhesion in Drosophila melanogaster /." Doctoral thesis, Umeå : Umeå University, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-971.

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44

Lu, Bin. "Roles of cellular FLICE-inhibitory protein (c-FLIP) and Pl3K/Akt in Fas (CD95)-induced NF-[kappa]B activation and apoptosis through death effector domains." Morgantown, W. Va. : [West Virginia University Libraries], 2005. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4344.

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Thesis (Ph. D.)--West Virginia University, 2005.
Title from document title page. Document formatted into pages; contains viii, 95 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 82-95).
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45

Rice, Kevin M. "Effects of aging on pressure-induced MAPK activation in the rat aorta." Huntington, WV : [Marshall University Libraries], 2005. http://www.marshall.edu/etd/descript.asp?ref=526.

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46

Bull, Natalie D. "Modulation of rat retinal glutamate transporters by PKC : physiological and ischaemic outcomes /." [St. Lucia, Qld.], 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16813.pdf.

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47

Cheng, Kai. "Identification of Pctaire1 as a p35-interacting protein and a novel substrate for Cdk5 /." View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BICH%202003%20CHENG.

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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2003.
Includes bibliographical references (leaves 153-177). Also available in electronic version. Access restricted to campus users.
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48

Chen, Mingzi. "Mos regulation in activating the MAP kinase pathway /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/9195.

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49

Raman, Malavika. "Identification of intracellular signaling pathways regulated by the TAO family of mammalian STE20p kinases." Access to abstract only; dissertation is embargoed until after 5/15/2007, 2006. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=163.

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50

Craig, Karen Leigh. "Characterization and phosphorylation site mapping of human pleckstrin /." *McMaster only, 1996.

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