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Protein kinase inhibitor effects on P-glycoprotein (P-gp) activity and expression in various cell linesPogorzelec, Michael P.J. 13 January 2015 (has links)
Little is known about potential influences of kinase pathway modulation on expression and activity of P-glycoprotein (P-gp). A protein kinase inhibitor (PKI) library was screened, to determine its effects on activity and expression of P-gp, in various cell lines.
Cell lines were incubated with PKI for 24 h. Subsequent P-gp substrate accumulation studies were performed. Changes in P-gp activity and/or expression ≥ 25% compared to control were considered hits. Kinase pathways identified as P-gp activity hits were examined for their ability to modulate permeability.
PKI families GSK-3, Craf1 and VEGFR2 and Tie-2, significantly modulated P-gp activity in the MDCK cell line. PKI families GSK-3, Iκκ and Jnk2/3 significantly modulated P-gp activity in the Caco-2 cell line. Few P-gp activity hits significantly modulated P-gp expression.
PKIs modulate P-gp activity more than P-gp expression in a cell line dependent manner, excluding GSK-3 PKI family, which appears to be cell line independent.
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Mechanism underlying the maturation of AMPA receptors in zebrafishAroonassala Patten, Shunmoogum 11 1900 (has links)
Glutamate AMPA receptors (AMPARs) are major excitatory receptors in the vertebrate CNS. In many biological systems there are changes in the properties of AMPARs during development that are essential for providing an increase in efficiency of information transfer between neurons and a refinement of motor co-ordination and sensory perception and cognition. It is not surprising that improper development or loss of function of AMPARs can lead to many neurological disorders such as epilepsy and amyotrophic lateral sclerosis. Thus, determining the mechanisms by which AMPARs mature is of particular importance. The objectives of my thesis were to characterize the developmental changes in AMPAR-mediated currents in zebrafish Mauthner cells and to determine the mechanisms underlying any changes. The major findings reported in this thesis are that (1) there are developmental changes in the properties of AMPAR-currents as the Mauthner cell matures; (2) the mechanism underlying these changes is a switch in the composition of AMPA receptor subtypes; and (3) PKC is necessary for the developmental switch in AMPAR subtypes from slow receptors to fast receptors. These findings provide valuable insights into the mechanism underlying the development of AMPARs. In addition, they provide the first instance of a signalling link (PKC) required for the developmental subunit switch and the developmental speeding of AMPAR kinetics. / Physiology, Cell Biology and Developmental Biology
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Krylov and Finite State Projection methods for simulating stochastic biochemical kinetics via the Chemical Master EquationShevarl MacNamara Unknown Date (has links)
Computational and mathematical models of cellular processes promise great benets in important elds such as molecular biology and medicine. Increasingly, researchers are incorporating the fundamentally discrete and stochastic nature of biochemical processes into the mathematical models that are intended to represent them. This has led to the formulation of models for genetic networks as continuous-time, discrete state, Markov processes, giving rise to the so-called Chemical Master Equation (CME), which is a discrete, partial dierential equation, that governs the evolution of the associated probability distribution function (PDF). While promising many insights, the CME is computationally challenging, especially as the dimension of the model grows. In this thesis, novel methods are developed for computing the PDF of the Master Equation. The problems associated with the high-dimensional nature of the Chemical Master Equation are addressed by adapting Krylov methods, in combination with Finite State Projection methods, to derive algorithms well-suited to the Master Equation. Variations of the approach that incorporate the Strang splitting and a stochastic analogue of the total quasi-steady-state approximation are also derived for chemical systems with disparate rates. Monte Carlo approaches, such as the Stochastic Simulation Algorithm, that simulate trajectories of the process governed by the CME have been a very popular approach and we compare these with the PDF approaches developed in this thesis. The thesis concludes with a discussion of various implementation issues along with numerical results for important applications in systems biology, including the gene toggle, the Goldbeter-Koshland switch and the Mitogen-Activated Protein Kinase Cascade.
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Krylov and Finite State Projection methods for simulating stochastic biochemical kinetics via the Chemical Master EquationShevarl MacNamara Unknown Date (has links)
Computational and mathematical models of cellular processes promise great benets in important elds such as molecular biology and medicine. Increasingly, researchers are incorporating the fundamentally discrete and stochastic nature of biochemical processes into the mathematical models that are intended to represent them. This has led to the formulation of models for genetic networks as continuous-time, discrete state, Markov processes, giving rise to the so-called Chemical Master Equation (CME), which is a discrete, partial dierential equation, that governs the evolution of the associated probability distribution function (PDF). While promising many insights, the CME is computationally challenging, especially as the dimension of the model grows. In this thesis, novel methods are developed for computing the PDF of the Master Equation. The problems associated with the high-dimensional nature of the Chemical Master Equation are addressed by adapting Krylov methods, in combination with Finite State Projection methods, to derive algorithms well-suited to the Master Equation. Variations of the approach that incorporate the Strang splitting and a stochastic analogue of the total quasi-steady-state approximation are also derived for chemical systems with disparate rates. Monte Carlo approaches, such as the Stochastic Simulation Algorithm, that simulate trajectories of the process governed by the CME have been a very popular approach and we compare these with the PDF approaches developed in this thesis. The thesis concludes with a discussion of various implementation issues along with numerical results for important applications in systems biology, including the gene toggle, the Goldbeter-Koshland switch and the Mitogen-Activated Protein Kinase Cascade.
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Leishmania donovani lipophosphoglycan : effects on actin and phagosomal maturation /Holm, Åsa January 2003 (has links) (PDF)
Diss. (sammanfattning) Linköping : Univ., 2003. / Härtill 4 uppsatser.
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Glucose and insulin modulate phagocytosis and production of reactive oxygen metabolites in human neutrophil granulocytes /Saiepour, Daniel, January 2006 (has links)
Diss. (sammanfattning) Umeå : Umeå universitet, 2006. / Härtill 4 uppsatser.
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The role of nucleoside diphosphate kinase in plant mitochondria /Johansson, Monika, January 2006 (has links) (PDF)
Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv., 2006. / Härtill 4 uppsatser.
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Analysis of timekeeper implicates antagonism between CK2 and PP2A during Drosophila neurogenesisKunttas, Ezgi. January 1900 (has links)
Thesis (M.S.)--West Virginia University, 2008. / Title from document title page. Document formatted into pages; contains ix, 128 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 118-127).
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Kappa Opioid Receptor regulation of ERK1/2 MAP kinase signaling cascade molecular mechanisms modulating cocaine reward : a dissertation /Rasakham, Khampaseuth. January 1900 (has links)
Thesis (Ph. D.)--Northeastern University, 2008. / Title from title page (viewed March 3, 2009). Graduate School of Arts and Sciences, Dept. of Psychology. Includes bibliographical references (p. 148-156).
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The roles of ERK₁ and ERK₂ MAP kinase in neural development and diseaseSamuels, Ivy S. January 2008 (has links)
Thesis (Ph. D.)--Case Western Reserve University, 2008. / [School of Medicine] Department of Neurosciences. Includes bibliographical references.
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