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T Cell Activation Requires Glucose Retention and Use Via Mechanisms Modulated by MAPK Signaling

dc.contributor.advisorFrauwirth, Kenneth A.en_US
dc.contributor.authorMarko, Aimee Joyen_US
dc.date.accessioned2011-02-19T06:30:54Z
dc.date.available2011-02-19T06:30:54Z
dc.date.issued2010en_US
dc.identifier.urihttp://hdl.handle.net/1903/11079
dc.description.abstractT lymphocytes play a critical role in a cell-mediated immune response. During activation, extracellular and intracellular signals alter T cell metabolism in order to meet the energetic and biometabolic needs of a proliferating, active cell, but control of these phenomena is not well defined. The idea that metabolism can be regulated directly via receptor-mediated signals is being investigated. The T cell receptor (TCR) and CD28 pathways were stimulated and signaling was modified using chemical inhibitors of MAP kinases. Metabolic changes were monitored using assays for glucose uptake, hexokinase activity, glycolysis, Krebs Cycle, and pentose phosphate pathway. Two MAPK pathways (ERK, JNK) appear to be determining factors because their inhibition downregulated metabolism. Inhibition of another MAPK pathway (p38) causes some downregulation of these activities but the effect is not as strong as with the ERK and JNK inhibitors, suggesting that the p38 pathway is less important in regulating glucose metabolism.en_US
dc.titleT Cell Activation Requires Glucose Retention and Use Via Mechanisms Modulated by MAPK Signalingen_US
dc.typeThesisen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.contributor.departmentCell Biology & Molecular Geneticsen_US
dc.subject.pqcontrolledMolecular Biologyen_US
dc.subject.pqcontrolledImmunologyen_US
dc.subject.pqcontrolledCellular Biologyen_US
dc.subject.pquncontrolledGlucose uptakeen_US
dc.subject.pquncontrolledGlycolysisen_US
dc.subject.pquncontrolledKrebs Cycle and Pentose Phosphate Pathwayen_US
dc.subject.pquncontrolledMAPK signalen_US
dc.subject.pquncontrolledT cellen_US
dc.subject.pquncontrolledTranscription factoren_US


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