Dissertation/Thesis Abstract

T cell activation requires glucose retention and use via mechanisms modulated by MAPK signaling
by Marko, Aimee Joy, M.S., University of Maryland, College Park, 2010, 66; 1489155
Abstract (Summary)

T 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.

Indexing (document details)
Advisor: Frauwirth, Kenneth A.
Commitee: Mosser, David M., Stewart, Richard C., Wu, Louisa P.
School: University of Maryland, College Park
Department: Cell Biology & Molecular Genetics
School Location: United States -- Maryland
Source: MAI 49/04M, Masters Abstracts International
Subjects: Molecular biology, Cellular biology, Immunology
Keywords: Glucose uptake, Glycolysis, Krebs cycle and pentose phosphate pathway, MAPK signal, T cell, Transcription factor
Publication Number: 1489155
ISBN: 978-1-124-48690-1
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