Current Search: Undergraduate Honors Theses (x) » Biological Science (x) » Life sciences (x)
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Title
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Chromatin Structural Changes Linking Flavonoid Luteolin's Function to Genomic Targets.
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Creator
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Koerner, Joshua, Biological Science
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Abstract/Description
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Many non-inherited factors play a role in the epidemiology of cancer. Several studies have suggested that a dietary increase in fruits and vegetables containing compounds such as Luteolin, used in this study, would reduce the new instances of cancer by 20% and potentially prevent 200,000 cancer-related deaths annually. One hallmark of cancer is the reorganization of DNA inside the cell. Each cell in the human body contains approximately four meters of DNA organized into a compartment, the...
Show moreMany non-inherited factors play a role in the epidemiology of cancer. Several studies have suggested that a dietary increase in fruits and vegetables containing compounds such as Luteolin, used in this study, would reduce the new instances of cancer by 20% and potentially prevent 200,000 cancer-related deaths annually. One hallmark of cancer is the reorganization of DNA inside the cell. Each cell in the human body contains approximately four meters of DNA organized into a compartment, the nucleus, that is five one-hundredths of a millimeter. This almost unbelievable compaction is facilitated by the combination of negatively charged DNA with positively charged proteins to make a complex called chromatin. The organization of chromatin regulates access to DNA sequences. This project aimed to investigate factors that regulate the organization of chromatin, thereby regulating access to the genome. In this study we highlight five genomic locations where the structure of DNA changes in response to Luteolin treatment. We have potentially identified a new promoter region for the Abelson murine leukemia viral oncogene homolog 2, (ABL2) gene. Luteolin places a nucleosome in a transcriptionally active region of hydroxytryptamine receptor 2B (HTR2B) to inhibit the possible production of the gene product. Luteolin may be establishing transcriptional competence of cyclin-dependent kinase inhibitor 2A (CDKN2A) through regulation of chromatin structure around Sp1 binding sites in the promoter. Luteolin alters chromatin structure around the Sp1 binding sites in the promoter region of kisspeptin-1 (KiSS1), which could be a preliminary step to achieving transcriptional competence. Luteolin treatment alters the chromatin structure of the myelocytomatosis viral oncogene homolog (Myc) promoter in order to potentially re-establish steady state expression in a previously deregulated gene.
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Date Issued
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2012
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Identifier
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FSU_migr_uhm-0079
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Format
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Thesis
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Title
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Hallmark Pathology of Temporal Lobe Epilepsy: Loss of Layer III Pyramidal Neurons in the Entorhinal Cortex and its Relation to Distribution of NMDA Receptor Subunits.
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Creator
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Richardson, Max, Biological Science
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Abstract/Description
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Neuronal loss in Layer III of the medial entorhinal cortex (MEA) is a characteristic phenomenon associated with Temporal Lobe Epilepsy. The immediately adjacent lateral entorhinal cortex (LEA) does not exhibit such loss. The current study uses indirect immunofluorescence assays in the third layer of both the medial and lateral entorhinal cortex to detect differences in protein expression of the most prevalent N-methyl-D-aspartate receptor (NMDAR) subunit isoforms in the adult cortex: the...
Show moreNeuronal loss in Layer III of the medial entorhinal cortex (MEA) is a characteristic phenomenon associated with Temporal Lobe Epilepsy. The immediately adjacent lateral entorhinal cortex (LEA) does not exhibit such loss. The current study uses indirect immunofluorescence assays in the third layer of both the medial and lateral entorhinal cortex to detect differences in protein expression of the most prevalent N-methyl-D-aspartate receptor (NMDAR) subunit isoforms in the adult cortex: the GluN1, GluN2A and GluN2B subunits. The latter two subunits confer varying levels of Ca2+ permeability and ostensibly the potential for excitotoxicity that may lead to characteristic loss of this particular population of neurons. We find that the level of GluN1 protein expression in the MEA and LEA is similar, suggesting that the number of NMDARs in the MEA and LEA is also similar, and that both GluN2A and GluN2B expression is higher in the MEA than in the LEA. These findings taken together may suggest a difference in subunit distribution and/or stoichiometry of NMDA receptors between the third layer of the MEA and LEA.
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Date Issued
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2012
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Identifier
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FSU_migr_uhm-0061
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Format
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Thesis
