Evidence for a role pf MAP kinases (ERK1 and pERK) in proliferating and differentiating odontogenic epithelia
| dc.contributor.author | Nickolaychuk, Brent R. | en_US |
| dc.date.accessioned | 2007-05-22T15:12:04Z | |
| dc.date.available | 2007-05-22T15:12:04Z | |
| dc.date.issued | 2001-01-01T00:00:00Z | en_US |
| dc.degree.discipline | Preventive Dental Science | en_US |
| dc.degree.level | Master of Science (M.Sc.) | en_US |
| dc.description.abstract | The epithelial rests of Malassez (ERM), remnants of odontogenic epithelium, have been implicated in maintaining the periodontal space by stimulating osteoclastic bone resorption and interstitial matrix degradation. While the binding of epidermal growth factor (EGF) to its receptor (EGFr) on ERM appears to play a central role in the functional activation of these cells, the nature of intracellular signaling pathways downstream of EGFr remains unclear. Mitogen-activated protein (MAP) kinases (or extracellular signal-regulated kinases - ERKs) have been described as downstream mediators of EGF-induced cellular activation in other tissues. The purpose of this study was to determine the expression pattern of ERK1 and its phosphorylated form (pERK) in proliferating and differentiating odontogenic epithelia, including ERM, in the presence or absence of inflammation. To this end, immunohistochemistry for ERK1, pERK, PCNA (marker for cycling cells), and PAN-cytokeratin (marker for epithelial differentiation) was performed on paraffin-embedded sections of dental follicles and odontogenic cysts. (Abstract shortened by UMI.) | en_US |
| dc.format.extent | 4345700 bytes | |
| dc.format.extent | 184 bytes | |
| dc.format.mimetype | application/pdf | |
| dc.format.mimetype | text/plain | |
| dc.identifier.uri | http://hdl.handle.net/1993/1987 | |
| dc.language.iso | eng | en_US |
| dc.rights | open access | en_US |
| dc.title | Evidence for a role pf MAP kinases (ERK1 and pERK) in proliferating and differentiating odontogenic epithelia | en_US |
| dc.type | master thesis | en_US |