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LEADER 03641ctm 2200529 i 4500

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003 OCoLC;

005 20240122153501.0;

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035 a| (Sirsi) o166343235;

035 a| (OCoLC)166343235;

049 a| EREE;

050 4 a| QH603.C43b| C43 2005;

100 1 a| Chappell, William H.,e| author.=| ^A720735;

245 10 a| Notch-1 signaling regulates the expression of the phosphatase and tensin homolog deleted on chromosome 10 tumor suppressor gene in human embryonic kidney 293 cells /c| by William H. Chappell.;

264 0 c| 2005.;

300 a| 75 leaves :b| illustrations (some color) ;c| 28 cm;

336 a| textb| txt2| rdacontent;

337 a| unmediatedb| n2| rdamedia;

338 a| volumeb| nc2| rdacarrier;

502 b| M.S.c| East Carolina Universityd| 2005;

500 a| Presented to the faculty of the Department of Biology.;

500 a| Advisor: Fred E. Bertrand;

520 3 a| Notch-1 is an evolutionarily conserved transmembrane receptor that is associated with binary cell choice in progenitor cells. Aberrant Notch-1 signaling has been reported to cause oncogenesis in different cell types and is capable of interacting with other signaling pathways. Constitutively active Notch-1 was introduced into 293 HEK fibroblast cells in order to examine crosstalk between Notch-1 and other signaling pathways, such as Ras/Raf/MEK/ERK. Stable Notch-1 expressing cells developed a more rounded morphology and contained an increased level of activated ERK-1,-2. In addition, total and phosphorylated species of FAK were decreased when compared to controls. Further analysis revealed an increase in total and phosphorylated PTEN protein in the presence of Notch-1. Examination of the human PTEN promoter yielded the identification of two potential CBF-1/RBP-Jk binding sites. A luciferase reporter assay for PTEN promoter activation was used to examine this potential interaction. An increase of promoter activity was observed in Notch-1 cells. These data suggest another mode of interaction between Notch-1 and Ras/Raf/MEK/ERK and also a role for Notch-1 in regulating PTEN.;

504 a| Includes bibliographical references (leaves 61-69).;

650 0 a| Cell receptorsx| Research.=| ^A9189;

650 0 a| Stem cellsx| Research.=| ^A707564;

650 0 a| Carcinogenesisx| Research.=| ^A1259;

650 7 a| Carcinogenesisx| Research.2| fast0| (OCoLC)fst00846982;

650 7 a| Cell receptorsx| Research.2| fast0| (OCoLC)fst01424817;

650 7 a| Stem cellsx| Research.2| fast0| (OCoLC)fst01132977;

655 7 a| Academic theses.2| fast0| (OCoLC)fst01726453;

655 7 a| Academic theses.2| lcgft;

655 7 a| Thèses et écrits académiques.2| rvmgf0| (CaQQLa)RVMGF-000001173;

655 2 a| Academic Dissertation.0| (DNLM)D019478?| UNAUTHORIZED;

700 1 a| Bertrand, Fred E.,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| East Carolina University.b| Department of Biology.=| ^A637467;

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/11907;

949 a| Click on web addressw| asish| joyner101;

949 a| Click on web addressw| asish| hsl111;

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Notch-1 signaling regulates the expression of the phosphatase and tensin homolog deleted on chromosome 10 tumor suppressor gene in human embryonic kidney 293 cells / by William H. Chappell.

Author/creator	Chappell, William H. author.
Other author	Bertrand, Fred E., degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	2005.
Description	75 leaves : illustrations (some color) ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	Cell receptors--Research. Stem cells--Research. Carcinogenesis--Research.

Summary	Notch-1 is an evolutionarily conserved transmembrane receptor that is associated with binary cell choice in progenitor cells. Aberrant Notch-1 signaling has been reported to cause oncogenesis in different cell types and is capable of interacting with other signaling pathways. Constitutively active Notch-1 was introduced into 293 HEK fibroblast cells in order to examine crosstalk between Notch-1 and other signaling pathways, such as Ras/Raf/MEK/ERK. Stable Notch-1 expressing cells developed a more rounded morphology and contained an increased level of activated ERK-1,-2. In addition, total and phosphorylated species of FAK were decreased when compared to controls. Further analysis revealed an increase in total and phosphorylated PTEN protein in the presence of Notch-1. Examination of the human PTEN promoter yielded the identification of two potential CBF-1/RBP-Jk binding sites. A luciferase reporter assay for PTEN promoter activation was used to examine this potential interaction. An increase of promoter activity was observed in Notch-1 cells. These data suggest another mode of interaction between Notch-1 and Ras/Raf/MEK/ERK and also a role for Notch-1 in regulating PTEN.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Fred E. Bertrand
Dissertation note	M.S. East Carolina University 2005
Bibliography note	Includes bibliographical references (leaves 61-69).
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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Notch-1 signaling regulates the expression of the phosphatase and tensin homolog deleted on chromosome 10 tumor suppressor gene in human embryonic kidney 293 cells / by William H. Chappell.

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