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003 OCoLC;

005 20250422153006.0;

008 071103s2006 xx a bm 000 0 eng d;

035 a| (Sirsi) o180688757;

035 a| (OCoLC)180688757;

049 a| EREE;

050 4 a| QR400b| .L35 2006;

100 1 a| Lambert, Phelps J.,e| author.?| UNAUTHORIZED;

245 12 a| A role for VEGFRs in regulating KSHV latency /c| by Phelps J. Lambert.;

264 0 c| 2006.;

300 a| viii, 60 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| 2006;

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

500 a| Advisor: Shaw M. Akula;

520 3 a| Kaposi's sarcoma associated herpesvirus (KSHV) is responsible for causing a number of diseases, including Kaposi's sarcoma (KS), primary effusion lymphoma (PEL) and multicentric Castleman disease. When KSHV infects a cell it first exists in a relatively dormant, or latent state. The virus becomes significantly more pathogenic when it switches to its lytic state, in which it actively replicates within the cell, causes the cell to burst, and spreads throughout the body. As such, understanding the mechanisms that govern the virus' switch, or reactivation, from its latent to lytic state will help in the future development of anti-KSHV therapies. It is currently known that KSHV infected cells are much more likely to undergo reactivation if they are in the S, or DNA synthesis phase of their cell cycle. It is further known that vascular endothelial growth factor (VEGF), plays a significant role in causing cells to progress to S phase of their cell cycle. What is not known is how VEGF mediates cell cycle progression in KSHV infected cells. We hypothesized VEGF signaling plays a crucial role in KSHV reactivation. Testing our hypothesis in KSHV infected B cells (BCBL-1), we found that VEGF signaling through VEGFR-2 stimulated cell cycle progression and KSHV reactivation while signaling through VEGFR-1 inhibited it. We further found that VEGFR-1 signaling works, at least in part, by inhibiting VEGFR-2 signaling through the molecule nitric oxide. Overall, the results from this study document a divergent role for VEGF signaling in regulating the KSHV reactivation process.;

504 a| Includes bibliographical references (leaves 42-54).;

650 0 a| Herpesviruses.=| ^A144272;

650 0 a| Kaposi's sarcoma.=| ^A708280;

650 0 a| Vascular endothelial growth factors.=| ^A708320;

650 0 a| Vascular endothelium.=| ^A575285;

650 0 a| Growth factors.=| ^A194099;

650 0 a| Cell cycle.=| ^A4972;

650 2 a| Sarcoma, Kaposi.0| (DNLM)D012514=| ^A964398;

650 2 a| Endothelium, Vascular.0| (DNLM)D004730=| ^A956394;

650 2 a| Growth Substances.0| (DNLM)D006133=| ^A920141;

650 2 a| Cell Cycle.0| (DNLM)D002453=| ^A919206;

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

650 7 a| Cell cycle.2| fast0| (OCoLC)fst00850178;

650 7 a| Growth factors.2| fast0| (OCoLC)fst00948607;

650 7 a| Herpesviruses.2| fast0| (OCoLC)fst00955650;

650 7 a| Kaposi's sarcoma.2| fast0| (OCoLC)fst00986150;

650 7 a| Vascular endothelial growth factors.2| fast0| (OCoLC)fst01200619;

650 7 a| Vascular endothelium.2| fast0| (OCoLC)fst01164498;

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;

700 1 a| Akula, Shaw M.,e| degree supervisor.1| https://id.oclc.org/worldcat/entity/E39PCjKQf4c4xJJb73dbXvgWcK=| ^A1406820;

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

856 41 z| Access via ScholarShipu| http://hdl.handle.net/10342/12553;

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

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

994 a| C0b| ERE;

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999 a| ASK AT SPECIAL COLLECTIONS DESKw| ASISc| 1i| MQ2266406l| JSCJTHDm| JOYNERr| Ys| Yt| JSCJTHDu| 11/3/2007x| ETDz| JSPECCOLLo| .STAFF. 0;

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A role for VEGFRs in regulating KSHV latency / by Phelps J. Lambert.

Author/creator	Lambert, Phelps J. author.
Other author	Akula, Shaw M., degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	2006.
Description	viii, 60 leaves : illustrations (some color) ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	Herpesviruses. Kaposi's sarcoma. Vascular endothelial growth factors. Vascular endothelium. Growth factors. Cell cycle. Sarcoma, Kaposi. Endothelium, Vascular. Growth Substances. Cell Cycle.

Summary	Kaposi's sarcoma associated herpesvirus (KSHV) is responsible for causing a number of diseases, including Kaposi's sarcoma (KS), primary effusion lymphoma (PEL) and multicentric Castleman disease. When KSHV infects a cell it first exists in a relatively dormant, or latent state. The virus becomes significantly more pathogenic when it switches to its lytic state, in which it actively replicates within the cell, causes the cell to burst, and spreads throughout the body. As such, understanding the mechanisms that govern the virus' switch, or reactivation, from its latent to lytic state will help in the future development of anti-KSHV therapies. It is currently known that KSHV infected cells are much more likely to undergo reactivation if they are in the S, or DNA synthesis phase of their cell cycle. It is further known that vascular endothelial growth factor (VEGF), plays a significant role in causing cells to progress to S phase of their cell cycle. What is not known is how VEGF mediates cell cycle progression in KSHV infected cells. We hypothesized VEGF signaling plays a crucial role in KSHV reactivation. Testing our hypothesis in KSHV infected B cells (BCBL-1), we found that VEGF signaling through VEGFR-2 stimulated cell cycle progression and KSHV reactivation while signaling through VEGFR-1 inhibited it. We further found that VEGFR-1 signaling works, at least in part, by inhibiting VEGFR-2 signaling through the molecule nitric oxide. Overall, the results from this study document a divergent role for VEGF signaling in regulating the KSHV reactivation process.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Shaw M. Akula
Dissertation note	M.S. East Carolina University 2006
Bibliography note	Includes bibliographical references (leaves 42-54).
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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