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035 a| (Sirsi) o648767442;

035 a| (OCoLC)648767442;

040 a| EREc| EREd| EREd| UtOrBLW;

049 a| EREE;

090 a| QH465;

100 1 a| Loftin, Charles William.?| UNAUTHORIZED;

245 10 a| Repair of clustered DNA lesions in double strand break repair deficient human tumor cells /c| by Charles William Loftin.;

260 a| [Greenville, N.C.] :b| East Carolina University,c| 2010.;

300 a| 95 pages :b| ills. (some color), digital, PDF file;

336 a| text2| rdacontent;

337 a| computer2| rdamedia;

338 a| online resource2| rdacarrier;

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

500 a| Advisor: Alexandros Georgakilas.;

500 a| Title from PDF t.p. (viewed Sep. 27, 2010).;

502 b| M.S.c| East Carolina Universityd| 2010.;

504 a| Includes bibliographical references.;

520 3 a| DNA-dependent protein kinase (DNA-PK) is a holoenzyme of three subunits, Ku70, Ku80, and the DNA-Pk catalytic subunit (DNA-PKcs). DNA-PK serves a role in non-homologous end joining to repair double stranded breaks, and has a suggested role in the expression of base excision repair (BER) proteins. Repair of DNA damage is vital to the prevention of malignant mutations. Oxidative induced clustered DNA lesions (OCDLs) is the occurrence of two or more closely located DNA lesions, and have been shown to be poorly repaired. DNA-PKcs is the phosphorylating unit of DNA-PK. DNA-PKcs deficient cells show increased radiosensitivity and decreased repairability. This study aimed to evaluate the role of DNA-PK in OCDL repair in DNA-PKcs deficient cells. This study showed decreased OCDL repair and a decreased expression of the BER protein XRCC1 in cells treated with DNA-PKcs specific inhibitors compared to non-treated cells. This study proposes that DNA-PK is involved in response to single and complex damage, and that inhibition of DNA-PKcs results in poor OCDL repair. Interest is growing in protein kinase inhibitors as supplemental aids to chemo and radiotherapies. This study and others indicates that DNA-PK is important to proficient DNA repair, indicating that DNA-PKcs inhibitors may have clinical relevance as supplemental aids to current cancer therapies in killing targeted cells.;

538 a| System requirements: Adobe Reader.;

538 a| Mode of access: World Wide Web.;

650 0 a| DNA damage.=| ^A273441;

650 0 a| Protein kinases.=| ^A396687;

650 0 a| DNA repair.=| ^A15081;

650 0 a| Tumor suppressor proteins.=| ^A1032333;

653 a| Biology, General;

700 1 a| Georgakilas, Alexandros G.=| ^A1114884;

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

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/2727;

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998 a| 2284754;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 2284754-1001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 7/19/2010x| ETDz| JERESOURCE;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 2284754-2001l| HSLELECm| HSLr| Ys| Yt| HEETDu| 7/19/2010x| ETDz| HERESOURCE;

Repair of clustered DNA lesions in double strand break repair deficient human tumor cells / by Charles William Loftin.

Author/creator	Loftin, Charles William
Other author	Georgakilas, Alexandros G.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Publication Info	[Greenville, N.C.] : East Carolina University, 2010.
Description	95 pages : ills. (some color), digital, PDF file
Supplemental Content	Access via ScholarShip
Subjects	DNA damage. Protein kinases. DNA repair. Tumor suppressor proteins.

Summary	DNA-dependent protein kinase (DNA-PK) is a holoenzyme of three subunits, Ku70, Ku80, and the DNA-Pk catalytic subunit (DNA-PKcs). DNA-PK serves a role in non-homologous end joining to repair double stranded breaks, and has a suggested role in the expression of base excision repair (BER) proteins. Repair of DNA damage is vital to the prevention of malignant mutations. Oxidative induced clustered DNA lesions (OCDLs) is the occurrence of two or more closely located DNA lesions, and have been shown to be poorly repaired. DNA-PKcs is the phosphorylating unit of DNA-PK. DNA-PKcs deficient cells show increased radiosensitivity and decreased repairability. This study aimed to evaluate the role of DNA-PK in OCDL repair in DNA-PKcs deficient cells. This study showed decreased OCDL repair and a decreased expression of the BER protein XRCC1 in cells treated with DNA-PKcs specific inhibitors compared to non-treated cells. This study proposes that DNA-PK is involved in response to single and complex damage, and that inhibition of DNA-PKcs results in poor OCDL repair. Interest is growing in protein kinase inhibitors as supplemental aids to chemo and radiotherapies. This study and others indicates that DNA-PK is important to proficient DNA repair, indicating that DNA-PKcs inhibitors may have clinical relevance as supplemental aids to current cancer therapies in killing targeted cells.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Alexandros Georgakilas.
General note	Title from PDF t.p. (viewed Sep. 27, 2010).
Dissertation note	M.S. East Carolina University 2010.
Bibliography note	Includes bibliographical references.
Technical details	System requirements: Adobe Reader.
Technical details	Mode of access: World Wide Web.

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Repair of clustered DNA lesions in double strand break repair deficient human tumor cells / by Charles William Loftin.

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