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LEADER 04476ctm 2200625 i 4500

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003 OCoLC;

005 20260127093919.0;

008 071119s2007 xx a bm 000 0 eng d;

035 a| (Sirsi) o181588405;

035 a| (OCoLC)181588405;

049 a| EREE;

050 4 a| QH609b| .P43 2007;

100 1 a| Peddi, Prakash,e| author.?| UNAUTHORIZED;

245 10 a| Role of DNA-PKCS in the processing of double stranded breaks and oxidative clustered DNA lesions in the human breast cancer cell line MCF-7 /c| by Prakash Peddi.;

264 0 c| 2007.;

300 a| xii, 88 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| 2007;

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

500 a| Advisor: Alexandros Georgakilas;

520 0 a| Double stranded breaks (DSBs) and non-DSB oxidative clustered DNA lesions (OCDLs) are the most lethal forms of DNA damage and can be induced by a number of external agents, including ionizing radiation and radiomimetic drugs. DSBs can result from several normal cellular responses and also during repair of OCDLs. Efficient repair of DNA DSBs is essential for the maintenance of chromosomal integrity. DNA-dependent protein kinase (DNA-PK) is the central protein participating in non homologous end joining pathway (NHEJ) and is composed of a heterotrimer of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and Ku (composed of Ku 70 and Ku 80). DNA-PKcs closely interacts with proteins like Ku, which is involved in repair of closely spaced lesions. Targeted silencing of DNA-PKcs using RNA interference methodology resulted in reduced repair of clustered DNA lesions and DSBs produced as a result of [gamma]-irradiation. Reducing the activity of DNA-PKcs using a specific inhibitor 1- (2-hydroxy4-morpholin-4yl-phenyl)-ethanone, also known as IC86621, delayed the processing of clusters and DSBs produced as a result of exposure to [gamma]-rays. Evaluation of y-H2AX foci formation confirms delayed processing of DSBs in MCF-7 cells with reduced expression or reduced activity of DNA-PKcs. We propose that inhibition of double strand break repair pathway blocks leads to inhibiting the efficient repair of clustered DNA lesions. The functional significance and mechanisms of interaction between these two pathways require further investigation.;

504 a| Includes bibliographical references (leaves 80-88).;

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

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

650 0 a| DNA-binding proteins.=| ^A260138;

650 0 a| Breastx| Cancerx| Research.=| ^A491048;

650 0 a| Precancerous conditions.=| ^A7886;

650 2 a| DNA Repair.0| (DNLM)D004260=| ^A923057;

650 2 a| DNA Damage.0| (DNLM)D004249=| ^A926668;

650 2 a| DNA-Binding Proteins.0| (DNLM)D004268=| ^A926280;

650 2 a| Precancerous Conditions.0| (DNLM)D011230=| ^A948923;

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

650 7 a| DNA-binding proteins.2| fast0| (OCoLC)fst00886613;

650 7 a| DNA damage.2| fast0| (OCoLC)fst00886581;

650 7 a| DNA repair.2| fast0| (OCoLC)fst00886599;

650 7 a| Precancerous conditions.2| fast0| (OCoLC)fst01074845;

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| Georgakilas, Alexandros G.,e| degree supervisor.1| https://id.oclc.org/worldcat/entity/E39PCjFXfvtJXMyHCbk7p6pfhd=| ^A1114884;

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

856 41 z| Access via ScholarShipu| http://hdl.handle.net/10342/12678;

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

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

994 a| C0b| ERE;

596 a| 1 4;

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999 a| ASK AT SPECIAL COLLECTIONS DESKw| ASISc| 1i| MQ2268709l| JSCJTHDm| JOYNERr| Ys| Yt| JSCJTHDu| 11/20/2007x| ETDz| JSPECCOLLo| .STAFF. 0;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 1272644-3001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 12/18/2025x| ETDz| JERESOURCE;

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Role of DNA-PKCS in the processing of double stranded breaks and oxidative clustered DNA lesions in the human breast cancer cell line MCF-7 / by Prakash Peddi.

Author/creator	Peddi, Prakash author.
Other author	Georgakilas, Alexandros G., degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	2007.
Description	xii, 88 leaves : illustrations (some color) ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	DNA repair. DNA damage. DNA-binding proteins. Breast--Cancer. --Research. Precancerous conditions. DNA Repair. DNA Damage. DNA-Binding Proteins. Precancerous Conditions.

Subject	Double stranded breaks (DSBs) and non-DSB oxidative clustered DNA lesions (OCDLs) are the most lethal forms of DNA damage and can be induced by a number of external agents, including ionizing radiation and radiomimetic drugs. DSBs can result from several normal cellular responses and also during repair of OCDLs. Efficient repair of DNA DSBs is essential for the maintenance of chromosomal integrity. DNA-dependent protein kinase (DNA-PK) is the central protein participating in non homologous end joining pathway (NHEJ) and is composed of a heterotrimer of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and Ku (composed of Ku 70 and Ku 80). DNA-PKcs closely interacts with proteins like Ku, which is involved in repair of closely spaced lesions. Targeted silencing of DNA-PKcs using RNA interference methodology resulted in reduced repair of clustered DNA lesions and DSBs produced as a result of [gamma]-irradiation. Reducing the activity of DNA-PKcs using a specific inhibitor 1- (2-hydroxy4-morpholin-4yl-phenyl)-ethanone, also known as IC86621, delayed the processing of clusters and DSBs produced as a result of exposure to [gamma]-rays. Evaluation of y-H2AX foci formation confirms delayed processing of DSBs in MCF-7 cells with reduced expression or reduced activity of DNA-PKcs. We propose that inhibition of double strand break repair pathway blocks leads to inhibiting the efficient repair of clustered DNA lesions. The functional significance and mechanisms of interaction between these two pathways require further investigation.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Alexandros Georgakilas
Dissertation note	M.S. East Carolina University 2007
Bibliography note	Includes bibliographical references (leaves 80-88).
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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Role of DNA-PKCS in the processing of double stranded breaks and oxidative clustered DNA lesions in the human breast cancer cell line MCF-7 / by Prakash Peddi.

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