大葉大學圖書館 |

Induction of Markers of DNA Damage Signaling upon Reactivation of Epstein-Barr Virus: A Novel Role for ZEBRA and the Pre-replicative Phase of the Viral Lytic Cycle.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
書名/作者:	Induction of Markers of DNA Damage Signaling upon Reactivation of Epstein-Barr Virus: A Novel Role for ZEBRA and the Pre-replicative Phase of the Viral Lytic Cycle.
作者:	Wang'ondu, Ruth.
面頁冊數:	215 p.
附註:	Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.
Contained By:	Dissertation Abstracts International76-11B(E).
標題:	Cellular biology.
標題:	Microbiology.
ISBN:	9781321965476
摘要、提要註:	Epstein Barr virus (EBV), like other oncogenic viruses, manipulates cellular DNA damage signaling pathways during its life cycle. Activation of markers of DNA damage signaling during the EBV lytic cycle is hypothesized to occur in response to large amounts of exogenous double stranded DNA products generated during lytic EBV DNA replication. Here I show that viral DNA replication, per se, may not be the only trigger for induction of DNA damage signaling markers during the EBV lytic cycle. To study induction of DNA damage signaling markers during the pre-replicative stage of the EBV lifecycle, I relied on the characteristic, diffuse, nuclear distribution of early lytic proteins, the use of phosphonoacetic acid, an EBV replication inhibitor, and target cells that did not replicate EBV or lack EBV DNA. I showed that ATM and at least one of three substrates of ATM, namely H2AX, 53BP1, or P53, are phosphorylated upon EBV lytic reactivation in EBV-positive HEK and Burkitt lymphoma cell lines. Phosphorylated forms of ATM and its substrates were induced in lytically reactivated EBV positive cells during the pre-replicative state as well as during EBV DNA replication. I found that ZEBRA, a bZIP transcription factor that is sufficient and indispensable for EBV lytic replication, was capable of activating phosphorylation of ATM and H2AX independent of other EBV gene products. Two ZEBRA mutants deficient in DNA binding did not induce markers of DNA damage signaling. ATM and H2AX phosphorylation induced prior to EBV replication may be critical for creating a microenvironment conducive for progression of the lytic cycle and might also contribute to oncogenesis.
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3663682

Induction of Markers of DNA Damage Signaling upon Reactivation of Epstein-Barr Virus: A Novel Role for ZEBRA and the Pre-replicative Phase of the Viral Lytic Cycle.
Wang'ondu, Ruth.

Induction of Markers of DNA Damage Signaling upon Reactivation of Epstein-Barr Virus: A Novel Role for ZEBRA and the Pre-replicative Phase of the Viral Lytic Cycle. - 215 p.

Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.

Thesis (Ph.D.)--Yale University, 2015.

Epstein Barr virus (EBV), like other oncogenic viruses, manipulates cellular DNA damage signaling pathways during its life cycle. Activation of markers of DNA damage signaling during the EBV lytic cycle is hypothesized to occur in response to large amounts of exogenous double stranded DNA products generated during lytic EBV DNA replication. Here I show that viral DNA replication, per se, may not be the only trigger for induction of DNA damage signaling markers during the EBV lytic cycle. To study induction of DNA damage signaling markers during the pre-replicative stage of the EBV lifecycle, I relied on the characteristic, diffuse, nuclear distribution of early lytic proteins, the use of phosphonoacetic acid, an EBV replication inhibitor, and target cells that did not replicate EBV or lack EBV DNA. I showed that ATM and at least one of three substrates of ATM, namely H2AX, 53BP1, or P53, are phosphorylated upon EBV lytic reactivation in EBV-positive HEK and Burkitt lymphoma cell lines. Phosphorylated forms of ATM and its substrates were induced in lytically reactivated EBV positive cells during the pre-replicative state as well as during EBV DNA replication. I found that ZEBRA, a bZIP transcription factor that is sufficient and indispensable for EBV lytic replication, was capable of activating phosphorylation of ATM and H2AX independent of other EBV gene products. Two ZEBRA mutants deficient in DNA binding did not induce markers of DNA damage signaling. ATM and H2AX phosphorylation induced prior to EBV replication may be critical for creating a microenvironment conducive for progression of the lytic cycle and might also contribute to oncogenesis.

ISBN: 9781321965476Subjects--Topical Terms:

629801
Cellular biology.

Induction of Markers of DNA Damage Signaling upon Reactivation of Epstein-Barr Virus: A Novel Role for ZEBRA and the Pre-replicative Phase of the Viral Lytic Cycle.
LDR:02628nam a2200277 4500 001 440954
005 20160422125037.5
008 160525s2015 ||||||||||||||||| ||eng d
020 $a 9781321965476
035 $a (MiAaPQ)AAI3663682
035 $a AAI3663682
040 $a MiAaPQ $c MiAaPQ
100 1 $a Wang'ondu, Ruth. $3 629972
245 1 0 $a Induction of Markers of DNA Damage Signaling upon Reactivation of Epstein-Barr Virus: A Novel Role for ZEBRA and the Pre-replicative Phase of the Viral Lytic Cycle.
300 $a 215 p.
500 $a Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.
500 $a Adviser: I. George Miller.
502 $a Thesis (Ph.D.)--Yale University, 2015.
520 $a Epstein Barr virus (EBV), like other oncogenic viruses, manipulates cellular DNA damage signaling pathways during its life cycle. Activation of markers of DNA damage signaling during the EBV lytic cycle is hypothesized to occur in response to large amounts of exogenous double stranded DNA products generated during lytic EBV DNA replication. Here I show that viral DNA replication, per se, may not be the only trigger for induction of DNA damage signaling markers during the EBV lytic cycle. To study induction of DNA damage signaling markers during the pre-replicative stage of the EBV lifecycle, I relied on the characteristic, diffuse, nuclear distribution of early lytic proteins, the use of phosphonoacetic acid, an EBV replication inhibitor, and target cells that did not replicate EBV or lack EBV DNA. I showed that ATM and at least one of three substrates of ATM, namely H2AX, 53BP1, or P53, are phosphorylated upon EBV lytic reactivation in EBV-positive HEK and Burkitt lymphoma cell lines. Phosphorylated forms of ATM and its substrates were induced in lytically reactivated EBV positive cells during the pre-replicative state as well as during EBV DNA replication. I found that ZEBRA, a bZIP transcription factor that is sufficient and indispensable for EBV lytic replication, was capable of activating phosphorylation of ATM and H2AX independent of other EBV gene products. Two ZEBRA mutants deficient in DNA binding did not induce markers of DNA damage signaling. ATM and H2AX phosphorylation induced prior to EBV replication may be critical for creating a microenvironment conducive for progression of the lytic cycle and might also contribute to oncogenesis.
590 $a School code: 0265.
650 4 $a Cellular biology. $3 629801
650 4 $a Microbiology. $3 182563
690 $a 0379
690 $a 0410
710 2 $a Yale University. $t Reports on the course of instruction in Yale college. $3 374489
773 0 $t Dissertation Abstracts International $g 76-11B(E).
790 $a 0265
791 $a Ph.D.
792 $a 2015
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3663682