東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

The role of Epstein-Barr virus in mo...

Snow, Andrew Linnell.

FindBook

Google Book

Amazon

博客來

The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas./
作者:	Snow, Andrew Linnell.
面頁冊數:	105 p.
附註:	Source: Dissertation Abstracts International, Volume: 66-04, Section: B, page: 1971.
Contained By:	Dissertation Abstracts International66-04B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3171722
ISBN:	0542084759

The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas.
Snow, Andrew Linnell.

The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas. - 105 p.

Source: Dissertation Abstracts International, Volume: 66-04, Section: B, page: 1971.

Thesis (Ph.D.)--Stanford University, 2005.

Epstein-Barr virus (EBV) is an oncogenic herpesvirus associated with several B cell malignancies. Previous studies suggest that latent EBV infection contributes to lymphomagenesis by protecting B cell hosts from apoptosis. However, the relationship between EBV infection and sensitivity to death receptor (DR)-induced apoptosis is poorly understood. In this study, we provide the first evidence demonstrating EBV can protect a latently infected B cell lymphoma from apoptosis triggered through DRs. We showed that unlike uninfected control cells, BJAB lymphoma cells latently infected with the B95.8 strain of EBV (BJAB_B95) are completely resistant to apoptosis triggered through Fas or the TRAIL receptors DR4 and DR5. Caspase 8 activation was impaired and cFLIP recruitment was enriched in death inducing signaling complexes (DISCS) formed in EBV-infected BJAB cells relative to parent BJAB cells. Furthermore, the expression of the EBV latent membrane protein 1 (LMP1) alone could reduce caspase activation and confer partial resistance to death receptor apoptosis in BJAB cells. This protective effect was dependent on LMP1-induced NF-kappaB activation, which in turn upregulated cFLIP expression in LMP1+ BJAB cells. Finally, we showed that inhibition of NF-kappaB blocked cFLIP upregulation, reversed LMP1-mediated protection from DR apoptosis and sensitized BJAB_B95 cells to DR apoptosis as well. Thus, latent EBV can block DR apoptosis in host B cells, in part through the anti-apoptosic function of LMP1. Understanding the mechanisms by which latent EBV infection contributes to apoptosis resistance will hopefully improve our understanding and treatment of various EBV-associated neoplasms.

ISBN: 0542084759Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas.
LDR:02653nmm 2200289 4500 001 1815681
005 20060710080803.5
008 130610s2005 eng d
020 $a 0542084759
035 $a (UnM)AAI3171722
035 $a AAI3171722
040 $a UnM $c UnM
100 1 $a Snow, Andrew Linnell. $3 1905095
245 1 4 $a The role of Epstein-Barr virus in modulating death receptor-mediated apoptosis in latently infected B cell lymphomas.
300 $a 105 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-04, Section: B, page: 1971.
500 $a Adviser: Olivia M. Martinez.
502 $a Thesis (Ph.D.)--Stanford University, 2005.
520 $a Epstein-Barr virus (EBV) is an oncogenic herpesvirus associated with several B cell malignancies. Previous studies suggest that latent EBV infection contributes to lymphomagenesis by protecting B cell hosts from apoptosis. However, the relationship between EBV infection and sensitivity to death receptor (DR)-induced apoptosis is poorly understood. In this study, we provide the first evidence demonstrating EBV can protect a latently infected B cell lymphoma from apoptosis triggered through DRs. We showed that unlike uninfected control cells, BJAB lymphoma cells latently infected with the B95.8 strain of EBV (BJAB_B95) are completely resistant to apoptosis triggered through Fas or the TRAIL receptors DR4 and DR5. Caspase 8 activation was impaired and cFLIP recruitment was enriched in death inducing signaling complexes (DISCS) formed in EBV-infected BJAB cells relative to parent BJAB cells. Furthermore, the expression of the EBV latent membrane protein 1 (LMP1) alone could reduce caspase activation and confer partial resistance to death receptor apoptosis in BJAB cells. This protective effect was dependent on LMP1-induced NF-kappaB activation, which in turn upregulated cFLIP expression in LMP1+ BJAB cells. Finally, we showed that inhibition of NF-kappaB blocked cFLIP upregulation, reversed LMP1-mediated protection from DR apoptosis and sensitized BJAB_B95 cells to DR apoptosis as well. Thus, latent EBV can block DR apoptosis in host B cells, in part through the anti-apoptosic function of LMP1. Understanding the mechanisms by which latent EBV infection contributes to apoptosis resistance will hopefully improve our understanding and treatment of various EBV-associated neoplasms.
590 $a School code: 0212.
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Health Sciences, Oncology. $3 1018566
690 $a 0982
690 $a 0410
690 $a 0992
710 2 0 $a Stanford University. $3 754827
773 0 $t Dissertation Abstracts International $g 66-04B.
790 1 0 $a Martinez, Olivia M., $e advisor
790 $a 0212
791 $a Ph.D.
792 $a 2005
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3171722