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 interaction of Chlamydia trachom...

Balsara, Zarine Rohinton.

FindBook

Google Book

Amazon

博客來

The interaction of Chlamydia trachomatis with mammalian host cells.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The interaction of Chlamydia trachomatis with mammalian host cells./
作者:	Balsara, Zarine Rohinton.
面頁冊數:	216 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2349.
Contained By:	Dissertation Abstracts International67-05B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3217669
ISBN:	9780542691867

The interaction of Chlamydia trachomatis with mammalian host cells.
Balsara, Zarine Rohinton.

The interaction of Chlamydia trachomatis with mammalian host cells. - 216 p.

Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2349.

Thesis (Ph.D.)--Harvard University, 2006.

The obligate intracellular lifestyle of Chlamydia trachomatis poses significant challenges to the survival of the organism. Therefore, C. trachomatis have evolved strategies to exploit the host to ensure an abundant supply of cellular resources and to preserve the integrity of the host cell. In the first part of this thesis, I explored a number of cellular processes targeted by C. trachomatis to promote bacterial survival within the host cell. In the second part, I examined the converse of this host-pathogen interaction by addressing which eukaryotic genes control C. trachomatis replication within the host.

ISBN: 9780542691867Subjects--Topical Terms:

1017734
Biology, Microbiology.

The interaction of Chlamydia trachomatis with mammalian host cells.
LDR:04296nmm 2200313 4500 001 1829028
005 20071106080107.5
008 130610s2006 eng d
020 $a 9780542691867
035 $a (UMI)AAI3217669
035 $a AAI3217669
040 $a UMI $c UMI
100 1 $a Balsara, Zarine Rohinton. $3 1917900
245 1 4 $a The interaction of Chlamydia trachomatis with mammalian host cells.
300 $a 216 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2349.
500 $a Adviser: Michael Starnbach.
502 $a Thesis (Ph.D.)--Harvard University, 2006.
520 $a The obligate intracellular lifestyle of Chlamydia trachomatis poses significant challenges to the survival of the organism. Therefore, C. trachomatis have evolved strategies to exploit the host to ensure an abundant supply of cellular resources and to preserve the integrity of the host cell. In the first part of this thesis, I explored a number of cellular processes targeted by C. trachomatis to promote bacterial survival within the host cell. In the second part, I examined the converse of this host-pathogen interaction by addressing which eukaryotic genes control C. trachomatis replication within the host.
520 $a One mechanism whereby C. trachomatis ensure an adequate supply of cellular resources is through manipulation of the host cell cycle. I demonstrated that C. trachomatis-infected cells proliferate more slowly than uninfected cells. I correlated this phenotype with a reduction in levels of the cyclin-dependent kinase, cdk1, and an N-terminal truncation of the mitotic cyclin B1 in infected cells. Because interruption of the cell cycle often serves as a trigger for apoptosis, it is no surprise that C. trachomatis have also developed strategies to promote host cell survival. My studies have pointed to a role for the C. trachomatis protein, CrpA, in this process. By degrading the pro-apoptotic factor BNIP3L, CrpA may help to regulate the balance of pro- and anti-apoptotic factors within infected cells. However, the observation that CrpA alone could not protect host cells against externally-induced apoptosis suggests that other C. trachomatis proteins are necessary for the cumulative cell survival effect. Studies on another C. trachomatis protein, Cap1, suggested that this bacterial factor interacts with a member of the eukaryotic nuclear pore complex. Despite the implication that C. trachomatis may disrupt trafficking of molecules across the nuclear membrane, I have not yet shown that the bacteria perturb nuclear-cytoplasmic transport of molecules during infection.
520 $a To regulate all of these cellular processes, C. trachomatis must secrete virulence factors into the host cytosol. One way C. trachomatis may protect these factors from proteolytic destruction is by exploiting the host ubiquitin-proteasome pathway. Working with Shahram Misaghi, I identified two C. trachomatis-encoded cysteine proteases that function as deubiquitinating and deneddylating enzymes (DUBS). This finding offers the possibility that these DUBs may control the half-life and activity of bacterial and/or host proteins during C. trachomatis infection. Additionally, these DUBs may protect other C. trachomatis proteins from processing and presentation to the host immune system.
520 $a My studies end with an examination of the host response to C. trachomatis infection. Taking advantage of differences in susceptibility to C. trachomatis infection between two inbred strains of mice, Isaac Bernstein-Hanley and I mapped three quantitative trait loci (QTL) linked to host susceptibility to systemic C. trachomatis infection. Functional analysis of candidate genes within one of these QTL has revealed a role for a member of the IFNgamma-inducible family of GTPases in influencing the permissiveness of host cells to C. trachomatis infection. Through these studies we have developed an appreciation for the complex interplay between C. trachomatis and the host.
590 $a School code: 0084.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0410
690 $a 0982
710 2 0 $a Harvard University. $3 528741
773 0 $t Dissertation Abstracts International $g 67-05B.
790 1 0 $a Starnbach, Michael, $e advisor
790 $a 0084
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3217669