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Murine coronavirus-induced apoptosis and cell cycle dysregulation.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Murine coronavirus-induced apoptosis and cell cycle dysregulation./
作者:	Chen, Chun-Jen.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2002,
面頁冊數:	182 p.
附註:	Source: Dissertations Abstracts International, Volume: 65-05, Section: B.
Contained By:	Dissertations Abstracts International65-05B.
標題:	Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3077618
ISBN:	9780493980690

Murine coronavirus-induced apoptosis and cell cycle dysregulation.
Chen, Chun-Jen.

Murine coronavirus-induced apoptosis and cell cycle dysregulation. - Ann Arbor : ProQuest Dissertations & Theses, 2002 - 182 p.

Source: Dissertations Abstracts International, Volume: 65-05, Section: B.

Thesis (Ph.D.)--The University of Texas at Austin, 2002.

This item must not be sold to any third party vendors.

Mouse hepatitis virus (MHV), a murine coronavirus, is an enveloped virus with a large, single-stranded positive-sense RNA genome. The present study examined two major biological events, MHV-induced apoptosis and cell cycle dysregulation, that occurred in MHV-infected cells. MHV infection in cultured cells generally results in cell death. MHV infection in murine fibroblast cells, 17Cl-1, induced morphological and biochemical features of apoptotic cell death. Active MHV replication was required for triggering apoptosis. Furthermore, as a result of the expression of an MHV envelope protein, E protein, apoptosis was induced in mouse DBT cells, suggesting that E protein may be an apoptosis inducer. MHV induced caspase-dependent apoptosis, and blocking apoptosis by a pan-caspase inhibitor sustained both cell survival and virus production. Caspase cascades can be activated by two major pathways, i.e., mitochondria- and death receptor-mediated pathways. Overexpression of Bcl-2 delayed MHV-induced apoptosis, indicating the activation of a mitochondria-mediated pathway. Analysis of the subcellular localization of cytochrome c and caspase-9 suggested an unusual event of apoptosome formation in association with mitochondria in MHV-infected 17Cl-1 cells. We also detected receptor-mediated pathway-related events, including an increase in the amount of Fas (APO-1/CD95), caspase-8 activation, caspase-8-mediated Bid cleavage, and subsequent translocation of truncated Bid to mitochondria. Unexpectedly, caspase-8 and Bid cleavages were blocked by Bcl-2 overexpression, indicating that these events occurred mostly downstream of mitochondria. These data suggest that mitochondria play a central role in regulating MHV-induced apoptosis. We found that expression of an MHV nonstructural protein, p28, in cultured cells arrested the cell cycle in the G0/G1 phase. p28-induced G0/G1 cell cycle arrest was mostly caused by the accumulation of pRb in its active, hypo-/unphosphorylated form. Because the accumulation of p53 and the cyclin-dependent kinase inhibitor p21Cip1 occurred in p28-expressing cells, p53-mediated activation of p21Cip1 is one mechanism to activate pRb and to arrest p28-expressing cells in G 0/G1 phase. MHV infection in asynchronously growing cells also led to the inhibition of cell proliferation and the accumulation of infected cells in the G0/G1 phase of cell cycle. (Abstract shortened by UMI.).

ISBN: 9780493980690Subjects--Topical Terms:

536250
Microbiology.
Subjects--Index Terms:

Apoptosis

Murine coronavirus-induced apoptosis and cell cycle dysregulation.
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520 $a Mouse hepatitis virus (MHV), a murine coronavirus, is an enveloped virus with a large, single-stranded positive-sense RNA genome. The present study examined two major biological events, MHV-induced apoptosis and cell cycle dysregulation, that occurred in MHV-infected cells. MHV infection in cultured cells generally results in cell death. MHV infection in murine fibroblast cells, 17Cl-1, induced morphological and biochemical features of apoptotic cell death. Active MHV replication was required for triggering apoptosis. Furthermore, as a result of the expression of an MHV envelope protein, E protein, apoptosis was induced in mouse DBT cells, suggesting that E protein may be an apoptosis inducer. MHV induced caspase-dependent apoptosis, and blocking apoptosis by a pan-caspase inhibitor sustained both cell survival and virus production. Caspase cascades can be activated by two major pathways, i.e., mitochondria- and death receptor-mediated pathways. Overexpression of Bcl-2 delayed MHV-induced apoptosis, indicating the activation of a mitochondria-mediated pathway. Analysis of the subcellular localization of cytochrome c and caspase-9 suggested an unusual event of apoptosome formation in association with mitochondria in MHV-infected 17Cl-1 cells. We also detected receptor-mediated pathway-related events, including an increase in the amount of Fas (APO-1/CD95), caspase-8 activation, caspase-8-mediated Bid cleavage, and subsequent translocation of truncated Bid to mitochondria. Unexpectedly, caspase-8 and Bid cleavages were blocked by Bcl-2 overexpression, indicating that these events occurred mostly downstream of mitochondria. These data suggest that mitochondria play a central role in regulating MHV-induced apoptosis. We found that expression of an MHV nonstructural protein, p28, in cultured cells arrested the cell cycle in the G0/G1 phase. p28-induced G0/G1 cell cycle arrest was mostly caused by the accumulation of pRb in its active, hypo-/unphosphorylated form. Because the accumulation of p53 and the cyclin-dependent kinase inhibitor p21Cip1 occurred in p28-expressing cells, p53-mediated activation of p21Cip1 is one mechanism to activate pRb and to arrest p28-expressing cells in G 0/G1 phase. MHV infection in asynchronously growing cells also led to the inhibition of cell proliferation and the accumulation of infected cells in the G0/G1 phase of cell cycle. (Abstract shortened by UMI.).
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