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Regulation of programmed cell death ...

Ogg, Paul David.

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Regulation of programmed cell death by herpes simplex virus type-1.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Regulation of programmed cell death by herpes simplex virus type-1./
作者:	Ogg, Paul David.
面頁冊數:	156 p.
附註:	Source: Dissertation Abstracts International, Volume: 66-04, Section: B, page: 1902.
Contained By:	Dissertation Abstracts International66-04B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3172427
ISBN:	0542096013

Regulation of programmed cell death by herpes simplex virus type-1.
Ogg, Paul David.

Regulation of programmed cell death by herpes simplex virus type-1. - 156 p.

Source: Dissertation Abstracts International, Volume: 66-04, Section: B, page: 1902.

Thesis (Ph.D.)--The University of Iowa, 2005.

Successful replication and spread of Herpes Simplex Virus (HSV-1) depends on survival of infected cells long enough for completion of viral replication. Infected cells are targeted for destruction by extracellular immune responses and by intracellular sensors that can initiate a program of cell death (PCD). HSV-1 encodes a battery of factors that disable or delay these anti-viral defenses. Data presented in this thesis characterize two viral factors, UL34 and US3, that mediate the viral defense against programmed cell death.

ISBN: 0542096013Subjects--Topical Terms:

1017719
Biology, Molecular.

Regulation of programmed cell death by herpes simplex virus type-1.
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500 $a Supervisor: Richard J. Roller.
502 $a Thesis (Ph.D.)--The University of Iowa, 2005.
520 $a Successful replication and spread of Herpes Simplex Virus (HSV-1) depends on survival of infected cells long enough for completion of viral replication. Infected cells are targeted for destruction by extracellular immune responses and by intracellular sensors that can initiate a program of cell death (PCD). HSV-1 encodes a battery of factors that disable or delay these anti-viral defenses. Data presented in this thesis characterize two viral factors, UL34 and US3, that mediate the viral defense against programmed cell death.
520 $a Multiple pathways of PCD likely mediate redundant cell disassembly functions. Results described in this thesis demonstrate that US3 is sufficient to block apoptosis, a caspase-dependent pathway of PCD, and suggest that UL34 may block a caspase-independent pathway. As UL34 is not sufficient to block apoptosis, HSV may rely on each factor to block a different pathway of PCD.
520 $a Three UL34-interacting proteins were previously identified in a yeast-two-hybrid screen. One of these proteins, Clone Number Four (CFN), is a protein of unknown function that we demonstrate is a member of a family of genes that are highly conserved in species as divergent as humans and fish.
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