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Characterization of the Bcl-2 homolo...
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The Johns Hopkins University.
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Characterization of the Bcl-2 homologues encoded by the gamma herpesviruses.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Characterization of the Bcl-2 homologues encoded by the gamma herpesviruses./
作者:
Bellows, David S.
面頁冊數:
152 p.
附註:
Adviser: J. Marie Hardwick.
Contained By:
Dissertation Abstracts International63-03B.
標題:
Biology, Microbiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3046418
ISBN:
049360555X
Characterization of the Bcl-2 homologues encoded by the gamma herpesviruses.
Bellows, David S.
Characterization of the Bcl-2 homologues encoded by the gamma herpesviruses.
- 152 p.
Adviser: J. Marie Hardwick.
Thesis (Ph.D.)--The Johns Hopkins University, 2002.
Apoptosis is an evolutionarily conserved genetic suicide program required for development and tissue homeostasis in metazoans. In addition, apoptosis has been proposed as an intrinsic defense against invading viruses. Cysteine proteases called caspases drive the program. Bcl-2 proteins regulate caspase activation and are themselves regulated by protease cleavage that can convert anti-death proteins into potent killers in a proposed feed-forward loop. All the gamma herpesviruses studied to date have been found to encode a functional Bcl-2 homolog, implying a requirement for Bcl-2-mediated protection in the gamma herpesvirus life cycle.
ISBN: 049360555XSubjects--Topical Terms:
1017734
Biology, Microbiology.
Characterization of the Bcl-2 homologues encoded by the gamma herpesviruses.
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Apoptosis is an evolutionarily conserved genetic suicide program required for development and tissue homeostasis in metazoans. In addition, apoptosis has been proposed as an intrinsic defense against invading viruses. Cysteine proteases called caspases drive the program. Bcl-2 proteins regulate caspase activation and are themselves regulated by protease cleavage that can convert anti-death proteins into potent killers in a proposed feed-forward loop. All the gamma herpesviruses studied to date have been found to encode a functional Bcl-2 homolog, implying a requirement for Bcl-2-mediated protection in the gamma herpesvirus life cycle.
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These studies were designed to examine the regulation of Bcl-2 proteins encoded by the gamma herpesviruses. The first series of experiments shows that the virus-encoded Bcl-2 proteins escape caspase-mediated conversion to proapoptotic molecules, either by elimination of the caspase recognition site or by mutation of their C-terminal regions to a non-lethal protein, or both. The second set of experiments show that BALF1, the putative second Bcl-2 homolog encoded by Epstein-Barr virus (EBV), is a negative regulator of the antiapoptotic EBV Bcl-2 homolog, BHRF1. The mechanism of BALF1 inhibition of BHRF1 function is apparently independent of a direct interaction between the two proteins since they localize to different compartments within the cell. The last series of experiments show that BALF1 accelerates the apoptotic morphology of cells exposed to a death stimulus and that this acceleration is dominant to BHRF1-mediated protection. In addition, BALF1 associates with Aven, a cellular Bcl-2 interacting factor that regulates apoptosome formation, providing a potential mechanism for BALF1 activity.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3046418
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