JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Peng, W.
Right arrow Articles by Jones, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Peng, W.
Right arrow Articles by Jones, C.

 Previous Article  |  Next Article 

Journal of Virology, October 2003, p. 10714-10718, Vol. 77, No. 19
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.19.10714-10718.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Gene That Encodes the Herpes Simplex Virus Type 1 Latency-Associated Transcript Influences the Accumulation of Transcripts (Bcl-xL and Bcl-xS) That Encode Apoptotic Regulatory Proteins

Weiping Peng,1 Gail Henderson,1 Guey-Chuen Perng,2 Anthony B. Nesburn,2 Steven L. Wechsler,2 and Clinton Jones1*

Department of Veterinary and Biomedical Sciences, University of Nebraska—Lincoln, Lincoln, Nebraska 68583-0905,1 Department of Ophthalmology, University of California Irvine College of Medicine, Irvine, California 92697-43752

Received 1 April 2003/ Accepted 14 July 2003

The herpes simplex virus type 1 latency-associated transcript (LAT) inhibits apoptosis. We demonstrate here that LAT influences the accumulation of the Bcl-xL transcript versus the Bcl-xS transcript in Neuro-2A cells. Bcl-xL encodes an antiapoptotic protein, whereas Bcl-xS encodes a proapoptotic protein. Promoting the accumulation of Bcl-xL in neurons may inhibit apoptosis, thus enhancing the latency-reactivation cycle.


* Corresponding author. Mailing address: Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln, Fair St. at East Campus Loop, Lincoln, NE 68583-0905. Phone: (402) 472-1890. Fax: (402) 472-9690. E-mail: cjones{at}unlnotes.unl.edu.


Journal of Virology, October 2003, p. 10714-10718, Vol. 77, No. 19
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.19.10714-10718.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2003 by the American Society for Microbiology. All rights reserved.