Abstract:
:The herpes simplex virus type 1 (HSV-1) latency associated transcript (LAT) gene's anti-apoptosis activity plays a central, but not fully elucidated, role in enhancing the virus's reactivation phenotype. In transient transfection experiments, LAT increases cell survival following an apoptotic insult in the absence of other HSV-1 genes. However, the high background of untransfected cells has made it difficult to demonstrate that LAT inhibits specific apoptotic factors such as caspases. Here we report that, in mouse neuroblastoma cell lines (C1300) stably expressing high levels of LAT, cold shock induced apoptosis was blocked as judged by increased survival, protection against DNA fragmentation (by DNA ladder assay), and inhibition of caspase 3 cleavage and activation (Western blots). To our knowledge, this is the first report providing direct evidence that LAT blocks two biochemical hallmarks of apoptosis, caspase 3 cleavage and DNA laddering, in the absence of other HSV-1 gene products.
journal_name
Virologyjournal_title
Virologyauthors
Carpenter D,Hsiang C,Brown DJ,Jin L,Osorio N,BenMohamed L,Jones C,Wechsler SLdoi
10.1016/j.virol.2007.07.023subject
Has Abstractpub_date
2007-12-05 00:00:00pages
12-8issue
1eissn
0042-6822issn
1096-0341pii
S0042-6822(07)00493-Xjournal_volume
369pub_type
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