Abstract
The herpes simplex virus type 1 latency-associated transcript (LAT) inhibits apoptosis. We demonstrate here that LAT influences the accumulation of the Bcl-x(L) transcript versus the Bcl-x(S) transcript in Neuro-2A cells. Bcl-x(L) encodes an antiapoptotic protein, whereas Bcl-x(S) encodes a proapoptotic protein. Promoting the accumulation of Bcl-x(L) in neurons may inhibit apoptosis, thus enhancing the latency-reactivation cycle.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Apoptosis*
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Herpesvirus 1, Human / genetics*
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Humans
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MicroRNAs
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Proto-Oncogene Proteins c-bcl-2 / genetics*
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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RNA, Messenger / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Tumor Cells, Cultured
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Viral Proteins / genetics*
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Virus Latency
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bcl-X Protein
Substances
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BCL2L1 protein, human
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MicroRNAs
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Proto-Oncogene Proteins c-bcl-2
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RNA, Messenger
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Viral Proteins
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bcl-X Protein
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latency associated transcript, herpes simplex virus-1