Abstract
The positive transcription elongation factor b complexes comprise CDK9 and a C-type cyclin, required for the efficient expression of both eukaryotic and primate lentivirus-encoded genes. Cyclin K/CPR4 is the least studied of the positive transcription elongation factor b-forming cyclins. Here, we demonstrate that cyclin K/CPR4-containing positive transcription elongation factor b complexes are unresponsive to Tat and HEXIM1-mediated inactivation. Enhancing expression of cyclin K/CPR4 inhibited the human and simian immunodeficiency viral replication. These data indicate that cyclin K/CPR4 functions as a natural inhibitor of primate lentiviruses.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cyclins / antagonists & inhibitors*
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Cyclins / metabolism
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DNA Replication / genetics
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HIV Long Terminal Repeat / genetics
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HIV-1 / genetics
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Humans
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Lentiviruses, Primate / genetics*
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Positive Transcriptional Elongation Factor B / antagonists & inhibitors*
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RNA-Binding Proteins / pharmacology*
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Transcription Factors
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Transcription, Genetic
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Virus Replication / genetics
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tat Gene Products, Human Immunodeficiency Virus / pharmacology*
Substances
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Cyclins
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HEXIM1 protein, human
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RNA-Binding Proteins
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Transcription Factors
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tat Gene Products, Human Immunodeficiency Virus
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Positive Transcriptional Elongation Factor B