Myc is required for the maintenance of Kaposi's sarcoma-associated herpesvirus latency.

@article{Li2010MycIR,
  title={Myc is required for the maintenance of Kaposi's sarcoma-associated herpesvirus latency.},
  author={Xudong Li and Shijia Chen and Jun Feng and Hongyu Deng and Ren Sun},
  journal={Journal of virology},
  year={2010},
  volume={84 17},
  pages={8945-8}
}
Myc is deregulated by Kaposi's sarcoma-associated herpesvirus (KSHV) latent proteins, but its role in KSHV latency is not clear. We found that Myc knockdown with RNA interference (RNAi) induced KSHV reactivation and increased the protein and mRNA levels of RTA, a key viral regulator of KSHV reactivation. Myc knockdown increased, whereas Myc overexpression inhibited, RTA promoter activity. KSHV reactivation and the activation of the RTA promoter induced by Myc depletion were inhibited by c-Jun N… CONTINUE READING

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Myc knockdown inhibited primary effusion lymphoma ( PEL ) cell proliferation through inducing apoptosis and G(1 ) cell cycle arrest .
Myc knockdown inhibited primary effusion lymphoma ( PEL ) cell proliferation through inducing apoptosis and G(1 ) cell cycle arrest .
Myc knockdown inhibited primary effusion lymphoma ( PEL ) cell proliferation through inducing apoptosis and G(1 ) cell cycle arrest .
Myc knockdown inhibited primary effusion lymphoma ( PEL ) cell proliferation through inducing apoptosis and G(1 ) cell cycle arrest .
Proto-Oncogene Proteins c-mycGene product is element in pathwayCell Cycle
Myc knockdown inhibited primary effusion lymphoma ( PEL ) cell proliferation through inducing apoptosis and G(1 ) cell cycle arrest .
Proto-Oncogene Proteins c-mycGene product plays role in biological processCell Proliferation
Myc knockdown inhibited primary effusion lymphoma ( PEL ) cell proliferation through inducing apoptosis and G(1 ) cell cycle arrest .
Myc knockdown inhibited primary effusion lymphoma ( PEL ) cell proliferation through inducing apoptosis and G(1 ) cell cycle arrest .
Myc knockdown inhibited primary effusion lymphoma ( PEL ) cell proliferation through inducing apoptosis and G(1 ) cell cycle arrest .
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