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  1. Structural rearrangements in the nucleus localize latent HIV proviruses to a perinucleolar compartment supportive of reactivation
  2. A Reliable Primary Cell Model for HIV Latency: The QUECEL (Quiescent Effector Cell Latency) Method
  3. HIV-1 persists in treated patients because of shutdown of the cellular factor P-TEFb
  4. Cross-talk between microglia and neurons regulates HIV latency
  5. Multiple Histone Lysine Methyltransferases Are Required for the Establishment and Maintenance of HIV-1 Latency
  6. Phosphorylation of HEXIM1 at Tyr271 and Tyr274 Promotes Release of P-TEFb from the 7SK snRNP Complex and Enhances Proviral HIV Gene Expression
  7. Short chain fatty acids potently induce latent HIV-1 in T-cells by activating P-TEFb and multiple histone modifications
  8. Transcriptional control of HIV latency: Cellular signaling pathways, epigenetics, happenstance and the hope for a cure
  9. Negative Elongation Factor Is Required for the Maintenance of Proviral Latency but Does Not Induce Promoter-Proximal Pausing of RNA Polymerase II on the HIV Long Terminal Repeat
  10. Phosphorylation of CDK9 at Ser175 Enhances HIV Transcription and Is a Marker of Activated P-TEFb in CD4+ T Lymphocytes
  11. Control of HIV Latency by Epigenetic and Non-Epigenetic Mechanisms
  12. T-Cell Receptor Signaling Enhances Transcriptional Elongation from Latent HIV Proviruses by Activating P-TEFb through an ERK-Dependent Pathway
  13. Two Distinct Pathways for Cyclooxygenase-2 Protein Degradation
  14. Regulation of intracellular cyclooxygenase levels by gene transcription and protein degradation
  15. The 19-amino Acid Cassette of Cyclooxygenase-2 Mediates Entry of the Protein into the Endoplasmic Reticulum-associated Degradation System