Koh Fujinaga, PhD

Assistant Professor

My main research interest is understanding the regulatory mechanism of eukaryotic gene expression. I have studied HIV transcription as a model system. However, my research topics are not limited to HIV and AIDS. The elongation control of HIV transcritpion which I have been studying during the past two decades is now recognized as a common regulatory mechanism in most cellular gene transcription. Since transcriptional regulation plays a central role in most biological pathways and diseases, I began to study the mechanisms of transcriptional regulation and misregulation in various diseases including cardiac hypertrophy, cancers such as breast cancer, leukemia and lymphoma, and autoimmune and inflammatory diseases.
Education
Postdoctoral Studies, - Graduate Division, University of California, San Francisco
Publications
  1. Nucleolar protein NOP2/NSUN1 suppresses HIV-1 transcription and promotes viral latency by competing with Tat for TAR binding and methylation.
  2. P-TEFb as A Promising Therapeutic Target.
  3. Fused in sarcoma silences HIV gene transcription and maintains viral latency through suppressing AFF4 gene activation.
  4. P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress.
  5. HEXIM1-Tat chimera inhibits HIV-1 replication.
  6. HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies.
  7. Bromodomain-containing protein 4-independent transcriptional activation by autoimmune regulator (AIRE) and NF-?B.
  8. Susceptibility of Human Endogenous Retrovirus Type K to Reverse Transcriptase Inhibitors.
  9. Hili Inhibits HIV Replication in Activated T Cells.
  10. Euphorbia Kansui Reactivates Latent HIV.
  11. FBXO3 Protein Promotes Ubiquitylation and Transcriptional Activity of AIRE (Autoimmune Regulator).
  12. Stress from Nucleotide Depletion Activates the Transcriptional Regulator HEXIM1 to Suppress Melanoma.
  13. The two sides of Tat.
  14. Molecular mechanisms of HIV latency.
  15. CDK11 in TREX/THOC Regulates HIV mRNA 3' End Processing.
  16. An In-Depth Comparison of Latency-Reversing Agent Combinations in Various In Vitro and Ex Vivo HIV-1 Latency Models Identified Bryostatin-1+JQ1 and Ingenol-B+JQ1 to Potently Reactivate Viral Gene Expression.
  17. Visualization of positive transcription elongation factor b (P-TEFb) activation in living cells.
  18. Cyclin-dependent kinase 12 increases 3' end processing of growth factor-induced c-FOS transcripts.
  19. Genetic analysis of the structure and function of 7SK small nuclear ribonucleoprotein (snRNP) in cells.
  20. 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.
  21. Release of positive transcription elongation factor b (P-TEFb) from 7SK small nuclear ribonucleoprotein (snRNP) activates hexamethylene bisacetamide-inducible protein (HEXIM1) transcription.
  22. Bromodomain and extra-terminal (BET) bromodomain inhibition activate transcription via transient release of positive transcription elongation factor b (P-TEFb) from 7SK small nuclear ribonucleoprotein.
  23. Histone deacetylase inhibitors (HDACis) that release the positive transcription elongation factor b (P-TEFb) from its inhibitory complex also activate HIV transcription.
  24. Bromodomain and extra-terminal (BET) bromodomain inhibition activate transcription via transient release of positive transcription elongation factor b (P-TEFb) from 7SK small nuclear ribonucleoprotein.
  25. PKC phosphorylates HEXIM1 and regulates P-TEFb activity.
  26. Functional characterization of a human cyclin T1 mutant reveals a different binding surface for Tat and HEXIM1.
  27. Activation of P-TEFb at sites of dual HIV/TB infection, and inhibition of MTB-induced HIV transcriptional activation by the inhibitor of CDK9, Indirubin-3'-monoxime.
  28. HIV-1 inhibits autophagy in bystander macrophage/monocytic cells through Src-Akt and STAT3.
  29. Cyclin T1 stabilizes expression levels of HIV-1 Tat in cells.
  30. Dominant negative mutant cyclin T1 proteins that inhibit HIV transcription by forming a kinase inactive complex with Tat.
  31. HEXIM1 regulates 17beta-estradiol/estrogen receptor-alpha-mediated expression of cyclin D1 in mammary cells via modulation of P-TEFb.
  32. The positive transcription elongation factor b is an essential cofactor for the activation of transcription by myocyte enhancer factor 2.
  33. Dominant negative mutant cyclin T1 proteins inhibit HIV transcription by specifically degrading Tat.
  34. Cyclin box structure of the P-TEFb subunit cyclin T1 derived from a fusion complex with EIAV tat.
  35. The breast cell growth inhibitor, estrogen down regulated gene 1, modulates a novel functional interaction between estrogen receptor alpha and transcriptional elongation factor cyclin T1.
  36. Dynamics of human immunodeficiency virus transcription: P-TEFb phosphorylates RD and dissociates negative effectors from the transactivation response element.
  37. A minimal chimera of human cyclin T1 and tat binds TAR and activates human immunodeficiency virus transcription in murine cells.
  38. Optimized chimeras between kinase-inactive mutant Cdk9 and truncated cyclin T1 proteins efficiently inhibit Tat transactivation and human immunodeficiency virus gene expression.
  39. Extracellular Nef protein activates signal transduction pathway from Ras to mitogen-activated protein kinase cascades that leads to activation of human immunodeficiency virus from latency.
  40. P-TEFb containing cyclin K and Cdk9 can activate transcription via RNA.
  41. Structure-based computational database screening, in vitro assay, and NMR assessment of compounds that target TAR RNA.
  42. Interaction between P-TEFb and the C-terminal domain of RNA polymerase II activates transcriptional elongation from sites upstream or downstream of target genes.
  43. Binding of Tat to TAR and recruitment of positive transcription elongation factor b occur independently in bovine immunodeficiency virus.
  44. Interactions between equine cyclin T1, Tat, and TAR are disrupted by a leucine-to-valine substitution found in human cyclin T1.
  45. Tat transactivation: a model for the regulation of eukaryotic transcriptional elongation.
  46. Interactions between Tat and TAR and human immunodeficiency virus replication are facilitated by human cyclin T1 but not cyclins T2a or T2b.
  47. Interactions between human cyclin T, Tat, and the transactivation response element (TAR) are disrupted by a cysteine to tyrosine substitution found in mouse cyclin T.
  48. The ability of positive transcription elongation factor B to transactivate human immunodeficiency virus transcription depends on a functional kinase domain, cyclin T1, and Tat.
  49. The HIV transactivator TAT binds to the CDK-activating kinase and activates the phosphorylation of the carboxy-terminal domain of RNA polymerase II.