Kylene Kehn-Hall

Drug 9AA reactivates p21/Waf1 and Inhibits HIV-1 progeny formation.

Effect of transcription peptide inhibitors on HIV-1 replication.

CDK13, a new potential human immunodeficiency virus type 1 inhibitory factor regulating viral mRNA splicing.

Lysine methylation of HIV-1 Tat regulates transcriptional activity of the viral LTR.

Retroviral proteomics and interactomes: intricate balances of cell survival and viral replication.

Cyclin dependent kinases as attractive targets to prevent transcription from viral genomes.

9-Aminoacridine inhibition of HIV-1 Tat dependent transcription.

The utilization of humanized mouse models for the study of human retroviral infections.

Novel insights into transcriptional elongation: ubiquitination of HEXIM1 and p-TEFb activity.

Chromatin dynamics associated with HIV-1 Tat-activated transcription.

Novel HIV-1 therapeutics through targeting altered host cell pathways.

Cell-type-specific proteome and interactome: using HIV-1 Tat as a test case.

Human T-lymphotropic virus type 1 transcription and chromatin-remodeling complexes.

Inhibition of human immunodeficiency virus type-1 by cdk inhibitors.

Absence of DICER in monocytes and its regulation by HIV-1.

Transcription through the HIV-1 nucleosomes: effects of the PBAF complex in Tat activated transcription.

The identification of unique serum proteins of HIV-1 latently infected long-term non-progressor patients.

Methylation of the tumor suppressor protein, BRCA1, influences its transcriptional cofactor function.

microRNA machinery is an integral component of drug-induced transcription inhibition in HIV-1 infection.

Direct detection of diverse metabolic changes in virally transformed and tax-expressing cells by mass spectrometry.

Erratum to: microRNA machinery is an integral component of drug-induced transcription inhibition in HIV-1 infection.

Reverse-phase phosphoproteome analysis of signaling pathways induced by Rift valley fever virus in human small airway epithelial cells.

Analysis of the roles of HIV-derived microRNAs.

Developments in antivirals against influenza, smallpox and hemorrhagic fever viruses.

Inhibition of Tat-mediated HIV-1 replication and neurotoxicity by novel GSK3-beta inhibitors.

Alteration in superoxide dismutase 1 causes oxidative stress and p38 MAPK activation following RVFV infection.

Varying modulation of HIV-1 LTR activity by Baf complexes.

Rapid, non-targeted discovery of biochemical transformation and biomarker candidates in oncovirus-infected cell lines using LAESI mass spectrometry.

Induction of DNA damage signaling upon Rift Valley fever virus infection results in cell cycle arrest and increased viral replication.

Modulation of GSK-3β activity in Venezuelan equine encephalitis virus infection.

p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.

Use of ATP analogs to inhibit HIV-1 transcription.

Localization and sub-cellular shuttling of HTLV-1 tax with the miRNA machinery.

Curcumin inhibits Rift Valley fever virus replication in human cells.

Exosomes derived from HIV-1-infected cells contain trans-activation response element RNA.

The use of NanoTrap particles as a sample enrichment method to enhance the detection of Rift Valley Fever Virus.

Design of Potential Bisubstrate Inhibitors against Mycobacterium tuberculosis (Mtb) 1-Deoxy-D-Xylulose 5-Phosphate Reductoisomerase (Dxr)-Evidence of a Novel Binding Mode.

Nuclear import and export inhibitors alter capsid protein distribution in mammalian cells and reduce Venezuelan Equine Encephalitis Virus replication.

Novel neuroprotective GSK-3β inhibitor restricts Tat-mediated HIV-1 replication.

Reactive oxygen species activate NFκB (p65) and p53 and induce apoptosis in RVFV infected liver cells.

The use of Nanotrap particles for biodefense and emerging infectious disease diagnostics.

Proteomic strategies for the discovery of novel diagnostic and therapeutic targets for infectious diseases.

The role of IKKβ in Venezuelan equine encephalitis virus infection.

Multi-faceted proteomic characterization of host protein complement of Rift Valley fever virus virions and identification of specific heat shock proteins, including HSP90, as important viral host factors.

The use of Nanotrap particles technology in capturing HIV-1 virions and viral proteins from infected cells.

Transcriptional Gene Silencing (TGS) via the RNAi Machinery in HIV-1 Infections.

1E7-03, a Small Molecule Targeting Host Protein Phosphatase-1, Inhibits HIV-1 Transcription.

Inhibition of host extracellular signal-regulated kinase (ERK) activation decreases new world alphavirus multiplication in infected cells.