Olaf Kutsch

Tumor necrosis factor-related apoptosis-inducing ligand induces caspase-dependent interleukin-8 expression and apoptosis in human astroglioma cells.

Direct and quantitative single-cell analysis of human immunodeficiency virus type 1 reactivation from latency.

CD154-CD40-induced reactivation of latent HIV-1 infection.

Dynamics of HIV-1 recombination in its natural target cells.

Bis-anthracycline antibiotics inhibit human immunodeficiency virus type 1 transcription.

Tat inhibitors, a new approach: interview with Olaf Kutsch, Ph.D. Interview by John S. James.

T-cell line for HIV drug screening using EGFP as a quantitative marker of HIV-1 replication.

Nef-mediated suppression of T cell activation was lost in a lentiviral lineage that gave rise to HIV-1.

A high-throughput drug screening system for HIV-1 transcription inhibitors.

High throughput drug screening for human immunodeficiency virus type 1 reactivating compounds.

Optimization of HIV-1 infectivity assays.

The quality of chimpanzee T-cell activation and simian immunodeficiency virus/human immunodeficiency virus susceptibility achieved via antibody-mediated T-cell receptor/CD3 stimulation is a function of the anti-CD3 antibody isotype.

Human immunodeficiency virus type 2 (HIV-2)/HIV-1 envelope chimeras detect high titers of broadly reactive HIV-1 V3-specific antibodies in human plasma.

Determinants of the establishment of human immunodeficiency virus type 1 latency.

Effective activation alleviates the replication block of CCR5-tropic HIV-1 in chimpanzee CD4+ lymphocytes.

Adjusting transgene expression levels in lymphocytes with a set of inducible promoters.

Hit-and-run stimulation: a novel concept to reactivate latent HIV-1 infection without cytokine gene induction.

Suppressor of cytokine signaling 3 inhibits antiviral IFN-beta signaling to enhance HIV-1 replication in macrophages.

A screen to identify small molecule inhibitors of protein-protein interactions in mycobacteria.

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

Targeted disruption of the CCR5 gene in human hematopoietic stem cells stimulated by peptide nucleic acids.

Validating a firefly luciferase-based high-throughput screening assay for antimalarial drug discovery.

Facts and fiction: cellular models for high throughput screening for HIV-1 reactivating drugs.

Kinase control prevents HIV-1 reactivation in spite of high levels of induced NF-κB activity.

Selected drugs with reported secondary cell-differentiating capacity prime latent HIV-1 infection for reactivation.

Host factor transcriptional regulation contributes to preferential expression of HIV type 1 in IL-4-producing CD4 T cells.

Effective non-viral delivery of siRNA to acute myeloid leukemia cells with lipid-substituted polyethylenimines.

An AP-1 binding site in the enhancer/core element of the HIV-1 promoter controls the ability of HIV-1 to establish latent infection.

Copper-boosting compounds: a novel concept for antimycobacterial drug discovery.

Kinase control of latent HIV-1 infection: PIM-1 kinase as a major contributor to HIV-1 reactivation.

Copper complexation screen reveals compounds with potent antibiotic properties against methicillin-resistant Staphylococcus aureus.

Stable Phenotypic Changes of the Host T Cells Are Essential to the Long-Term Stability of Latent HIV-1 Infection.

Disulfiram and Copper Ions Kill Mycobacterium tuberculosis in a Synergistic Manner.

The host cell side of latent HIV-1 infection.

RNAP II processivity is a limiting step for HIV-1 transcription independent of orientation to and activity of endogenous neighboring promoters.

Targeting CXCR4/SDF-1 axis by lipopolymer complexes of siRNA in acute myeloid leukemia.

Combinatorial phenotypic screen uncovers unrecognized family of extended thiourea inhibitors with copper-dependent anti-staphylococcal activity.

Protein Phosphatase, Mg2+/Mn2+-dependent 1A controls the innate antiviral and antibacterial response of macrophages during HIV-1 and Mycobacterium tuberculosis infection.

A Macrophage Infection Model to Predict Drug Efficacy Against Mycobacterium Tuberculosis.

8-Hydroxyquinolines Are Boosting Agents of Copper-Related Toxicity in Mycobacterium tuberculosis.

Mycobacterium tuberculosis exploits the PPM1A signaling pathway to block host macrophage apoptosis.