HIV protease inhibitors block the zinc metalloproteinase ZMPSTE24 and lead to an accumulation of prelamin A in cells

sumsung submitted, created time 1 year 5 months (www.pnas.org)

HIV protease inhibitors (HIV-PIs) target the HIV aspartyl protease, which cleaves the HIV gag-pol polyprotein into shorter proteins required for the production of new virions.

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Amnesia produced by altered release of neurotransmitters after intraamygdala injections of a protein synthesis inhibitor

sumsung submitted, created time 1 year 5 months (www.pnas.org)

Amnesia produced by protein synthesis inhibitors such as anisomycin provides major support for the prevalent view that the formation of long-lasting memories requires de novo protein synthesis. However, inhibition of protein synthesis might disrupt other neural functions to interfere with memory formation.

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Design of helical, oligomeric HIV-1 fusion inhibitor peptides with potent activity against enfuvirtide-resistant virus

bianjie submitted, created time 1 year 5 months (www.pnas.org)

Enfuvirtide (ENF), the first approved fusion inhibitor (FI) for HIV, is a 36-aa peptide that acts by binding to the heptad repeat 1 (HR1) region of gp41 and preventing the interaction of the HR1 and HR2 domains, which is required for virus-cell fusion.

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Mechanisms of host cell exit by the intracellular bacterium Chlamydia

gh0706 submitted, created time 1 year 6 months (www.pnas.org)

The mechanisms that mediate the release of intracellular bacteria from cells are poorly understood, particularly for those that live within a cellular vacuole. The release pathway of the obligate intracellular bacterium Chlamydia from cells is unknown. Kevin Hybiske and Richard S. Stephens identified that Chlamydia release occurred by two mutually exclusive pathways by using a GFP-based approach to visualize chlamydial inclusions within cells by live fluorescence videomicroscopy.

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AS602868, a dual inhibitor of IKK2 and FLT3 to target AML cells

athena submitted, created time 1 year 8 months (www.nature.com)

"Acute myeloid leukemia (AML) cells carry molecular defects that promote their leukemic proliferation, resistance to apoptosis and defect in differentiation. Pharmacological targeting of the nuclear factor kappaB (NF-B) pathway has been shown to promote apoptosis of primary AML cells and to sensitize blasts to neoplastic drugs (Frelin, Blood 2005, 105, 804). The Fms-like tyrosine kinase 3 (FLT3), which sustains proliferation of normal hematopoietic progenitors is frequently overexpressed or mutated in AML patients."

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Evaluation of a cyclophilin inhibitor in hepatitis C virus-infected chimeric mice in vivo

fiona submitted, created time 1 year 8 months (www3.interscience.wiley.com)

"Cyclosporin A (CsA) inhibits replication of the HCV subgenomic replicon, and this effect is believed to not be mediated by its immunosuppressive action."

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