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High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE144992 | GEO | 2020/08/05

REPOSITORIES: GEO

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High-throughput phenotypic screen and transcriptional analysis identify new compounds and targets for macrophage reprogramming.

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High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming II

Project description:Purpose: To understand compound effects on human macrophage repolarization in the transcriptional level

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High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming I

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High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming III

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High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming

Project description:High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming

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High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming I

Project description:High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming I

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High throughput phenotypic screen and transcriptional analysis identify new compounds, targets and pathways for macrophage reprogramming II

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A Yeast/Drosophila Screen to Identify New Compounds Overcoming Frataxin Deficiency.

Project description:Friedreich's ataxia (FA) is a rare neurodegenerative disease which is very debilitating for the patients who progressively lose their autonomy. The lack of efficient therapeutic treatment of the disease strongly argues for urgent need to search for new active compounds that may stop the progression of the disease or prevent the appearance of the symptoms when the genetic defect is diagnosed early enough. In the present study, we used a yeast strain with a deletion of the frataxin homologue gene as a model of FA cells in a primary screen of two chemical libraries, a fraction of the French National Chemical Library (5500 compounds) and the Prestwick collection (880 compounds). We ran a secondary screen on Drosophila melanogaster flies expressing reduced levels of frataxin during larval development. Half of the compounds selected in yeast appeared to be active in flies in this developmental paradigm, and one of the two compounds with highest activities in this assay partially rescued the heart dilatation phenotype resulting from heart specific depletion of frataxin. The unique complementarity of these two frataxin-deficient models, unicellular and multicellular, appears to be very efficient to select new compounds with improved selectivity, bringing significant perspectives towards improvements in FA therapy.

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