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Regulation of T cell gene expression by Halofuginone (HF)

ABSTRACT: T cell differentiation to the Th17 effector subset requires stimulation through the T cell and co-stimulatory receptors, together with cytokine stimulation by TGFb and IL-6. The small molecule halofuginone (HF) inhibits Th17 cell development and induces a pattern of stress-regulated gene expression that mimics amino acid starvation. We used global transcript profiling to ask how halofuginone modulates gene expression induced during T cell activaiton and Th17 differentiation Keywords: T cell activation/ differentiation timecourse

ORGANISM(S): Mus musculus

PROVIDER: GSE15624 | GEO | 2009/04/10

SECONDARY ACCESSION(S): PRJNA116595

REPOSITORIES: GEO

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Transcription profiling of mouse T cells treated with halofuginone to investigate regulation of Y cell gene expression by Halofuginone (HF)

Project description:T cell differentiation to the Th17 effector subset requires stimulation through the T cell and co-stimulatory receptors, together with cytokine stimulation by TGFb and IL-6. The small molecule halofuginone (HF) inhibits Th17 cell development and induces a pattern of stress-regulated gene expression that mimics amino acid starvation. We used global transcript profiling to ask how halofuginone modulates gene expression induced during T cell activaiton and Th17 differentiation Experiment Overall Design: Purified mouse CD4+ CD25- T cells were activated under Th17 polarizing cytokine conditions and treated with either halofuginone or its inactive derivative, MAZ1310, for 3- or 6-hours.

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Microarray profiling reveals Integrated Stress Response is activated by Halofuginone in mammary epithelial cells

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Proteome expression changes upon Halofuginone treatment

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Microarray profiling reveals Integrated Stress Response is activated by Halofuginone in mammary epithelial cells

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Halofuginone is a potent inhibitor of SARS-CoV-2 Infection and Replication [Exp2]

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