Number of the records: 1  

GAR22: A novel target gene of thyroid hormone receptor causes growth inhibition in human erythroid cells

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    SYSNO ASEP0333660
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleGAR22: A novel target gene of thyroid hormone receptor causes growth inhibition in human erythroid cells
    Author(s) Gamper, I. (DE)
    Koh, K.-R. (DE)
    Ruau, D. (DE)
    Ullrich, K. (DE)
    Bartůňková, Jana (UMG-J)
    Piroth, D. (DE)
    Hacker, C. (DE)
    Bartůněk, Petr (UMG-J) RID
    Zenke, M. (DE)
    Number of authors9
    Source TitleExperimental Hematology. - : Elsevier - ISSN 0301-472X
    Roč. 37, č. 5 (2009), s. 539-548
    Number of pages10 s.
    Languageeng - English
    CountryUS - United States
    KeywordsThyroid hormone receptor ; GAR22 ; erythropoiesis
    Subject RIVEB - Genetics ; Molecular Biology
    R&D ProjectsLC06077 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    CEZAV0Z50520514 - UMG-J (2005-2011)
    UT WOS000265626900002
    DOI10.1016/j.exphem.2009.02.002
    AnnotationThyroid hormone receptors (TRs) are ligand-dependent transcription factors with a major impact on erythroid cell development. Here we investigated TR activity on red cell gene expression using a genome-wide approach with DNA microarrays and identified TR target genes. Ligand-activated TR effectively accelerated red cell progenitor differentiation in vitro concomitantly with inducing growth arrest. We demonstrate that activated TR induced specific gene expression patterns of up- or down-regulated genes, including distinct clusters associated with accelerated differentiation in response to treatment. Mining for T3 induced genes identified BTEB1 and GAR22 as TR target genes. BTEB1 is a known TR target gene while GAR22, initially identified as a putative tumor suppressor, represents a novel TR target gene. We demonstrate that ectopic GAR22 expression in red cell progenitors lengthens the cell cycle and causes growth inhibition, but leaves red cell gene expression unaffected.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2010
Number of the records: 1  

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