Tilman Borggrefe

Summary

Publications

  1. pmc Histone demethylase KDM5A is an integral part of the core Notch-RBP-J repressor complex
    Robert Liefke
    Max Planck Institute of Immunobiology, Freiburg, Germany
    Genes Dev 24:590-601. 2010
  2. doi request reprint Fine-tuning of the intracellular canonical Notch signaling pathway
    Tilman Borggrefe
    Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany
    Cell Cycle 11:264-76. 2012
  3. doi request reprint Interactions between subunits of the Mediator complex with gene-specific transcription factors
    Tilman Borggrefe
    Max Planck Institute of Immunobiology and Epigenetics, Stubeweg 51, D 79108 Freiburg, Germany
    Semin Cell Dev Biol 22:759-68. 2011
  4. doi request reprint RNA helicase Ddx5 and the noncoding RNA SRA act as coactivators in the Notch signaling pathway
    Claudia Jung
    Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany
    Biochim Biophys Acta 1833:1180-9. 2013
  5. pmc Essential role of Mediator subunit Med1 in invariant natural killer T-cell development
    Xiaojing Yue
    The Max Planck Institute of Immunobiology and Epigenetics, D 79108 Freiburg, Germany
    Proc Natl Acad Sci U S A 108:17105-10. 2011
  6. pmc ETO, but not leukemogenic fusion protein AML1/ETO, augments RBP-Jkappa/SHARP-mediated repression of notch target genes
    Daniela Salat
    Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology, Stubeweg 51, 79108 Freiburg, Germany
    Mol Cell Biol 28:3502-12. 2008

Collaborators

  • Franz Oswald
  • Maria Dominguez
  • Robert Liefke
  • Claudia Jung
  • Gerhard Mittler
  • Xiaojing Yue
  • Daniela Salat
  • Ana Izcue
  • Patrick Rodriguez
  • Dolores Ferres-Marco
  • Cristobal Alvarado
  • Jörg Wiedenmann

Detail Information

Publications6

  1. pmc Histone demethylase KDM5A is an integral part of the core Notch-RBP-J repressor complex
    Robert Liefke
    Max Planck Institute of Immunobiology, Freiburg, Germany
    Genes Dev 24:590-601. 2010
    ..KDM5A interacts physically with RBP-J; this interaction is conserved in Drosophila and is crucial for Notch-induced growth and tumorigenesis responses...
  2. doi request reprint Fine-tuning of the intracellular canonical Notch signaling pathway
    Tilman Borggrefe
    Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany
    Cell Cycle 11:264-76. 2012
    ..Furthermore, we review how the canonical (RBP-J dependent) Notch pathway is fine-tuned by downstream effectors and feedback loops in mammals...
  3. doi request reprint Interactions between subunits of the Mediator complex with gene-specific transcription factors
    Tilman Borggrefe
    Max Planck Institute of Immunobiology and Epigenetics, Stubeweg 51, D 79108 Freiburg, Germany
    Semin Cell Dev Biol 22:759-68. 2011
    ..The focus of the review is to summarize the current knowledge of transcription factor/Mediator interactions in higher eukaryotes and illuminate the physiological and gene-selective roles of Mediator...
  4. doi request reprint RNA helicase Ddx5 and the noncoding RNA SRA act as coactivators in the Notch signaling pathway
    Claudia Jung
    Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany
    Biochim Biophys Acta 1833:1180-9. 2013
    ..Together, our data demonstrate that Ddx5 and SRA function as coactivators of Notch signaling...
  5. pmc Essential role of Mediator subunit Med1 in invariant natural killer T-cell development
    Xiaojing Yue
    The Max Planck Institute of Immunobiology and Epigenetics, D 79108 Freiburg, Germany
    Proc Natl Acad Sci U S A 108:17105-10. 2011
    ..Thus, Med1 is essential for a complete intrathymic development of iNKT cells...
  6. pmc ETO, but not leukemogenic fusion protein AML1/ETO, augments RBP-Jkappa/SHARP-mediated repression of notch target genes
    Daniela Salat
    Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology, Stubeweg 51, 79108 Freiburg, Germany
    Mol Cell Biol 28:3502-12. 2008
    ..Therefore, we propose that AML1/ETO can disturb the normal, repressive function of ETO at Notch target genes. This activating (or derepressing) effect of AML1/ETO may contribute to its oncogenic potential in myeloid leukemia...