Publications by authors named "Joern Lausen"

Article Synopsis
  • Erythropoiesis, the formation of red blood cells, is regulated by transcription factors like TAL1, which either activate or repress gene expression through epigenetic mechanisms.
  • TAL1 works with the cofactor PRMT6 to regulate the ID3 gene, essential for hematopoietic cell differentiation, by modifying histones and affecting ID3 expression.
  • Enhancing ID3 expression through manipulation may improve the in vitro differentiation of stem cells (hCD34+) into erythrocytes, providing insights into both normal and pathological red blood cell development.
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The feed-forward loop between the transcription factors Ppar-gamma and C/ebp-alpha is critical for lineage commitment during adipocytic differentiation. Ppar-gamma interacts with epigenetic cofactors to activate C/ebp-alpha and the downstream adipocytic gene expression program. Therefore, knowledge of the epigenetic cofactors associated with Ppar-gamma, is central to understanding adipocyte differentiation in normal differentiation and disease.

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The establishment of cell type specific gene expression by transcription factors and their epigenetic cofactors is central for cell fate decisions. Protein arginine methyltransferase 6 (PRMT6) is an epigenetic regulator of gene expression mainly through methylating arginines at histone H3. This way it influences cellular differentiation and proliferation.

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A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain gene expression patterns during hematopoiesis. In this network, transcription factors regulate each other and are involved in regulatory loops with microRNAs. The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes six mature microRNAs.

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Article Synopsis
  • The study investigates how leukemic cells find refuge in the bone marrow and the role of specific adhesion molecules, CD44 and E-selectin, in chronic myeloid leukemia (CML).
  • Researchers hypothesized that inhibiting the adhesion of CML-initiating cells to the bone marrow's E-selectin could enhance the effectiveness of imatinib treatment, and found that combining the E-selectin inhibitor GMI-1271 with imatinib improved survival in mice by reducing leukemic cell interactions with the bone marrow.
  • The findings suggest that targeting specific molecular pathways, such as the modulation of adhesion molecules like CD44 and the phosphorylation of SCL/TAL1, could lead to better treatment strategies for CML in humans
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Hematopoietic differentiation is directed by transcription factors such as RUNX1. RUNX1 binds to specific DNA binding sites in regulatory elements of genes and recruits epigenetic cofactors to target loci. In this way histone modification patterns and the chromatin environment are altered, which results in adjusted gene expression.

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