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@ARTICLE{Staehle:303647,
      author       = {H. F. Staehle and C. Koellerer and A. M. Staehle and J.
                      Schulze and P. Eble and A. Müller and F. Zell and J. M.
                      Müller and F. Perner and A. Attia and J.-P. Mallm$^*$ and
                      O. Pozdnyakova and K. Rippe$^*$ and B. Brors$^*$ and L.
                      Feuerbach$^*$ and C. D. Imbusch$^*$ and E. Metzger and R.
                      Schüle and H. L. Pahl and J. S. Jutzi},
      title        = {{L}ysine-specific demethylase 1 regulates hematopoietic
                      stem cell expansion and myeloid cell differentiation.},
      journal      = {Cell death $\&$ disease},
      volume       = {16},
      number       = {1},
      issn         = {2041-4889},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2025-01711},
      pages        = {619},
      year         = {2025},
      abstract     = {The lysine-specific demethylase 1 (LSD1) regulates
                      hematopoietic stem cell differentiation and has been
                      identified as a therapeutic target in hematological
                      disorders. LSD1 demethylates mono and dimethylated histones
                      3 at lysine 4 and 9. In addition, it acts as a scaffold for
                      the formation of chromatin-modifying complexes that
                      regulates the transcription of myeloid-lineage-specific
                      genes in complex with GFI1, a transcriptional repressor.
                      While both enzymatic and non-enzymatic functions of LSD1
                      have been well defined, the relative importance of these two
                      functions in hematopoiesis remains incompletely understood.
                      Here, we investigated the contribution of enzymatic and
                      non-enzymatic functions of LSD1 to myelopoiesis. We show
                      that myeloid differentiation is independent of the enzymatic
                      functions of LSD1 but requires the non-enzymatic,
                      scaffolding function, which directs GFI1 binding to target
                      sequences. In the absence of the LSD1 protein, GFI1 DNA
                      binding is diminished, and myeloid cell differentiation
                      arrests at an immature, myelomonocytic-like cell stage,
                      which overexpresses Prtn3. We provide functional data
                      implicating Prtn3 as an effector of the stem cell expansion
                      and myeloid maturation block caused by the loss of LSD1.},
      cin          = {W192 / B066 / B330 / HD01},
      ddc          = {570},
      cid          = {I:(DE-He78)W192-20160331 / I:(DE-He78)B066-20160331 /
                      I:(DE-He78)B330-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40813574},
      pmc          = {pmc:PMC12354751},
      doi          = {10.1038/s41419-025-07951-z},
      url          = {https://inrepo02.dkfz.de/record/303647},
}