% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Gerber:163640,
      author       = {Gerber, Julia P and Russ, Jenny and Chandrasekar, Vijay and
                      Offermann, Nina and Lee, Hang-Mao and Spear, Sarah and
                      Guzzi, Nicola and Maida, Simona and Pattabiraman,
                      Sundararaghavan and Zhang, Ruoyu and Kayvanjoo, Amir H and
                      Datta, Preeta and Kasturiarachchi, Jagath and Sposito,
                      Teresa and Izotova, Natalia and Händler, Kristian and
                      Adams, Peter D and Marafioti, Teresa and Enver, Tariq and
                      Wenzel, Jörg and Beyer, Marc-Daniel and Mass, Elvira and
                      Bellodi, Cristian and Schultze, Joachim and Capasso, Melania
                      and Nimmo, Rachael and Salomoni, Paolo},
      title        = {{A}berrant chromatin landscape following loss of the {H}3.3
                      chaperone {D}axx in haematopoietic precursors leads to
                      {P}u.1-mediated neutrophilia and inflammation.},
      journal      = {Nature cell biology},
      volume       = {23},
      number       = {12},
      issn         = {1465-7392},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DZNE-2022-00386},
      pages        = {1224 - 1239},
      year         = {2021},
      abstract     = {Defective silencing of retrotransposable elements has been
                      linked to inflammageing, cancer and autoimmune diseases.
                      However, the underlying mechanisms are only partially
                      understood. Here we implicate the histone H3.3 chaperone
                      Daxx, a retrotransposable element repressor inactivated in
                      myeloid leukaemia and other neoplasms, in protection from
                      inflammatory disease. Loss of Daxx alters the chromatin
                      landscape, H3.3 distribution and histone marks of
                      haematopoietic progenitors, leading to engagement of a
                      Pu.1-dependent transcriptional programme for myelopoiesis at
                      the expense of B-cell differentiation. This causes
                      neutrophilia and inflammation, predisposing mice to develop
                      an autoinflammatory skin disease. While these molecular and
                      phenotypic perturbations are in part reverted in animals
                      lacking both Pu.1 and Daxx, haematopoietic progenitors in
                      these mice show unique chromatin and transcriptome
                      alterations, suggesting an interaction between these two
                      pathways. Overall, our findings implicate retrotransposable
                      element silencing in haematopoiesis and suggest a cross-talk
                      between the H3.3 loading machinery and the pioneer
                      transcription factor Pu.1.},
      keywords     = {Animals / Autoimmune Diseases: genetics / Autoimmune
                      Diseases: pathology / B-Lymphocytes: cytology / Cell Line /
                      Chromatin: genetics / Chromatin: pathology / Co-Repressor
                      Proteins: genetics / Hematopoietic Stem Cells: cytology /
                      Histones: metabolism / Humans / Inflammation: pathology /
                      Leukocyte Disorders: congenital / Leukocyte Disorders:
                      pathology / Mice / Mice, Inbred C57BL / Mice, Knockout /
                      Molecular Chaperones: genetics / Myelopoiesis: genetics /
                      Proto-Oncogene Proteins: metabolism / Retroelements:
                      genetics / Skin Diseases: genetics / Skin Diseases:
                      immunology / Skin Diseases: pathology / Trans-Activators:
                      metabolism / Chromatin (NLM Chemicals) / Co-Repressor
                      Proteins (NLM Chemicals) / Daxx protein, mouse (NLM
                      Chemicals) / Histones (NLM Chemicals) / Molecular Chaperones
                      (NLM Chemicals) / Proto-Oncogene Proteins (NLM Chemicals) /
                      Retroelements (NLM Chemicals) / Trans-Activators (NLM
                      Chemicals) / proto-oncogene protein Spi-1 (NLM Chemicals)},
      cin          = {AG Salomoni / Schultze - PRECISE / $R\&D$ PRECISE / AG
                      Capasso / AG Bano / AG Beyer},
      ddc          = {570},
      cid          = {I:(DE-2719)1013032 / I:(DE-2719)1013031 /
                      I:(DE-2719)5000031 / I:(DE-2719)1013033 / I:(DE-2719)1013003
                      / I:(DE-2719)1013035},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 351 - Brain Function
                      (POF4-351) / 354 - Disease Prevention and Healthy Aging
                      (POF4-354)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-351 /
                      G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34876685},
      pmc          = {pmc:PMC8683376},
      doi          = {10.1038/s41556-021-00774-y},
      url          = {https://pub.dzne.de/record/163640},
}