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Targeted disruption of the PU.1 gene results in multiple hematopoietic abnormalities

Academic Article
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Overview

authors

  • McKercher, S. R.
  • Torbett, Bruce
  • Anderson, K. L.
  • Henkel, G. W.
  • Vestal, D. J.
  • Baribault, H.
  • Klemsz, M.
  • Feeney, Ann
  • Wu, G. E.
  • Paige, C. J.
  • Maki, R. A.

publication date

  • October 1996

journal

  • EMBO Journal  Journal

abstract

  • PU.1 is a member of the ets family of transcription factors and is expressed exclusively in cells of the hematopoietic lineage. Mice homozygous for a disruption in the PU.1 DNA binding domain are born alive but die of severe septicemia within 48 h. The analysis of these neonates revealed a lack of mature macrophages, neutrophils, B cells and T cells, although erythrocytes and megakaryocytes were present. The absence of lymphoid commitment and development in null mice was not absolute, since mice maintained on antibiotics began to develop normal appearing T cells 3-5 days after birth. In contrast, mature B cells remained undetectable in these older mice. Within the myeloid lineage, despite a lack of macrophages in the older antibiotic-treated animals, a few cells with the characteristics of neutrophils began to appear by day 3. While the PU.1 protein appears not to be essential for myeloid and lymphoid lineage commitment, it is absolutely required for the normal differentiation of B cells and macrophages.

subject areas

  • Animals
  • B-Lymphocytes
  • Binding Sites
  • Cell Differentiation
  • DNA
  • Flow Cytometry
  • Hematopoiesis
  • Macrophages
  • Mice
  • Neutrophils
  • Proto-Oncogene Proteins
  • T-Lymphocytes
  • Trans-Activators
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Research

keywords

  • PU-1
  • ets family
  • hematopoiesis
  • transcription factor
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Identity

PubMed Central ID

  • PMC452309

International Standard Serial Number (ISSN)

  • 0261-4189

PubMed ID

  • 8896458
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Additional Document Info

start page

  • 5647

end page

  • 5658

volume

  • 15

issue

  • 20

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