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Both E12 and E47 allow commitment to the B cell lineage

Academic Article
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Overview

authors

  • Bain, G.
  • Maandag, E. C. R.
  • Riele, Hpjt
  • Feeney, Ann
  • Sheehy, A.
  • Schlissel, M.
  • Shinton, S. A.
  • Hardy, R. R.
  • Murre, C.

publication date

  • February 1997

journal

  • Immunity  Journal

abstract

  • The E2A gene products, E12 and E47, are required for proper B cell development. Mice lacking the E2A gene products generate only a very small number of B220+ cells, which lack immunoglobulin DJ(H) rearrangements. We have now generated mice expressing either E12 or E47. B cell development in mice expressing E12 but lacking E47 is perturbed at the pro-B cell stage, and these mice lack IgM+B220+ B cells in both bone marrow and spleen. IgM+B220+ B cells can be detected, albeit at significantly reduced levels, in the bone marrow and spleen of mice lacking E12. Ectopic expression of both E12 and E47 in a null mutant background shows that E12 and E47 act in concert to promote B lineage development. Taken together, the data indicate that both E12 and E47 allow commitment to the B cell lineage and act synergistically to promote B lymphocyte maturation.

subject areas

  • Animals
  • B-Lymphocytes
  • Cell Differentiation
  • DNA-Binding Proteins
  • Drug Synergism
  • Gene Rearrangement, B-Lymphocyte
  • Mice
  • Mice, Mutant Strains
  • Mice, Transgenic
  • TCF Transcription Factors
  • Transcription Factor 7-Like 1 Protein
  • Transcription Factors
  • Transcription, Genetic
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Identity

International Standard Serial Number (ISSN)

  • 1074-7613

Digital Object Identifier (DOI)

  • 10.1016/s1074-7613(00)80421-5

PubMed ID

  • 9047236
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Additional Document Info

start page

  • 145

end page

  • 154

volume

  • 6

issue

  • 2

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