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Myc-mediated proliferation and lymphomagenesis, but not apoptosis, are compromised by e2f1 loss

Academic Article
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Overview

authors

  • Baudino, T. A.
  • Maclean, K. H.
  • Brennan, J.
  • Parganas, E.
  • Yang, C. Y.
  • Aslanian, A.
  • Lees, J. A.
  • Sherr, C. J.
  • Roussel, M. F.
  • Cleveland, John

publication date

  • April 2003

journal

  • Molecular Cell  Journal

abstract

  • Myc and E2f1 promote cell cycle progression, but overexpression of either can trigger p53-dependent apoptosis. Mice expressing an Emu-Myc transgene in B lymphocytes develop lymphomas, the majority of which sustain mutations of either the Arf or p53 tumor suppressors. Emu-Myc transgenic mice lacking one or both E2f1 alleles exhibited a slower onset of lymphoma development associated with increased expression of the cyclin-dependent kinase inhibitor p27(Kip1) and a reduced S phase fraction in precancerous B cells. In contrast, Myc-induced apoptosis and the frequency of Arf and p53 mutations in lymphomas were unaffected by E2f1 loss. Therefore, Myc does not require E2f1 to induce Arf, p53, or apoptosis in B cells, but depends upon E2f1 to accelerate cell cycle progression and downregulate p27(Kip1).

subject areas

  • ADP-Ribosylation Factor 1
  • Animals
  • Apoptosis
  • Cell Cycle Proteins
  • Cell Division
  • Cell Transformation, Neoplastic
  • Cyclin-Dependent Kinase Inhibitor p27
  • DNA-Binding Proteins
  • E2F Transcription Factors
  • E2F1 Transcription Factor
  • Female
  • Genotype
  • Lymphoma
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Mutation
  • Proto-Oncogene Proteins c-myc
  • S Phase
  • Transcription Factors
  • Transgenes
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
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Identity

International Standard Serial Number (ISSN)

  • 1097-2765

Digital Object Identifier (DOI)

  • 10.1016/s1097-2765(03)00102-3

PubMed ID

  • 12718877
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Additional Document Info

start page

  • 905

end page

  • 914

volume

  • 11

issue

  • 4

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