Pre-B cell receptor-mediated activation of BCL6 induces pre-B cell quiescence through transcriptional repression of MYC Academic Article uri icon


MeSH Major

  • Cell Cycle Checkpoints
  • Cell Division
  • DNA-Binding Proteins
  • Pre-B Cell Receptors
  • Precursor Cells, B-Lymphoid
  • Proto-Oncogene Proteins c-myc
  • Transcription, Genetic


  • Initial cell surface expression of the pre-B cell receptor induces proliferation. After 2 to 5 divisions, however, large pre-BII (Fraction C') cells exit cell cycle to become resting, small pre-BII cells (Fraction D). The mechanism by which pre-BII cells exit cell cycle, however, is currently unclear. The checkpoint at the Fraction C'-D transition is critical for immunoglobulin light chain gene recombination and to prevent malignant transformation into acute lymphoblastic leukemia. Here we demonstrate that inducible activation of pre-B cell receptor signaling induces cell-cycle exit through up-regulation of the transcriptional repressor BCL6. Inducible activation of BCL6 downstream of the pre-B cell receptor results in transcriptional repression of MYC and CCND2. Hence, pre-B cell receptor-mediated activation of BCL6 limits pre-B cell proliferation and induces cellular quiescence at the small pre-BII (Fraction D) stage.

publication date

  • October 13, 2011



  • Academic Article



  • eng

PubMed Central ID

  • PMC3204735

Digital Object Identifier (DOI)

  • 10.1182/blood-2011-01-331181

PubMed ID

  • 21856866

Additional Document Info

start page

  • 4174

end page

  • 8


  • 118


  • 15