The p53 tumor suppressor protein is a critical regulator of hematopoietic stem cell behavior

Yan Liu, Shannon E. Elf, Takashi Asai, Yasuhiko Miyata, Yuhui Liu, Goro Sashida, Gang Huang, Silvana Di Giandomenico, Andrew Koff, Stephen D. Nimer

Research output: Contribution to journalReview articlepeer-review

53 Scopus citations


In response to diverse stresses, the tumor suppressor p53 differentially regulates its target genes, variably inducing cell cycle arrest, apoptosis or senescence. Emerging evidence indicates that p53 plays an important role in regulating hematopoietic stem cell (HSC) quiescence, self-renewal, apoptosis and aging. The p53 pathway is activated by DNA damage, defects in ribosome biogenesis, oxidative stress and oncogene induced p19ARF upregulation. We present an overview of the current state of knowledge about p53 (and its target genes) in regulating HSC behavior, with the hope that understanding the molecular mechanisms that control p53 activity in HSCs and how p53 mutations affect its role in these events may facilitate the development of therapeutic strategies for eliminating leukemia (and cancer) propagating cells.

Original languageEnglish (US)
Pages (from-to)3120-3124
Number of pages5
JournalCell Cycle
Issue number19
StatePublished - Oct 1 2009
Externally publishedYes


  • Aging
  • Apoptosis
  • Gfi-1
  • Hematopoietic stem cell
  • Leukemia stem cell
  • Necdin
  • Quiescence
  • Self-renewal
  • Slug
  • p21
  • p53

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


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