Table 1.

Transcription factors implicated in quiescence and dormancy

Transcription factorFunctionReferences
TP53 Preserves quiescence of HSCs primarily by transcriptionally promoting expression of growth factor independent 1 (Gfi-1) and Necdin as inhibitors of HSC proliferation 56,69  
c-Myc, N-Myc, and L-Myc Double-deficiency of c-Myc and N-Myc inhibits proliferation of myeloid progenitor cells but promotes cell cycling of HSCs and results in depleted HSC pool 70  
c-Myb Reduces proliferation but promotes differentiation of HSCs 71  
HLF, Pbx1, Evi-1, Nurr1, Nrf2, C/EBPα, PU.1, YY1, Gfi-1, Fhl2, Hoxb5, and Tcf15 Maintain quiescence 26,72-83  
ELF4 and Id1 Deletion preserves quiescence in HSCs 84,85  
Hoxb3 and Hoxb4 Deletion impairs the proliferation of HSCs 86,87  
Hoxb4 or Hoxb7 Overexpression substantially enhances the expansion capacity of HSCs 87,88  
Gata 2 Inhibits proliferation and increases quiescence in HSCs by repressing gene expression of CCND1, CDK4, and CDK6 89  
Gata 3 Essential for HSC entry into the cell cycle 90  
FoxM1 Essential for quiescence maintenance in HSCs by inducing expression of Nurr1, which preserves quiescence of HSCs via inducing expression of p21 and p27 78  
FoxO1, FoxO3, and FoxO4 Deletion of which increases cell cycling and apoptosis in quiescent HSCs via alteration of the expression of their target genes, including cyclin G2, cyclin D, p21, and p27 91,92  
Foxo3 Enhances autophagy 93  
RUNX1 Induces the expression of multiple ribosome protein genes and controls ribosome biogenesis 94  
Transcription factorFunctionReferences
TP53 Preserves quiescence of HSCs primarily by transcriptionally promoting expression of growth factor independent 1 (Gfi-1) and Necdin as inhibitors of HSC proliferation 56,69  
c-Myc, N-Myc, and L-Myc Double-deficiency of c-Myc and N-Myc inhibits proliferation of myeloid progenitor cells but promotes cell cycling of HSCs and results in depleted HSC pool 70  
c-Myb Reduces proliferation but promotes differentiation of HSCs 71  
HLF, Pbx1, Evi-1, Nurr1, Nrf2, C/EBPα, PU.1, YY1, Gfi-1, Fhl2, Hoxb5, and Tcf15 Maintain quiescence 26,72-83  
ELF4 and Id1 Deletion preserves quiescence in HSCs 84,85  
Hoxb3 and Hoxb4 Deletion impairs the proliferation of HSCs 86,87  
Hoxb4 or Hoxb7 Overexpression substantially enhances the expansion capacity of HSCs 87,88  
Gata 2 Inhibits proliferation and increases quiescence in HSCs by repressing gene expression of CCND1, CDK4, and CDK6 89  
Gata 3 Essential for HSC entry into the cell cycle 90  
FoxM1 Essential for quiescence maintenance in HSCs by inducing expression of Nurr1, which preserves quiescence of HSCs via inducing expression of p21 and p27 78  
FoxO1, FoxO3, and FoxO4 Deletion of which increases cell cycling and apoptosis in quiescent HSCs via alteration of the expression of their target genes, including cyclin G2, cyclin D, p21, and p27 91,92  
Foxo3 Enhances autophagy 93  
RUNX1 Induces the expression of multiple ribosome protein genes and controls ribosome biogenesis 94  
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