Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation.
KP Foley, GA McArthur, C Quéva, PJ Hurlin, P Soriano, RN Eisenman
EMBO J | Published : 1998
The switch from transcriptionally activating MYC-MAX to transcriptionally repressing MAD1-MAX protein heterodimers has been correlated with the initiation of terminal differentiation in many cell types. To investigate the function of MAD1-MAX dimers during differentiation, we disrupted the Mad1 gene by homologous recombination in mice. Analysis of hematopoietic differentiation in homozygous mutant animals revealed that cell cycle exit of granulocytic precursors was inhibited following the colony-forming cell stage, resulting in increased proliferation and delayed terminal differentiation of low proliferative potential cluster-forming cells. Surprisingly, the numbers of terminally differentia..View full abstract
Awarded by NICHD NIH HHS
Awarded by NHLBI NIH HHS
Awarded by NCI NIH HHS