In this study, Greenberg et al. demonstrate that hematopoietic stem cells (HSCs) utilize a novel mechanism involving the CD53-mediated dimerization partner, Rb-like, E2F and multi-vulval class B (DREAM) complex to revert to a quiescent state after exposure to inflammatory and proliferative stress, thus safeguarding their functional integrity.
In this issue of Blood, Greenberg et al1 show that hematopoietic stem cells (HSCs) employ a novel mechanism via promotion of the CD53-mediated dimerization partner, Rb-like, E2F and multi-vulval class B (DREAM) com-plex to return to quiescence after inflammatory and proliferative stress, thereby protecting them from functional decline.
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