352 Perinatal Heart Development: Identification and Characterization of a Transitional Program That Controls Cell Cycle Arrest and Terminal Differentiation of the Heart

2012 ◽  
Vol 28 (5) ◽  
pp. S229
Author(s):  
L. Kouri ◽  
P.G. Burgon
PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e76987 ◽  
Author(s):  
Lisa Heron-Milhavet ◽  
Celine Franckhauser ◽  
Anne Fernandez ◽  
Ned J. Lamb

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e108858 ◽  
Author(s):  
Véronique Joliot ◽  
Ouardia Ait-Mohamed ◽  
Valentine Battisti ◽  
Julien Pontis ◽  
Ophélie Philipot ◽  
...  

Blood ◽  
2004 ◽  
Vol 103 (4) ◽  
pp. 1286-1295 ◽  
Author(s):  
Carl R. Walkley ◽  
Louise E. Purton ◽  
Hayley J. Snelling ◽  
Yang-Dar Yuan ◽  
Hideaki Nakajima ◽  
...  

Abstract Retinoids are potent inducers of cell cycle arrest and differentiation of numerous cell types, notably granulocytes. However the mechanisms by which retinoids mediate cell cycle arrest during differentiation remain unclear. We have used myeloid differentiation to characterize the molecular pathways that couple cell cycle withdrawal to terminal differentiation. Using primary cells from mice deficient for either the cyclin-dependent kinase inhibitor (CDKi) p27Kip1, the Myc antagonist Mad1, or both Mad1 and p27Kip1, we observed that signals mediated through retinoic acid receptor α (RARα), but not RARβ or γ, required both Mad1 and p27Kip1 to induce cell cycle arrest and to accelerate terminal differentiation of granulocytes. Although RARα did not directly regulate Mad1 or p27Kip1, the RARα target gene C/EBPϵ directly regulated transcription of Mad1. Induction of C/EBPϵ activity in granulocytic cells led to rapid induction of Mad1 protein and transcript, with direct binding of C/EBPϵ to the Mad1 promoter demonstrated through chromatin immunoprecipitation assay. These data demonstrate that cell cycle arrest in response to RARα specifically requires Mad1 and p27Kip1 and that Mad1 is transcriptionally activated by CCAAT/enhancer-binding protein ϵ (C/EBPϵ). Moreover, these data demonstrate selectivity among the RARs for cell cycle arrest pathways and provide a direct mechanism to link differentiation induction and regulation of the Myc antagonist Mad1.


Oncotarget ◽  
2016 ◽  
Vol 7 (17) ◽  
pp. 24027-24049 ◽  
Author(s):  
Cristina Florean ◽  
Michael Schnekenburger ◽  
Jin-Young Lee ◽  
Kyung Rok Kim ◽  
Aloran Mazumder ◽  
...  

1998 ◽  
Vol 36 (9-10) ◽  
pp. 791-804 ◽  
Author(s):  
J.R. Ciacci-Zanella ◽  
A.H. Merrill ◽  
E. Wang ◽  
C. Jones

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