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Nature Communications|December 8, 2015
Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progressionAmy Tarangelo, Nathanael Lo, Rebecca Teng, et al.
Molecular and Cellular Biology|January 27, 2010
Regulation of RB transcription in vivo by RB family membersDeborah L Burkhart, Lynn K Ngai, Caitlin M Roake, et al.
Cell Reports|March 5, 2020
Direct Comparison of Mononucleated and Binucleated Cardiomyocytes Reveals Molecular Mechanisms Underlying Distinct Proliferative CompetenciesRebecca Windmueller, John P Leach, Apoorva Babu, et al.
Cell Stem Cell|October 23, 2008
Hematopoietic stem cell quiescence is maintained by compound contributions of the retinoblastoma gene familyPatrick Viatour, Tim C Somervaille, Shivkumar Venkatasubrahmanyam, et al.
Molecular and Cellular Biology|June 16, 2010
The repressing function of the oncoprotein BCL-3 requires CtBP, while its polyubiquitination and degradation involve the E3 ligase TBLR1Aurore Keutgens, Kateryna Shostak, Pierre Close, et al.
The Journal of Biological Chemistry|June 19, 2010
BCL-3 degradation involves its polyubiquitination through a FBW7-independent pathway and its binding to the proteasome subunit PSMB1Aurore Keutgens, Xin Zhang, Kateryna Shostak, et al.
The Journal of Cell Biology|November 10, 2010
G1 arrest and differentiation can occur independently of Rb family functionStacey E Wirt, Adam S Adler, Véronique Gebala, et al.
The Journal of Experimental Medicine|May 15, 2013
Inactivation of the RB family prevents thymus involution and promotes thymic function by direct control of Foxn1 expressionPhillip M Garfin, Dullei Min, Jerrod L Bryson, et al.
Molecular Cell|October 8, 2004
GSK3-mediated BCL-3 phosphorylation modulates its degradation and its oncogenicityPatrick Viatour, Emmanuel Dejardin, Michael Warnier, et al.
The Journal of Experimental Medicine|May 28, 2017
Rb family proteins enforce the homeostasis of quiescent hematopoietic stem cells by repressing Socs3 expressionEunsun Kim, Ying Cheng, Elisabeth Bolton-Gillespie, et al.
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