scholarly journals The Multiple Layers of Ubiquitin-Dependent Cell Cycle Control

2009 ◽  
Vol 109 (4) ◽  
pp. 1537-1548 ◽  
Author(s):  
Katherine Wickliffe ◽  
Adam Williamson ◽  
Lingyan Jin ◽  
Michael Rape
Stem Cells ◽  
2009 ◽  
Vol 27 (6) ◽  
pp. 1433-1442 ◽  
Author(s):  
Yun-Hua Zhu ◽  
Cheng-Wu Zhang ◽  
Li Lu ◽  
Oleg N. Demidov ◽  
Li Sun ◽  
...  

2017 ◽  
Vol 7 (10) ◽  
pp. 1168-1183 ◽  
Author(s):  
Svasti Haricharan ◽  
Nindo Punturi ◽  
Purba Singh ◽  
Kimberly R. Holloway ◽  
Meenakshi Anurag ◽  
...  

Oncotarget ◽  
2015 ◽  
Vol 7 (1) ◽  
pp. 622-637 ◽  
Author(s):  
Nithyananda Thorenoor ◽  
Petra Faltejskova-Vychytilova ◽  
Sonja Hombach ◽  
Jitka Mlcochova ◽  
Markus Kretz ◽  
...  

Blood ◽  
2012 ◽  
Vol 120 (26) ◽  
pp. 5118-5127 ◽  
Author(s):  
Vinod Pant ◽  
Alfonso Quintás-Cardama ◽  
Guillermina Lozano

Abstract Aberrations in the p53 tumor suppressor pathway are associated with hematologic malignancies. p53-dependent cell cycle control, senescence, and apoptosis functions are actively involved in maintaining hematopoietic homeostasis under normal and stress conditions. Whereas loss of p53 function promotes leukemia and lymphoma development in humans and mice, increased p53 activity inhibits hematopoietic stem cell function and results in myelodysplasia. Thus, exquisite regulation of p53 activity is critical for homeostasis. Most of our understanding of p53 function in hematopoiesis is derived from genetically engineered mice. Here we summarize some of these models, the various mechanisms that disrupt the regulation of p53 activity, and their relevance to human disease.


ChemInform ◽  
2009 ◽  
Vol 40 (26) ◽  
Author(s):  
Katherine Wickliffe ◽  
Adam Williamson ◽  
Lingyan Jin ◽  
Michael Rape

2020 ◽  
Vol 30 (14) ◽  
pp. 2829-2835.e5
Author(s):  
Emily K. Ho ◽  
Anaïs E. Tsai ◽  
Tim Stearns

2012 ◽  
Vol 199 (1) ◽  
pp. 77-95 ◽  
Author(s):  
Matteo J. Marzi ◽  
Eleonora M. R. Puggioni ◽  
Valentina Dall'Olio ◽  
Gabriele Bucci ◽  
Loris Bernard ◽  
...  

The cancer-associated loss of microRNA (miRNA) expression leads to a proliferative advantage and aggressive behavior through largely unknown mechanisms. Here, we exploit a model system that recapitulates physiological terminal differentiation and its reversal upon oncogene expression to analyze coordinated mRNA/miRNA responses. The cell cycle reentry of myotubes, forced by the E1A oncogene, was associated with a pattern of mRNA/miRNA modulation that was largely reciprocal to that induced during the differentiation of myoblasts into myotubes. The E1A-induced mRNA response was preponderantly Retinoblastoma protein (Rb)-dependent. Conversely, the miRNA response was mostly Rb-independent and exerted through tissue-specific factors and Myc. A subset of these miRNAs (miR-1, miR-34, miR-22, miR-365, miR-29, miR-145, and Let-7) was shown to coordinately target Rb-dependent cell cycle and DNA replication mRNAs. Thus, a dual level of regulation—transcriptional regulation via Rb–E2F and posttranscriptional regulation via miRNAs—confers robustness to cell cycle control and provides a molecular basis to understand the role of miRNA subversion in cancer.


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