The Role of the Retinoblastoma Protein in Health, Malignancy, and the Pathogenesis of Retinoblastoma

2003 ◽  
pp. 143-202
Keyword(s):  
Retinoblastoma Protein

scholarly journals Role of the Retinoblastoma Protein in Differentiation and Senescence

2003 ◽  
Vol 2 (2) ◽  
pp. 124-130 ◽  
Author(s):  
David M. Thomas ◽  
Hai-Su Yang ◽  
Kamilah Alexander ◽  
Philip W. Hinds
Keyword(s):  
Retinoblastoma Protein

The Role of Decreased Retinoblastoma Protein Expression in Acute Myelomonocytic and Monoblastic Leukemias

1995 ◽  
Vol 17 (1-2) ◽  
pp. 135-137 ◽  
Author(s):  
Rudolf Weide ◽  
Behnoush Parviz ◽  
Karl-Heinz Pfluuger ◽  
Hubert Kouppler ◽  
Bernhard Wourmann ◽  
...  
Keyword(s):  
Protein Expression ◽  
Retinoblastoma Protein

scholarly journals Role of Drosophila retinoblastoma protein instability element in cell growth and proliferation

Cell Cycle ◽  
2015 ◽  
Vol 14 (4) ◽  
pp. 589-597 ◽  
Author(s):  
Jared S Elenbaas ◽  
Rima Mouawad ◽  
R William Henry ◽  
David N Arnosti ◽  
Sandhya Payankaulam
Keyword(s):  
Cell Growth ◽  
Retinoblastoma Protein ◽  
Protein Instability ◽  
Cell Growth And Proliferation

scholarly journals Role of LXCXE motif-dependent interactions in the activity of the retinoblastoma protein

Oncogene ◽  
2001 ◽  
Vol 20 (43) ◽  
pp. 6152-6163 ◽  
Author(s):  
Ho Man Chan ◽  
Linda Smith ◽  
Nicholas B La Thangue
Keyword(s):  
Retinoblastoma Protein ◽  
Lxcxe Motif

scholarly journals p53 Regulation of G2 Checkpoint Is Retinoblastoma Protein Dependent

2000 ◽  
Vol 20 (12) ◽  
pp. 4210-4223 ◽  
Author(s):  
Patricia M. Flatt ◽  
Luo Jia Tang ◽  
Caroline D. Scatena ◽  
Suzanne T. Szak ◽  
Jennifer A. Pietenpol
Keyword(s):  
Molecular Mechanisms ◽  
Cell Model ◽  
Retinoblastoma Protein ◽  
Genotoxic Stress ◽  
Cyclin B1 ◽  
Model Systems ◽  
Wild Type ◽  
G2 Checkpoint ◽  
Cdc2 Activity

ABSTRACT In the present study, we investigated the role of p53 in G2 checkpoint function by determining the mechanism by which p53 prevents premature exit from G2 arrest after genotoxic stress. Using three cell model systems, each isogenic, we showed that either ectopic or endogenous p53 sustained a G2arrest activated by ionizing radiation or adriamycin. The mechanism was p21 and retinoblastoma protein (pRB) dependent and involved an initial inhibition of cyclin B1-Cdc2 activity and a secondary decrease in cyclin B1 and Cdc2 levels. Abrogation of p21 or pRB function in cells containing wild-type p53 blocked the down-regulation of cyclin B1 and Cdc2 expression and led to an accelerated exit from G2after genotoxic stress. Thus, similar to what occurs in p21 and p53 deficiency, pRB loss can uncouple S phase and mitosis after genotoxic stress in tumor cells. These results indicate that similar molecular mechanisms are required for p53 regulation of G1 and G2 checkpoints.

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