c-ABL tyrosine kinase modulates p53-dependent p21 induction and ensuing cell fate decision in response to DNA damage

2014 ◽  
Vol 26 (2) ◽  
pp. 444-452 ◽  
Author(s):  
S.M. Nashir Udden ◽  
Yuiko Morita-Fujimura ◽  
Masanobu Satake ◽  
Shuntaro Ikawa
2011 ◽  
Vol 18 (11) ◽  
pp. 1771-1779 ◽  
Author(s):  
Z Wu ◽  
S T Lee ◽  
Y Qiao ◽  
Z Li ◽  
P L Lee ◽  
...  

2011 ◽  
Vol 101 (11) ◽  
pp. 2582-2591 ◽  
Author(s):  
Changjing Zhuge ◽  
Ying Chang ◽  
Yanjun Li ◽  
Yingyu Chen ◽  
Jinzhi Lei

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e55268 ◽  
Author(s):  
Siwei Tang ◽  
Huimin Bao ◽  
Yang Zhang ◽  
Jun Yao ◽  
Pengyuan Yang ◽  
...  

2019 ◽  
Vol 20 (19) ◽  
pp. 4768 ◽  
Author(s):  
Cheng-Yuan Sun ◽  
Xiao-Peng Zhang ◽  
Wei Wang

p53-targeted microRNAs (miRNAs) markedly affect cellular response to DNA damage. These miRNAs may contribute to either cell cycle arrest or apoptosis induction. However, how these miRNAs coordinate to modulate the decision between cell survival and death remains less understood. Here, we developed an integrated model of p53 signaling network to investigate how p53-targeted miR-192 and miR-22 modulate cellular outcome in response to DNA damage. By numerical simulations, we found that p53 is activated progressively depending on the extent of DNA damage. Upon moderate damage, p53 rises to medium levels and induces miR-192 to promote its own activation, facilitating p21 induction and cell cycle arrest. Upon severe damage, p53 reaches high levels and is fully activated due to phosphatase and tensin homolog (PTEN) induction. As a result, it transactivates miR-22 to repress p21 expression and activate E2F1, resulting in apoptosis. Therefore, miR-192 promotes primary activation of p53, while miR-22 promotes apoptosis by downregulating p21. This work may advance the understanding of the mechanism for cell fate decision between life and death by p53-inducible miRNAs.


2015 ◽  
Vol 11 (11) ◽  
pp. 2955-2963 ◽  
Author(s):  
L. R. de Oliveira ◽  
J. C. M. Mombach ◽  
G. Castellani

The mechanisms leading to the cell fate decision between apoptosis and senescence upon DNA damage are still unclear and have stochastic features.


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