The p53 Network

2007 ◽  
pp. 1-23 ◽  
Author(s):  
Arnold J. Levine ◽  
Jill Bargonetti ◽  
Gareth L. Bond ◽  
Josephine Hoh ◽  
Kenan Onel ◽  
...  
Keyword(s):  
P53 Network

Oscillatory Dynamics of P53 Network With Time Delays

2018 ◽  
Vol 21 (6) ◽  
pp. 411-419 ◽  
Author(s):  
Conghua Wang ◽  
Fang Yan ◽  
Yuan Zhang ◽  
Haihong Liu ◽  
Linghai Zhang
Keyword(s):  
Hopf Bifurcation ◽  
Cell Fate ◽  
Time Delays ◽  
Sustained Oscillation ◽  
Multiple Time ◽  
Cell Fate Decisions ◽  
Oscillatory Dynamics ◽  
Main Components ◽  
Parameter Values ◽  
P53 Network

Aims and Objective: A large number of experimental evidences report that the oscillatory dynamics of p53 would regulate the cell fate decisions. Moreover, multiple time delays are ubiquitous in gene expression which have been demonstrated to lead to important consequences on dynamics of genetic networks. Although delay-driven sustained oscillation in p53-based networks is commonplace, the precise roles of such delays during the processes are not completely known. Method: Herein, an integrated model with five basic components and two time delays for the network is developed. Using such time delays as the bifurcation parameter, the existence of Hopf bifurcation is given by analyzing the relevant characteristic equations. Moreover, the effects of such time delays are studied and the expression levels of the main components of the system are compared when taking different parameters and time delays. Result and Conclusion: The above theoretical results indicated that the transcriptional and translational delays can induce oscillation by undergoing a super-critical Hopf bifurcation. More interestingly, the length of these delays can control the amplitude and period of the oscillation. Furthermore, a certain range of model parameter values is essential for oscillation. Finally, we illustrated the main results in detail through numerical simulations.

scholarly journals A genome-scale protein interaction profile of Drosophila p53 uncovers additional nodes of the human p53 network

2010 ◽  
Vol 107 (14) ◽  
pp. 6322-6327 ◽  
Author(s):  
A. Lunardi ◽  
G. Di Minin ◽  
P. Provero ◽  
M. Dal Ferro ◽  
M. Carotti ◽  
...  
Keyword(s):  
Protein Interaction ◽  
A Genome ◽  
Genome Scale ◽  
P53 Network

Multi-scale modeling of cell survival and death mediated by the p53 network: a systems pharmacology framework

2015 ◽  
Vol 11 (11) ◽  
pp. 3011-3021 ◽  
Author(s):  
Yuan Wang ◽  
Zihu Guo ◽  
Xuetong Chen ◽  
Wenjuan Zhang ◽  
Aiping Lu ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cell Fate ◽  
Mammalian Cells ◽  
Regulatory Process ◽  
Systems Pharmacology ◽  
Multi Scale ◽  
Scale Modeling ◽  
Multi Scale Modeling ◽  
P53 Network

The determination of cell fate is a key regulatory process for the development of complex organisms that are controlled by distinct genes in mammalian cells.

scholarly journals Time delay as a key to apoptosis induction in the p53 network

2002 ◽  
Vol 29 (1) ◽  
pp. 135-140 ◽  
Author(s):  
G. Tiana ◽  
M.H. Jensen ◽  
K. Sneppen
Keyword(s):  
Time Delay ◽  
Apoptosis Induction ◽  
P53 Network

scholarly journals Modeling and controlling the two-phase dynamics of the p53 network: a Boolean network approach

2014 ◽  
Vol 16 (12) ◽  
pp. 125010 ◽  
Author(s):  
Guo-Qiang Lin ◽  
Bin Ao ◽  
Jia-Wei Chen ◽  
Wen-Xu Wang ◽  
Zeng-Ru Di
Keyword(s):  
Boolean Network ◽  
Network Approach ◽  
Two Phase ◽  
Phase Dynamics ◽  
P53 Network

scholarly journals miR-605joins p53 network to form a p53:miR-605:Mdm2 positive feedback loop in response to stress

2011 ◽  
Vol 30 (3) ◽  
pp. 524-532 ◽  
Author(s):  
Jiening Xiao ◽  
Huixian Lin ◽  
Xiaobin Luo ◽  
Xiaoyan Luo ◽  
Zhiguo Wang
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Positive Feedback Loop ◽  
Response To Stress ◽  
P53 Network

scholarly journals Cadmium Impairs p53 Activity in HepG2 Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
C. Urani ◽  
P. Melchioretto ◽  
M. Fabbri ◽  
G. Bowe ◽  
E. Maserati ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Conformational Changes ◽  
Protein Level ◽  
Cell Cycle Progression ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Cycle Arrest ◽  
Promote Cell Cycle Progression ◽  
Cycle Regulation ◽  
P53 Network

Cadmium and cadmium compounds are contaminants of the environment, food, and drinking water and are important constituents of cigarette smoke. Cd exposure has also been associated with airborne particulate CdO and with Cd-containing quantum dots in medical therapy. Adverse cadmium effects reported in the literature have stimulated during recent years an ongoing discussion to better elucidate cadmium outcomes at cell and molecular level. The present work is designed to gain an insight into the mechanism of p53 impairment at gene and protein level to understand Cd-induced resistance to apoptosis. We used a hepatoma cell line (HepG2) derived from liver, known to be metal responsive. At genotoxic cadmium concentrations no cell cycle arrest was observed. The p53 at gene and protein level was not regulated. Fluorescence images showed that p53 was correctly translocated into the nucleus but that the p21Cip1/WAF-1, a downstream protein of p53 network involved in cell cycle regulation, was not activated at the highest cadmium concentrations used. The miRNAs analysis revealed an upregulation of mir-372, an miRNA able to affect p21Cip1/WAF-1 expression and promote cell cycle progression and proliferation. The role of metallothioneins and possible conformational changes of p53 are discussed.

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