Identification of the function and regulatory network of circ_009773 in DNA damage induced by nanoparticles of neodymium oxide

2021 ◽  
pp. 105271
Author(s):  
Ling Liu ◽  
Yangyang Jia ◽  
Xia Zhang ◽  
Shijie Chen ◽  
Suhua Wang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Regulatory Network ◽  
Neodymium Oxide

Oscillatory Behaviors of Delayed p53 Regulatory Network with microRNA 192 in DNA Damage Response

2021 ◽  
Vol 31 (02) ◽  
pp. 2150020
Author(s):  
Chunyan Gao ◽  
Fangqi Chen
Keyword(s):  
Dna Damage ◽  
Time Delay ◽  
Dna Damage Response ◽  
Positive Feedback ◽  
Regulatory Network ◽  
Feedback Loop ◽  
Research Work ◽  
Positive Feedback Loop ◽  
Damage Response ◽  
High Level

This study develops a general model of delayed p53 regulatory network in the DNA damage response by introducing microRNA 192-mediated positive feedback loop based on the existing research work. Through theoretical analysis and numerical simulation, we find that the delay as a bifurcation parameter can drive the p53-Mdm2 module to undergo a supercritical Hopf bifurcation, thereby producing oscillation behavior. Moreover, we demonstrate how the positive feedback loop formed by p53* and microRNA 192 (miR-192) with the feature of double-negative regulation produces oscillations. Further, a comparison is given to demonstrate that microRNA 192-mediated positive feedback loop affects the robustness of system oscillations. In addition, we show that ataxia telangiectasia mutated kinase (ATM), once activated by DNA damage, makes p53* undergo two Hopf bifurcations. These results reveal that both time delay and miR-192 play tumor suppressing roles by promoting p53 oscillation or high level expression, which will provide a perspective for promoting the development of anti-cancer drugs by targeting miR-192 and time delay.

scholarly journals WIP1 Contributes to the Adaptation of Fanconi Anemia Cells to DNA Damage as Determined by the Regulatory Network of the Fanconi Anemia and Checkpoint Recovery Pathways

2019 ◽  
Vol 10 ◽  
Author(s):  
Alfredo Rodríguez ◽  
J. Jesús Naveja ◽  
Leda Torres ◽  
Benilde García de Teresa ◽  
Ulises Juárez-Figueroa ◽  
...  
Keyword(s):  
Dna Damage ◽  
Fanconi Anemia ◽  
Regulatory Network ◽  
Checkpoint Recovery ◽  
Recovery Pathways

Neighbourhoods in the yeast regulatory network in different physiological states

2020 ◽  
Author(s):  
Arthur M Lesk ◽  
Arun S Konagurthu
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Damage ◽  
Transcription Factor ◽  
Stress Response ◽  
Local Structure ◽  
Regulatory Network ◽  
Diauxic Shift ◽  
Central Node ◽  
Similarities And Differences

Abstract Motivation The gene expression regulatory network in yeast controls the selective implementation of the information contained in the genome sequence. We seek to understand how, in different physiological states, the network reconfigures itself to produce a different proteome. Results This article analyses this reconfiguration, focussing on changes in the local structure of the network. In particular, we define, extract and compare the 1-neighbourhoods of each transcription factor, where a 1-neighbourhood of a node in a network is the minimal subgraph of the network containing all nodes connected to the central node by an edge. We report the similarities and differences in the topologies and connectivities of these neighbourhoods in five physiological states for which data are available: cell cycle, DNA damage, stress response, diauxic shift and sporulation. Based on our analysis, it seems apt to regard the components of the regulatory network as ‘software’, and the responses to changes in state, ‘reprogramming’.

MINING TIME-DEPENDENT GENE FEATURES

2005 ◽  
Vol 03 (05) ◽  
pp. 1191-1205 ◽  
Author(s):  
ENRICO CAPOBIANCO
Keyword(s):  
Gene Expression ◽  
Dna Damage ◽  
Steady State ◽  
Mutual Information ◽  
Regulatory Network ◽  
Genomic Data ◽  
Genetic Regulatory Network ◽  
Time Dependent ◽  
Cascade Effects

This paper presents an application of the Independent Component Analysis (ICA) method to genomic data. In particular, experimentally produced perturbation effects over the E.coli bacterium are monitored through the changes of gene expression values observed at regular times, and until steady state has been reached. The aim is to control the response of the SOS system to DNA damage. We might assume that only part of the genetic regulatory network is affected directly by the perturbation conditions, as indirect cascade effects might also be present, and some genes may change just because of randomness. ICA decomposes the gene matrix and identifies groups of genes belonging to a certain estimated component by virtue of co-expression; it is of course of interest to establish co-regulation dynamics, which might underlie the captured correlation. Stronger forms of dependence, like Mutual Information, are thus computed and compared with linear correlation in order to validate the results and establish the role of the identified components in determining the network dynamics.

scholarly journals Study on regulatory network of proteins based on DNA damage

2014 ◽  
Vol 63 (1) ◽  
pp. 018702
Author(s):  
Geng Du-Yan ◽  
Xie Hong-Juan ◽  
Wan Xiao-Wei ◽  
Xu Gui-Zhi
Keyword(s):  
Dna Damage ◽  
Regulatory Network

A Regulatory Network of G2/M Phase Transition for DNA Damage

2013 ◽  
Vol 444-445 ◽  
pp. 1182-1186 ◽  
Author(s):  
L.W. Zhang ◽  
K.M. Liew
Keyword(s):  
Phase Transition ◽  
Dna Damage ◽  
Kinetic Parameters ◽  
Regulatory Network ◽  
Feedback Loop ◽  
Transition Process ◽  
Statistical Hypothesis ◽  
Statistical Hypothesis Testing ◽  
Phase Transition Process ◽  
M Phase

A regulatory network of G2/M phase transition influenced by different intensities of DNA damage is modeled. It contains the sub-modules of P53-Mdm2 feedback loop and G2/M phase transition process. To investigate the robustness of the regulatory network, a sensitivity analysis of kinetic parameters in the proposed mathematical model is implemented to select the most significant kinetic parameters, which are relevant to key proteins involved in G2/M phase transition. Subsequently, the statistical hypothesis testing is employed to evaluate the influence of perturbations on the G2/M regulatory network. The results indicate that G2/M regulatory network is robust to DNA damage signal when perturbations are very small that is consistent with the experimental observations.

scholarly journals Regulation of Mus81-Eme1 structure-specific endonuclease by Eme1 SUMO-binding and Rad3(ATR) kinase is essential in the absence of Rqh1(BLM) helicase

2021 ◽  
Author(s):  
C&eacutedric Giaccherini ◽  
Sarah Scaglione ◽  
St&eacutephane Coulon ◽  
Pierre-Marie Deh&eacute ◽  
Pierre Henri L GAILLARD
Keyword(s):  
Dna Damage ◽  
Regulatory Network ◽  
Dna Recombination ◽  
Dna Damage Checkpoint ◽  
Phosphorylation Sites ◽  
Late Replication ◽  
Blm Helicase ◽  
Atr Kinase ◽  
Replication Intermediates ◽  
Stimulation Of

The Mus81-Eme1 structure-specific endonuclease is crucial for the processing of DNA recombination and late replication intermediates. In fission yeast, stimulation of Mus81-Eme1 in response to DNA damage at the G2/M transition relies on Cdc2(CDK1) and DNA damage checkpoint-dependent phosphorylation of Eme1 and is critical for chromosome stability in absence of the Rqh1(BLM) helicase. Here we identify Rad3(ATR) checkpoint kinase consensus phosphorylation sites and two SUMO interacting motifs (SIM) within a short N-terminal domain of Eme1 that is required for cell survival in absence of Rqh1(BLM). We show that catalytic stimulation of Mus81-Eme1 depends entirely on direct phosphorylation of Eme1 by Rad3(ATR) and that while Eme1 also undergoes Chk1-mediated phosphorylation, this is not essential for catalytic modulation. Both Rad3(ATR)- and Chk1-mediated phosphorylation of Eme1 as well as the SIMs are independently critical for cell fitness in absence of Rqh1(BLM) and abrogating bimodal phosphorylation of Eme1 along with mutating the SIMs is incompatible with rqh1∆ cell viability. Our findings unravel an elaborate regulatory network that is essential for Mus81-Eme1 to fulfill functions that are essential in absence of Rqh1(BLM).

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