Bayleyegn2016 - interactions of CycE/Cdk2, Cdc25A, and P27 Kip1 in a core cancer subnetwork

  public model
Model Identifier
MODEL2003180002
Short description
Mathematical description of the interactions of CycE/Cdk2, Cdc25A, and P27Kip1 in a core cancer subnetwork. Model is encoded by Matthieu Maire/partially by Krishna Kumar Tiwari and submitted to BioModels by Krishna Kumar Tiwari.
Format
SBML (L2V4)
Related Publication
  • Mathematical description of the interactions of CycE/Cdk2, Cdc25A, and P27Kip1 in a core cancer subnetwork
  • Y.N.Bayleyegn, K.S.Govinder
  • wileyonlinelibrary , 2/ 2020 , Volume 30 , pages: 2961-2979 , DOI: 10.1002/mma.4213
  • School of Mathematics, Statistics and Computer Science, University of KwaZulu-Natal, Private Bag X54001, Durban 4000, South Africa
  • The Eukaryotic cell cycle is a repeated sequence of events that enables the division of a cell into two daughter cells. The cell cycle is classically divided into four phases: gap 1 (G1), synthesis (S), gap 2 (G2), and mitosis (M). In the G1 phase of the cell cycle, the cell physically grows and prepares for DNA replication. In the following, S, phase, the DNA is copied,while in the G2 phase, final preparations for cell division are made within the nucleus of the cell. In the last, M, phase, the cell divides into two daughter cells, which then begin a new cycle of division [1–4]. During the cell cycle process, there are different checkpoints that allow the cell to check for and repair DNA damage, as well as to control cell progression: the restriction (R) checkpoint between the G1 and S phases; the G2 checkpoint between the G2 and M phases; and the metaphase checkpoint between the metaphase and anaphases of the cell cycle [5]. At the R-checkpoint [6], either the cell commits to division and then progresses to the S phase or exits the cell cycle and enters the quiescent state (G0) [4]. In this study, we are particularly interested in the dynamics of the gene expression levels at the R-checkpoint. The cell-cycle process is orchestrated by the production and balance of chemical signals that activate and inhibit the cell-cycle progression genes that form a complex and highly integrated network [2]. In this network, activating and inhibitory signal molecules interact, forming positive-feedback and negative-feedback loops, which ultimately control the dynamics of the cell cycle. The two types of genes that are particularly important for regulating cell-cycle process are oncogenes (which are responsible for growth signals and promotion of cell-cycle progression) and tumor suppressor genes (TSGs) (which are responsible for inhibitory signals and retard or halt the cell cycle). If either (or both) of these genes malfunction, then cancer initiation (carcinogenesis) may occur.
Contributors
Submitter of the first revision: Krishna Kumar Tiwari
Submitter of this revision: Krishna Kumar Tiwari
Modellers: Krishna Kumar Tiwari

Metadata information

hasProperty (1 statement)
Mathematical Modelling Ontology Ordinary differential equation model

isDescribedBy (1 statement)
Curation status
Non-curated
Modelling approach(es)
ordinary differential equation model
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Model files
Bayleyegn2016.xml SBML L2V4 file for the model 17.96 KB Preview | Download

Additional files
Bayleyegn2016.cps COPASI 4.27 (built217) file for the model 47.20 KB Preview | Download
Bayleyegn2016.sedml SEDML file for the model 2.80 KB Preview | Download

  • Model originally submitted by : Krishna Kumar Tiwari
  • Submitted: Mar 18, 2020 6:50:47 PM
  • Last Modified: Mar 18, 2020 6:50:47 PM
Revisions
  • Version: 2 public model Download this version
    • Submitted on: Mar 18, 2020 6:50:47 PM
    • Submitted by: Krishna Kumar Tiwari
    • With comment: Edited model metadata online.