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In this study, we provide evidence that in the absence of DS, replication of the mini-EBV genome is still dependent on ORC and follows the once-per-cell cycle rule.
This paper presents the algorithmic methods needed for modeling complicated biochemical dynamics using rule-based models to represent expert knowledge in the context of cell cycle regulation and tumor growth.
From the cell cycle dependent rule profiles in Additional File 4, we constructed a model of yeast cell cycle transcriptional regulatory network.
Experiments using BRCA-null cells in which exogenous BRCA expression is induced to wild-type levels at the appropriate time in the cell cycle would rule out this possibility.
Although CBD has previously been implicated in the regulation of the cell cycle, we ruled out this possibility by studying BrdU incorporation and cell cycle progression.
The way to describe this is similar to the cell cycle transition rules, where intracellular protein amounts are taken into account in an upward causation manner.
We therefore performed a cell cycle analysis to rule out the possibility that up-regulation of survivin is due to merely an increase of a fraction of G2/M cells in the HER-2-overexpressing population.
First, we develop and test a preliminary cell cycle model using rules.
Hence, cell cycle arrest was ruled out as one of the mechanism of actions of the extracts.
In order to model a multicellular system, we extend the previous cell division rule (cell cycle transition from M phase to G1) to produce two distinct cells.
We selected 18 proteins connecting ERBB receptor signaling to the G1/S transition of cell cycle, and defined logical rules to describe their regulations with regard to literature information.
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