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Fig. 4 | BMC Systems Biology

Fig. 4

From: System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia

Fig. 4

Simulations of gene expression activities of cell cycle components. a-b Genetic synthesis rates, which are proportional to the transcription rates of genes, are computed herein as surrogates for gene expression activities. Simulation data of Cyclin D, Cyclin E, Cdk2 and Cdk4/6 (a) and multiple CKIs (b) under the circumstance that Maff and Egr3 are both highly-expressed (Maff +, Egr3 +) are shown. Subtypes of cyclins are not distinguished in modeling in order for simplifying computation (i.e. Cyclin D1, D2 and D3 are taken altogether as one molecule Cyclin D; E1 and E2 are taken together as E). In the labels, “Gene.Exp.” means gene expression, “~” means equivalency or proportionality. c-e: Experimental measurements of relative expressions of the cyclins (c), Cdks (d) and CKIs (e) when Maff and Egr3 are both highly-expressed (Maff +, Egr3 +; i.e. Day 14 of leukemia). Data are obtained by qRT-PCR; and it is shown that the simulation results are consistent with experimental data in terms of expressions of all CKIs, Cdks and Cyclins. Since the modeling does not distinguish molecular subtypes, simulation of Cyclin D expression amounts to the overall level of all subtypes, which is also consistent with the sum of D1, D2 and D3 in the experimental data

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