Table 5. Original and optPBN results for the Boolean model of apoptosis (case study 4).

	Apoptosis				C3ap17				NFkB
Exp	Orig.	Init.	Ext.	Meas.	Orig.	Init.	Ext.	Meas.	Orig.	Init.	Ext.	Meas.
Mock	0	0.0000	0.0054	0.00	0	0.0168	0.0082	0.00	0	0.0168	0.0027	0.00
FasL (2)	1	0.9208	0.7170	0.63	1	0.9505	0.8491	1.00	0	0.0198	0.1501	0.32
IL-1	0	0.0028	0.0063	0.00	0	0.0042	0.0013	0.03	1	0.8873	0.8481	1.00
TNF	0	0.0020	0.0018	0.10	0	0.4073	0.4049	0.39	1	0.7889	0.8723	0.98
UV1	1	0.9920	0.9868	1.00	1	0.9966	0.9901	1.00	0	0.0023	0.0033	0.26
UV2	0	0.4681	0.4914	0.49	0	0.0016	0.0012	0.00	1	0.3083	0.2932	0.46

The results from logical steady-state analysis in CellNetAnalyzer of the original Boolean model from Schlatter et al. [4] (Orig.) are shown in comparison to the optPBN results generated from the ‘initial apoptosis model’ (Init.), a probabilistic Boolean network (PBN) model which was modified from the original Boolean model, and from the ‘extended apoptosis model’ (Ext.), a PBN model variant with an additional literature-derived Boolean interaction from Caspase 8 to NFκB. The sum of optimal costs based on the calculation of sum of square error between simulated steady-state probabilities and measurement data (Meas.) are 1.002, 0.328, and 0.199, respectively. The inverse correlation between UVB irradiation (UV1 = 300 £/m², UV2 = 600 £/m²), NFκB and P17 form of activated Caspase 3 (C3ap17) activations, and apoptosis are observed in a limited qualitative manner in the original model in Boolean Network format, while this correlation is observed quantitatively in the initial and extended apoptosis models in PBN format. Note that the model fitting of NFκB in the case of Fas ligand activation, ‘FasL (2)’, in the extended apoptosis model is improved as a result from the additional molecular interaction derived from literature.