Unit testing.

<p>A) Ligand-receptor cooperativity for RTK submodel (dots-deterministic simulations; lines- hill equation fit) based on ligand-matched receptor expression (each receptor expressed in isolation and at appreciable levels). B-D) μ-Western blot data (left column) used to train simulated (right column) ERK (B), AKT (C), and mTOR (pEIF4E-BP1) (D) signaling dynamics in the proliferation and growth submodel. Serum and growth factor starved MCF10A cells were stimulated with indicated doses of EGF, insulin, and combinations (High/Low EGF 10/0.01 nM, High/Low Insulin 1721/0.17 nM) for 5, 30, 180, or 360 minutes. E) DNA damage-induced p53 responses to single-stranded breaks (top), double-stranded breaks (middle), and both (bottom), with (red) and without (blue) simulated repair. F) Stochastic simulations for how the number of p53 pulses (top), pulse height (middle) and width (bottom) depend on DNA damage level. G) Increasing amounts of TRAIL (increasingly warmer colors) decreases time to death (as indicated by cPARP spike) exponentially (right panel: red dots-simulation; line-exponential fit). H) Survival after 5 hours TRAIL treatment. Red dots-simulation; red line-sigmoid fit; black dots-flow cytometry data. I) Effects of PUMA, NOXA, ppERK and ppAKT on time-to-death in deterministic simulations. J) Simulated cell cycle initiation by increasing cyclin D mRNA levels in serum-starved cells indicates proper oscillatory behavior of cyclin-CDK complexes.