Figure 3

Experimental IKK and caspase data. (a) Measured biological data available in the Supplemental Data of Janes et al. [20]. For different concentrations of TNF (0 or 100 ng/ml) and IL-1ra (0 or 10 μg/ml), average IKK activity and cleaved caspase8 level are measured at thirteen time points, which start from 0 and end after 1440 minutes. (b) IKK activity versus time under three different conditions: no treatment (TNF = 0 ng/ml), treatment with TNF (TNF = 100 ng/ml, IL-1ra = 0 μg/ml), treatment with both TNF and IL-1ra (TNF = 100 ng/ml, IL-1ra = 10 μg/ml). From a communication system perspective, the “apoptosis” message is going to be transferred via IKK in the channel from the transmitter TNF to the receiver. Activation of TNF by increasing its concentration to 100 ng/ml can be viewed as TNF transmitting a signal. This signal is then propagated towards its downstream molecule IKK (Figure 1a). Activation of IKK eventually appears in long term, which means IKK has correctly received the signal from TNF. Adding IL-1ra, 10 μg/ml, acts as abnormality added to the communication channel, where IKK is located, and distorts the signal sent by TNF. This can be understood by looking at the decreased level of IKK activity in long term, which reflects the fact that IKK has not received the signal from TNF correctly. Hence, the “apoptosis” message has not been communicated successfully, and therefore the level of survival has increased [20]. (c) Cleaved caspase8 level versus time under three different conditions: no treatment (TNF = 0 ng/ml), treatment with TNF (TNF = 100 ng/ml, IL-1ra = 0 μg/ml), treatment with both TNF and IL-1ra (TNF = 100 ng/ml, IL-1ra = 10 μg/ml). See “Experimental data to demonstrate signal transmission error” in the Results section for further biological and communication engineering explanations.