Complement, for example, can be activated and fixed on the surface of microbes via properdin, or released from leukocytes [ 1] or the mannan associated serine protease pathway (in which mannose binding protein interacts with a serine protease that triggers the complement cascade) [ 2, 3, 4, 5].
Macrophages may for example be classically activated to trigger inflammation (M1), or alternatively activated which supports healing and vascularisation (M2).
In nutrient-deprived states, for example, autophagy can be activated to degrade cargoes for cell-autonomous energy production to promote cell survival.
For example, autophagy can be activated in an ATG5/ATG7 independent manner involving ULK1 and Rab9 [ 3].
For example, p53 can be activated by DNA damage to activate cell-cycle checkpoints or apoptosis, such that cells lacking p53 are prone to certain forms of mutation and genomic instability.
For example, the P53 pathway can control the Cell Cycle pathway by regulating the expression of p21 and can itself be activated by several pathways, for example the MAPK pathway.
6 For example, glycosyl hemiacetals can be activated directly using this combination of reagents; 6, 7 glycals can be oxidised to glycosyl epoxides for reaction with alcohols; 8 and this method is also often used to activate thioglycosides.
Previously, the main concern has been the risk of false negative results as a consequence of using only caspase fragmentation as marker of activity, based on the observation that, for example,, caspase-9 can be activated without proteolytic processing.
For example, L-Myb12 can be activated by any one of E-Jun-Fos, I-Rpol-Hnr, E-stat5b and L-Mcmd, so in Figure 10, g t (1), g t (9), g t (11) and g t (12) are used as the four inputs to an OR gate.
An example for this case is a reaction transforming educt A into product B that can alternatively be activated by two activators E1 and E2.
