Key characteristics of cellular signaling networks are explained at the beginning of the course (1.-15.) and illustrated on the examples covered in subsequent lectures (A.-I.).

1. Receptors couple ligand-binding and effector specificity
2. Signal is amplified on its way from receptor to effector
3. Signal transduction pathways converge, diverge, form nodules and interact with each other - crosstalk
4. Signal is transduced with the help of reversible posttranslational modifications and recognition codes
5. Change in proximity of signaling molecules is itself an important signal
6. Regulated folding and specific proteolysis can be used to transduce signals
7. Signal transduction is compartmentalized using membranes and protein skeletons
8. Information is transduced through both the amplitude and the frequency of messenger concentration changes
9. Signal components are highly mobile molecules
10. Complexity of signaling networks is achieved through combination of limited sets of elements
11. Cell responses to signals have cooperative character
12. Response to signal is always cell- and signal-context dependent
13. Quantity changes in signaling networks can lead to quality changes in cell responses
14. Signaling network robustness helps to distinguish signal from noise
15. Effector systems of the cell form one integrated network.

Outlines of signaling networks are explained; structure-function relationships of signaling proteins are presented.
A. cAMP – protein kinase A – CREB
A1. Protein kinase A structure-function
A2. PKA – CREB signaling
A3. Modularity in signaling
B. MAP kinase cascades – from mitogenic signals and stressors to Jun/Fos activation
C. Insulin receptor - PI3Kinases - PKB - FoxO transcription factor
D. GSK3 in PKB and Wnt signaling
E. Nuclear hormone receptors
E1. Receptor structure-function
E2. Coregulators, SREMs, chromatin environment
F. Tumor suppressor p53 – from genotoxic stress to the p53 oscillator and the activation of p21 gene
G. TGFβ signaling and CDK inhibitors – sensing gradients
H. NFκB/Rel pathways – two modalities of ubiquitin signaling
I. Myc/Max – pRb – E2F transcription factors – Myc as a regulator of transcription pausing.