1. FIGURE 15.1. Calcium ions entering the cytosol from the extracellular medium activate regulated exocytosis in the proximal axon terminal of a pain receptor nerve cell.

2. UNFIGURE 15.1.

3. FIGURE 15.2. ADP from damaged cells activates G q and hence phospholipase C  in platelets.

4. FIGURE 15.3. The inositol trisphosphategated calcium channel is a calcium- selective channel in the membrane of the endoplasmic reticulum. An increase of cytosolic calcium concentration in platelets makes them sticky, initiating blood clotting.

5. FIGURE 15.4. Scanning electron micrograph of a blood platelet on the damaged inner surface of a blood vessel. The platelet has activated, extending short processes called pseudopodia, and is ready to initiate blood clotting. Image by Mark Turmaine, Department of Cell and Developmental Biology, University College London. Reproduced by permission.

6. UNFIGURE 15.2.

7. FIGURE 15.5. Calcium and cyclic AMP activate distinct but overlapping sets of target processes in skeletal muscle cells.

8. FIGURE 15.6. Nerve cell mitochondria take up calcium from the cytosol. Experiment of William Coatesworth and Stephen Bolsover. First published in Cell Calcium 39, 217 (2006).

9. FIGURE 15.7. Cyclic adenosine monophosphate, also called cyclic AMP or just cAMP.

10. FIGURE 15.8. Scent-sensitive nerve cells send axons to the brain.

11. FIGURE 15.9. Scent chemicals activate G s and hence adenylate cyclase in scent- sensitive nerve cells. cAMP then opens a nonselective cation channel in the plasma membrane.

12. FIGURE 15.10. The PDGF receptor, like other growth factor receptors, activates the GTPase Ras and therefore the MAP kinase cascade.

13. FIGURE 15.11. Amino acid residues adjacent to phosphotyrosine recruit specific subtypes of SH2 domain.

14. FIGURE 15.12. The PDGF receptor, like other growth factor receptors, phosphorylates and hence activates phospholipase C .

15. FIGURE 15.13. The insulin receptor phosphorylates and hence activates PI 3-kinase.

16. FIGURE 15.14. PIP3 recruits protein kinase B (PKB) to the plasma membrane, where it is activated. Active PKB has many effects including exocytosis of vesicles containing glucose carriers. The action of PKB on the protein BAX will be described in Chapter 18.

17. FIGURE 15.15. Signaling from type 1 cytokine receptors.

18. FIGURE 15.16. Interactions of signaling pathways.