1. Healing by primary intention involves a lot of growth factors that orchestrate orderly cellularproliferation and matrix synthesis. Growth factors (such as VEGF and KGF) will bind towhich of the above receptors (encircle to receptor in the diagram)? Discuss how theseextracellular molecules induce their intracellular effects?2. A substance binds to the seven-pass G-protein which resulted in tachycardia, perspiration,decreased bowel peristalsis, and mydriasis. What is this hormone? What inactive protein isexchanged for the active form in this pathway?

Growth factors like VEGF (Vascular Endothelial Growth Factor) and KGF (Keratinocyte Growth Factor) bind to receptor tyrosine kinases. These receptors are located on the cell surface and have an extracellular binding domain and an intracellular domain with tyrosine kinase activity. When a growth factor binds to the receptor, it causes dimerization of the receptor, which then autophosphorylates its tyrosine residues. This phosphorylation serves as a docking site for proteins with SH2 domains, leading to the activation of several intracellular signaling pathways, such as the MAPK/ERK pathway, PI3K/Akt pathway, and JAK/STAT pathway. These pathways ultimately lead to cellular proliferation and matrix synthesis.

The hormone that binds to the seven-pass G-protein and results in tachycardia, perspiration, decreased bowel peristalsis, and mydriasis is likely adrenaline (also known as epinephrine). This hormone binds to the beta-adrenergic receptor, a seven-pass G-protein coupled receptor, and activates the G protein by causing it to exchange GDP for GTP. The G protein then activates adenylate cyclase, which converts ATP to cAMP, leading to the activation of protein kinase A (PKA). PKA then phosphorylates various target proteins, leading to the physiological effects observed.