NURS215 Lecture Notes - Lecture 3: Tyrosine Kinase, Ondansetron, Ion Channel

• School: University of Alberta
• Department: Nursing
• Course: NURS215
• Professor: Helena Schaefer

Document Summary

Note: more specific = narrower effect = fewer side effects: bi(cid:374)ds e(cid:374)doge(cid:374)ous su(cid:271)sta(cid:374)(cid:272)es (cid:894)hor(cid:373)o(cid:374)es, (cid:374)eurotra(cid:374)s(cid:373)itters, . (cid:895) Drugs need to match the existing target receptor binding site: receptor binding triggers a change within the cell or blocks the receptor, 6 major receptor types, g-protein (gpcr, ion channels, nuclear receptors. G-protein: g-protein (eg. :epinephrine)stimulates g-protein & second messenger systems = sympathomimetic stimulation. Inhibits depolarization = no pain transduction: most bind to voltage-gated channels, 3. Most bind in cytoplasm = change cell fx via dna: 4&5. Insulin cell membrane receptors = stimulate tyrosine kinase = activate cellular glucose uptake: transmembrane enzymes - enzymatic response within the cell, activated by ligand binding eg. insulin, non-enzyme signaling, http://www. dnatube. com/video/4103/cytokine-binding-or-jakstat-signaling-pathway, 6. Non-enzyme transmembrane eg. (cid:858)jak-stat(cid:859) signaling: eg. interferons, drug respo(cid:374)se depe(cid:374)ds o(cid:374) , receptor affinity, potency = strength, drug-receptor interactions, agonists, agonists, eg. Why does it work? (cid:858)stre(cid:374)gth(cid:859) of binding. Degree to which a drug induces maximum therapeutic effect.