Physiology 3140A Lecture Notes - Lecture 3: Metabotropic Glutamate Receptor, Retinitis Pigmentosa, Protein Kinase A
24 Nov 2016
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Nsaids: inhibit prostaglandin synthesis (pge2: blocks activity of. **do not memorize. know examples of disease caused by gpcr. > 1 g proteins: activation of different g proteins activates different specific pathways. Transmembrane spanning domain: 7 tmds ligand binding. Amino terminal domain: ligand binding, post-translational modification. Intracellular loop domain: 3 intracellular & extracellular loop, g protein coupling, regulatory protein interactions, interaction with g protein independent signaling proteins. Carboxyl-terminal domain: g protein coupling, regulatory protein interactions, interaction with g protein independent signaling proteins. Can have gpcrs bind/activate proteins independent of g proteins (g protein dependent and independent signaling) Hormone receptor (gnrh-r: long or short carboxyl/amino-terminal tails, long vs short extracellular domains, large vs small intracellular loops. Differences dictate the type of ligands, g proteins, and regulatory proteins that will associate with the receptor and define the molecular diversity of signaling. Having different structural regulation can further fine tune the type of gpcr signaling occurring. Diversity of physiological responses stimulated by gpcrs:
