BIOL 3510 1st Edition Lecture 19 Outline of Last Lecture I Cell Signaling II Four Basic Types of Cell Signaling III Timing of a Cell s Response IV Steroid and thyroid hormones Outline of Current Lecture I Three Types of Extracellular Receptors II GPCRs Activating G proteins upon Signal Binding III Bacteria Exploiting G protein Activity IV Actions Triggering Increases in Intracellular Ca2 Concentrations Current Lecture Three types of extracellular receptors 1 Ion channel coupled receptors signal binding opens the channel allowing ions to cross the plasma membrane 2 G protein coupled receptors signal binding to a G protein coupled receptor activates a Gprotein G proteins activate downstream channels or enzymes 3 Enzyme coupled receptor after signal binding these receptors act as enzyme or activate other enzymes G protein coupled receptors GPCRs have 7 transmembrane domains GPCRs activate G proteins upon signal binding G proteins 3 protein subunitis alpha binds GTP beta and gamma GPCR acts as a GPF guanine exchange factor for the G protein activating the alpha and betagamma subunits Alpha and beta gamma subunits have different downstream targets Hydrolysis of gTP to GDP inactivates the alpha subunit Re association with the alpha subunit GDP inactivates the beta gamma subunits Bacteria exploit G protein activity Vibria cholera produces cholera toxin These notes represent a detailed interpretation of the professor s lecture GradeBuddy is best used as a supplement to your own notes not as a substitute o Prevents Gs protein from hydrolyzing GTP in instestinal cels o Constitutively active Gs results in diarrhea and dehydration Bordetella pertussis produces pertussis toxin o Prevents Gs protein from exchanging GDP for GTP in the lungs o Constitutively inactive Gs stimulates coughing Some G proteins regulate ion channels Example heart muscle cells Acetylcholine inhibits muscle contraction via a GPCR signaling cascade G proteins can activate membrane bound enzymes creating small or second messengers The alpha subunit of Gs activates adenylyl cyclase generating cAMP from ATP cAMP activates cyclic AMP dependent protein kinase PKA PKA phosphorylates other proteins changing their activity Cyclic AMP phosphodiesterase continually converts cAMP to AMP Different cells have different responses to increased levels of cyclic AMP Response to a signal and the increase in cAMP can be rapid like skeletal muscle Response to a signal and the increase in cAMP can be slow like neuronal learning and memory Gs activates phospholipase C which cleaves inositol phospholipid to form the second messengers inositol 1 4 5 triphophate IPs and diacylglyercol DAG IPs moves to the ER where it binds to and opens Ca2 channels Ca2 and DAG activate protein kinase C PKC which phophorylates other downstream targets Many actions trigger an increase in intracellular Ca2 concentrations Sprem fertilizing an egg cell development Nerves signaling muscle cells contraction Secretory cells including neurons secretion Ca2 binds and affects the action of Ca2 responsive proteins like calmodulin Calmodulin activates Ca2 Calmodulin dependent protein kinases CaM kinases CaM kinase is involved in memory formation GPRC signaling allows for signal amplification Ex rod photoreceptor cells Signal light GPRF rhodopsin Signaling cascade results in the closure of cation channels and a voltage change
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