BIOL 3510 1st Edition Lecture 19 Outline of Last Lecture I. Cell SignalingII. Four Basic Types of Cell SignalingIII. Timing of a Cell’s ResponseIV. Steroid and thyroid hormones Outline of Current Lecture I. Three Types of Extracellular ReceptorsII. GPCRs Activating G-proteins upon Signal BindingIII. Bacteria Exploiting G-protein ActivityIV. Actions Triggering Increases in Intracellular Ca2+ ConcentrationsCurrent LectureThree types of extracellular receptors:1. Ion-channel-coupled-receptors: signal binding opens the channel allowing ions to cross the plasma membrane2. G-protein-coupled receptors: signal binding to a G-protein-coupled receptor activates a G-protein. G-proteins activate downstream channels or enzymes3. Enzyme-coupled receptor: after signal binding, these receptors act as enzyme or activate other enzymesG-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 subunitsBacteria exploit G-protein activity- Vibria cholera produces cholera toxinThese 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 celso Constitutively active Gs results in diarrhea and dehydration- Bordetella pertussis produces pertussis toxino Prevents Gs protein from exchanging GDP for GTP in the lungso Constitutively inactive Gs stimulates coughingSome G-proteins regulate ion channels- Example: heart muscle cells- Acetylcholine inhibits muscle contraction via a GPCR signaling cascadeG-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 AMPDifferent cells have different responses to increased levels of cyclic AMPResponse to a signal and the increase in cAMP can be rapid, like skeletal muscleResponse 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 inositol1,4,5 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 targetsMany actions trigger an increase in intracellular Ca2+ concentrations- Sprem fertilizing an egg cell = development- Nerves signaling muscle cells = contraction- Secretory cells (including neurons) = secretionCa2+ binds and affects the action of Ca2+ responsive proteins like calmodulinCalmodulin activates Ca2+/Calmodulin dependent protein kinases (CaM-kinases)CaM-kinase is involved in memory formationGPRC signaling allows for signal amplificationEx: rod photoreceptor cells- Signal: light- GPRF = rhodopsin- Signaling cascade results in the closure of cation channels and a voltage
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