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17 Cards in this Set
- Front
- Back
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Describe the steps necessary for activation and inaction of second messengers.
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Active Messenger:
ATP --> 3'5' cAMP via Adenylyl Cyclase Inactive Messenger: 3'5' cAMP --> AMP via cAMP PDE |
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Describe the basic steps that occur when a hormone binds a receptor.
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Hormone binds recepros (high affinity for each other) and GTP
GTP hydrolyzed to GDP H and R separate Results in cAMP formation |
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What are the characteristics that define a G-Protein?
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-Binds to adenylyl cyclase and regulate its activity
-Bind to hormone receptors and regulate their affinity for ligand -GTP binds the protein and alters their confrmn -Terminate their siginal by hydrolyzing GTP-->GDP (Nucleotide exchange) |
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How do a beta-agonist and alpha-agonist differ?
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Both will bind a G-protein linked receptor, however, beta-agonist will bind a stimulatory receptor which will in turn activate adenylyl cyclase
alpha2-agonist will bind inhibitory receptors and inhibit adenylyl cyclase |
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Using the heterotrimeric model, explain the steps that occur when a ligand binds a G-protein coupled receptor.
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Ligand binds receptor, receptor associates with G protein, alpha subunit dissociates and its GDP undergoes nucelotide exchange for GTP
alpha subunit acts on effectors GTP hydrolyzed to GDP alpha-GDP rejoina beta and gamma |
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What is the role of the gamma subunit of G-proteins?
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Tethers G-protein to cell membrane
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What causes cholera? Clinical manifestations?
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Bacterial toxin (an enzyme) causes cells in large intestine to produce large amount of cAMP and pump Na+ into large intestine
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What causes pertussis? Clinical manifestations?
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Pertussis caused by actions of a bacterial toxin (an enzyme).
Causes lymphocytosis and impaired ciliary function of respiratory epithelium |
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What reactions do the toxins of cholera and pertussis catalyze?
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NAD + Gs/i alpha --> ADP-ribose-Gs/i alpha + nicotinamide + H+
Gs for cholera Gi for pertussis |
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How do the cholera and pertussis toxins mediate their effects?
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Cholera: toxin prevents alpha-GTP-->alpha-GDP; thus, inhibiting shut-off mechanism for a stimulatory G-protein
Pertussis: Prevents Receptor-Ligand complex from binding with G-protein complex; thus blocking an inhibitory G-protein. |
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Provide an example of a downstream effect of cAMP.
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cAMP activates Protein Kinase A (which is cAMP dependent) which then goes on to phosphorylate enzymes, receptors, channels, etc
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What is Gt involved in? Golf?
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Gt = Transducin -- light receptors (rods)
Golf = olfaction |
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Under what protein can Ras be classified? What is its role?
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Ras has characteristics of G-protein even though it's strucually different
Ras is involved in growth signaling |
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If a patient presented with abnormally high PTH but normal serum Ca2+, what could be the problem?
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PTH resistance (insensitivity)
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What is pseudohypoparathyroidism? Clinical manifestations?
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AKA ALbright's Hereditary Osteodystrophy
Hormone-resistance disorder Manifests as skeletal abnormality, s hort stature, mental retardation |
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How does sex affect pseudopseudohypoparathyroidism?
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Effects G-s-alpha (RBC membranes only have 50% normal G-s-alpha activity)
Gene encoding G-s-alpha is imprinted (methylated). result is: Maternally inherited mutations cause osteodystrophy plus hormone resistance While paternally inherited mutations cause osteodystrophy alone (normal PTH levels maintain normal blood Ca2+) |
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How does McCune-Albright syndrome arise?
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activating G-s-a mutations
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