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18 Cards in this Set
- Front
- Back
In g-protein coupled receptors, what are the four main components?
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1. A receptor (inactive until binding)
2. A G-protein 3. An effector 4. A secondary messenger |
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How many subunits does a G-protein have and what are they?
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G-proteins are tri-meric - have an alpha, beta and gamma subunits.
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In g-protein coupled receptors, how is a signal detected and how does it activate the g-protein? What happens to the g-protein?
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Binding of a hormone causes a conformational change in the receptor, which then binds to the ALPHA subunit of G-protein. Alpha subunit changes conformation, looses GDP and gains a GTP
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After binding the the active receptor and exchanging GDP for GTP, what happens to the G-protein?
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GTP causes alpha subunit to disassociate from beta/gamma, then interacts with the EFFECTOR, activating it. Hydrolysis causes GTP-GDP change, alpha subunit then disassociates from effector, binds back with beta/gamma
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What is the most common type of effector, and what does an activated effector do most commonly? How are its effects carried through the cell?
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Most common = adenylyl cyclase. This catalyzes the creation of CYCLIC AMP (cAMP). cAMP = secondary messenger.
cAMP's effects are mediated through pKA (protein kinase A). |
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How do inhibitory signals work? What are some examples of inhibitory hormones?
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there can be inhibitory signals picked up and transmitted with inhibitory receptors/g proteins. Adenosine is one example.
Alpha-i subunit inhibits, same way as a normal alpha activates. Lowers production of cAMP. |
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Name 4 secondary messengers and the mediator that transmits their signal through the cell
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cAMP = pKA
cGMP = pKG DAG = pKC IP3 = opens Ca++ channels in ER |
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pKA - what subunits does it have, and what happens to them?
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pKA has 2 subunits - a regulatory and catalytic. cAMP binds regulatory, displacing it, allowing catalytic to go to work.
Catalytic subunit goes through NUCLEAR MEMBRANE. |
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Once the catalytic subunit translocates into the nucleus, what does it bind? How are genes turned on, and what are the DNA regions called that respond?
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Catalytic subunit binds CREB (cAMP response element biding protein), that binds to a CRE area of DNA (cAMP response element) - a CBP coactivator binds, helping to induce basal transcription.
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What kind of receptor detects epinephrine, and what secondary messenger is used?
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Epi is picked up by the Beta-Andrenergic receptor and uses cAMP as a secondary messenger. pKA phosphorylates, ups heart rate, glycogen metabolism, constricts vessels
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Acetycholine receptor - How is it different? How is cAMP involved? What's the secondary messenger?
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Acetycholine uses the muscarinic receptor. Binding of hormone causes alpha I subunit to GDP-GTP, disassociate. NOTE - beta/gamma subunit is business end - interacts with K+ channel, opens, REDUCES heart rate. GTP-GDP re-associates, turns off.
cAMP has NO ROLE. K++ channel is the secondary messenger. |
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Aside from the heart, what other organ should we think of with muscarinic acetycholine recptors?
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Overactive bladders - binding of acetycholine causes bladder contraction
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Heart failure and g-protein coupled receptors - what's the receptor used and what's the mechanism?
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B-andrenergic receptors, responsive to chatecholamines (adrenaline) - use cAMP, results in release of sarcoplasmic reticulum Ca+. Need to have difference in [Ca+] in cytosol vs. SR for normal heart function. Too much activation = weak heart.
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What drug can we use to fight heart failure?
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Beta blockers - stop the Beta-andronergic receptor, decrease cAMP production, keep Ca+ in the SR and lower [Ca+] in the cytosol = better heart function.
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If you use phospholipase C as an effector, what's the effect on the cell?
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Think Ca+ release from ER. Phospholipase C releases IP3 which opens CA+ channels. Phospholipase C also activates DAG, a protein the PM. Ca+ tells pKC to associate with DAG in the membrane and get activated.
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When i hear calcium/calmodulin regulation, what should i think of?
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think relaxation of smooth muscle and dilation of blood vessels.
Acetycholine can bind + activate Phospholipase C, which activates IP3 to release Ca+ from ER. Ca+ binds with CALMODULIN to activate nitric oxide, which diffuses. NO receptor on smooth muscles activated, turns on cGMP to pKG relaxes muscles = DILATION OF BLOOD VESSLES. |
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How is cholera related to G-proteins?
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Cholera toxin activates G-alpha unit, keeping it stimulated = up cAMP = up Cl- channel
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How is whooping cough related to g-proteins?
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Bortella pertussis - modifies G-alpha-I (inhibitory) - can't displace GDP for GTP, so inhibition never activated = hyperactivation, up cAMP, up fluid loss into lungs.
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