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31 Cards in this Set

  • Front
  • Back
what are the 6 steps for signalling transduction?
1. synthesis of signaling molecule by signaling cell.
2. release of the signal molecule
3. transport of the signal to the target cell
4. detection of the signla by the target cell
5. transmit signla w/i the cell, read signal, alter behavior
6. remove signal (usually terminates cellular response)
why do hormone receptors need to have a high affinity?
hormones reach their targets in very low concentrations
how many transmembrane helices do GCPR's have?
which subunit of the G protein is the GTPase?
the alpha subunit
When is a G protein activated, and what happens when it is activated?
it is activated when alpha binds GTP, then the beta-gamma subunit dissociates from alpha, and alpha+GTP modifies its target enzyme.
what are three ways that GCPR's are inactivated?
The C-term tail of the receptor becomes pi-ed and then arrestins block G protein interactions; hydrolysi of GTP in G alpha leads to its inactivation; once the receptor has been stimulated a few times it is internalized
how does cAMP activate PKA?
it binds PKA's two regulatory subunits which then disociate from catalytic subunits
what is an example of a txn factor that PKA activates?
It Pi's CREB which then bindsCBP to become a functional txn activator.
What is the main way cAMP is degraded? What are ways this can be inhibited?
via PDE's. caffeine inhibits PDE's and viagra inhibits PDE's of cGMP
what are the main effects of adrenergic stimulation?
increase heart rate, constriction of vessels of nonessential organs, liberation of glucose and fatty acids, relaxation of smooth muscle in the gut
in what two ways does PKA/cAMP stimulate glycogen breakdown?
it phosphorylates glycogen phosphorylase to activate it and pi's glycogen synthase to inactivate it.
Beta blockers help ailments associated with what?
stress, high BP, irregular heart rhythms, migranes, prophylaxis of 2nd MI
what are the effects of PTH
increases serum [Ca2+]
what pathways does PTH activate?
PKA and PKC pathways
how does the cholera toxin cause disease?
It locks the G alpha of the cAMP pathway to GTP, thus it is always active.
what kind of G protein activates PLC?
Which molecule cleaved by PLC is soluble and which one remains in the membrane?
IP3 is soluble while DAG remains in the membrane.
what are the receptors that usually stimulate PLC and what kind of responses do they have?
alpha1 adrenergic receptors which are important for contraction of smooth muscle and sphincters in gut, glandular secretions, pilomotor muscles, bladder and sex organs
Ca2+ released into the cytosol via IP3 does not last long. Why is this? (3 reasons)
IP3 is rapidly de-pi-ed and inactivated. Ca2+ that enters the cytosol is rapidly pumped out of cell. Some IP3 is pi-ed to IP4 which may promote refilling of intracellular calcium stores
What are DAG's two potential signalling roles?
It can be cleaved to release arachidonic acid or it can ctivate PKC (its main function)
How is PKC activated?
It binds Ca2+ from IP3, incorporates into the membrane, and is activated by DAG
How is PKC involved in diabetic retinopathy?
hyperglycemia causes overproduction of DAG in vascular cells thus PKC is activated more often. PKC pi's proteins involved in neovasculation, endothelial remodelling, etc.
How many calcium ions bind calmodulin?
4, bc calmodulin has 4 EF hand domains.
what are the two main targets allosterically activated by calcium-calmodulin?
calmodulin dependant protein kinases (CaM kinases) and the calcium ATPase pump
What are two ways the cAMP and Ca2+ pathways interact?
the txn factor CREB becomes a "super txn" factor if pi-ed by both PKC and PKA. Ca/calmodulin regulates some forms of cAMP, PDE, and AC.
calcineurin is a Ca regulated phosphatase that targets what?
NFAT, a txn factor used in T cell activation
what are three molecules that use Pi-ed RTK's as scaffolds?
PLC-gamma, SRC tyrosine kinases, Grb-2 (an adaptor protein for RAS)
What is the main cascade used to activate MAP kinase?
->MAP kinase
in order to be activated and move into the nucleus, MAP kinase must be...
how are RTK's downregulated?
protein phosphatases and endocytosis
how do farnesyl transferase inhibitors work?
they inhibit farnesylation which is necessary putting RAS in the plasma membrane. It has low toxicity but the problem is people eventually become resistant