Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

une ch 11

cell signaling by chemical messengers

QuestionAnswer
Be able to draw a cartoon of the insulin receptor that shows the cell membrane, two alpha-beta subunits, the membrane spanning region of the dimers, the insulin-binding site, the sites of tyrosine kinase domains, and the sites of auto-phosphorylation. Ignore grb2, PLC, PI3-kinase, and GAP1. p181
What is the effect of activating the Gas G protein? Stimulates adenylyl cyclase to produce cAMP, a 2nd messenger
What is the effect of activating the Gai G protein? Inhibits adenylyl cyclase.
What is the effect of activating the Gaq G protein? Activates phospholipase C (PLC).
Beginning with the response to a stimulus, list the common characteristics of all chemical messenger systems as they apply to the chemical messenger acetylcholine at the neuromuscular junction. action potential-> Ca channels open and Ca leaves and triggers fusion of the vesicle with the presynaptic membrane-> Ach released into synaptic cleft->Ach binds to receptors-> conformational change that lets Na leave and K go in-> muscle action potential
Describe the path taken by cortisol from the time it is released from the adrenal cortex until the time it affects gene transcription. cortisol leaves adrenal cortex-> travels on albumin/SHBG-> binds to receptor/conformational change-> receptor dimerizes->exposes nuclear translocation signal/allows hormone receptor complex to cross nuclear membrane->binds to GRE-> changes gene transcrip
In the Ras and MAP kinase pathway, how does the occupied receptor activate Grb2? autophosphorylation
Describe the path taken by cortisol from the time it is released from the adrenal cortex until the time it affects gene transcription. cortisol leaves adrenal cortex-> travels on albumin/SHBG-> binds to receptor/conformational change-> receptor dimerizes->exposes nuclear translocation signal/allows hormone receptor complex to cross nuclear membrane->binds to GRE-> changes gene transcrip
In the Ras and MAP kinase pathway, how does the occupied receptor activate Grb2? autophosphorylation-> phosphorylates tyrosyl residue that Grb2's SH2 domain can bind to
What is the last step in the pathway that is catalyzed by MAP-kinase and what is the effect? last step of MAP pathway is the induction or repression of gene transcription
What are the substrates and products of the reaction catalyzed by phospholipase C? PI 4,5 + water -> DAG + IP3
What are the substrates and products of the reaction catalyzed by phosphatidylinositol 3’ kinase? PI 4,5 + ATP-> PI 3,4,5 + ADP PI's third carbon gets phosphoylated and creates a docking site for pleckin homology domains
What is the function of a pleckstrin homology domain? to restrict diffusion of certain proteins in to the cell
In the insulin signal transduction pathway that leads to the activation of MAP kinase, what is the signal transducer protein that binds to the IRS? Grb2 is the protein that binds to phosphorylated IRS and activates MAP pathway. it can bind bc it has a SH2 domain
In the insulin signal transduction pathway that leads to an increase in the diacylglycerol and inositoltrisphosphate second messengers, what is the first signal transducer protein that binds to the IRS? Why does it bind to the IRS? PLC binds to IRS to activate pathway that creates DAG and IP3. PLC is capable of binding to IRS because it has a SH2 domain
Explain the sequence of reactions that occur following the binding of glucagon or epinephrine to a heptahelical receptor. epi 2 receptor-> GDP lets GTP take over-> GTP makes alpha and beta units of G protein all come apart/lipid anchored to membrane-> alpha subunit finds adenyl cyclase and turns ATP to cAMP->Gas inactivates itself by hydrolyzing own GTP to GDP and Pi
When epinephrine binds to α1-adrenergic receptor: activates Gaq-> PLC activated-> hydrolyzes PI-Biphosphate into DAG and IP3 (second messengers)
When epinephrine binds to b-adrenergic receptor: activates Gas-> activates adenyl cyclase-> to turn ATP to cAMP and PPi (second messenger)
When phosphatidyl inositol bisphosphate is hydrolyzed by phospholipase C (PLC), what is the next step in the signal transduction pathway for diacylglycerol (DAG)? DAG is created when PLC hydrolyzes PI Biphosphate. DAG then activates protein kinase C which then activates target proteins
When phosphatidyl inositol bisphosphate is hydrolyzed by phospholipase C (PLC), what are the next several steps in the signal transduction pathway for inositol trisphosphate (IP3)? IP3 is made when PLC hydrolyzes PI Biphosphate. IP3 then lets Ca leave ER and then activates enzymes in ca/calmodulin subunit-> binds to calmodulin proteins->changes protein conformation
Glucagon is released when blood sugar is low. How is its signal terminated (or lowered) following a high carbohydrate meal that increases the blood sugar? high blood sugar increases insulin. increased insulin inhibits glycogen release (any residual glycogen gets destroyed in liver), and increased insulin also activates phosphodiesterase which hydrolyzes cAMP
Concerning Dennis Veere who has cholera, how does the cholera toxin A change the metabolism of the intestinal cell? cholera toxin A enters GI tract-> it permanently ADP ribosylates a Gas protein (takes ADP ribose from NAD to put to Gas protein)-> Gas protein inc adenyl cyclase-> inc cAMP-> CFTR channel activated-> Cl and Na into intestine w water-> watery diarrhea
Created by: carolanimal