Question

Please answer all parts.

A.) GTP-bound G-protein will interact with an effector molecule. Name two effector molecules. What change occurs in the GTP once effector interaction occurs?

B.) Phosphorylation of GPCR (by GRK) results in binding sites for what molecule? What happens to the receptor at this point?

C.) Trimeric protein reforms in this part (what is the state of the guanine nucleotide (GTP or GDP)? How would a non-hydrolyzable GTP influence this signalling? What about if only GDP was present?

D.) Where is adenylyl cyclase located? From what is cAMP derived?

E.) What does cAMP target and what does that thing target?

F.) Phospholipase cleaves PIP2 to create two new second messengers. Why does DAG stay in the membrane while IP3 doesn’t?

G.) How does DAG vs. IP3 result in different signaling options?  How do they both feed into Protein Kinase C activation?

H.) How does Ca²⁺function in the cell in response to ER release? What are two examples of targets that Ca²⁺ can bind?

I.) Draw out PLC signaling cascade. Remember this is the effector target of GPCR-G protein activation. So you could include that part too.

J.) Draw out this pathway Adenylyl cyclase -> cAMP -> PKA -> CREB

Answer 1

A) The two effector molecules include the muscles and glands. Once the effector initiation occurs, the active GTP gets converted to the inactive GDP.

B) Phosphorylation of GPCR (by GRK) results in binding sites for the members of the arrestin family. Examples include the rod and cone receptors. The phosphorylation causes the termination of phototransduction.

C) When the trimeric protein reforms, the guanine is in the GTP form. A non-hydrolyzable GTP will affect the reformation of the trimeric protein by decreasing the dissociation of the subunits and increasing the affinity for the effector cells.

D) Adenylyl cyclase is located within the plasma membrane of the cells. The cAmp is derived from the ATP. Adenylyl cyclase synthesises the cyclic cAmp.