3.3 study guide Flashcards
Classical GPCR signaling involves three main components, a receptor, a G protein and an effector
enzyme. Which of these would be considered a receptor?
a. Rhodopsin
b. Ras
c. Adenylyl cyclase
d. Protein Kinase A
e. cGMP
Rhodopsin
For heterotrimeric G proteins, which subunit translocates to activate the downstream effector enzyme?
a. Alpha subunit
b. Beta subunit
c. Gamma subunit
d. All of these subunits
e. None of these subunits
Alpha subunit
How does cAMP affect the activity of Protein Kinase A (PKA or cAMP-dependent protein kinase)?
a. It causes the regulatory subunits to block the kinase active site
b. It causes PKA to be degraded
c. It causes the kinase catalytic subunits to be activated
d. It causes PKA to phosphorylate the beta-adrenergic receptor
e. cAMP does not affect PKA activity
It causes the kinase catalytic subunits to be activated
Which protein interacts with beta-adrenergic receptor that has been phosphorylated to promote signal
desensitization through endocytosis?
a. Beta arrestin
b. Adenylyl cyclase
c. Protein Kinase A
d. G Protein subunit alpha
e. Epinephrine
Beta arrestin
How does epinephrine regulate blood D-glucose levels?
a. By promoting movement of GLUT4 transporter to the plasma membrane
b. By activating glycogen synthase
c. By promoting release of D-glucose from glycogen
d. All of the above
e. None of the above
By promoting release of D-glucose from glycogen
Light, odorants and flavor molecules are all detected by GPCRs that activate effector enzyme activity
and results in second messenger production. What else do these pathways all have in common?
a. Production of NO
b. Modulation of ion channels
c. Activation of MAP kinase cascades
d. Receptor activity dependent on a chromophore
e. All of the above
Modulation of ion channels
How is the 11-cis-retinal chromophore attached to the opsin protein to make rhodopsin?
a. Hydrogen bonding to an Asp residue
b. Covalent linkage to a Ser alkoxide ion
c. Schiff base formation with a Lys residue
d. Covalent linkage to a His residue
e. Electrostatic interactions
Schiff base formation with a Lys residue
Which class of receptor binds DNA?
a. Steroid receptors
b. Tyrosine kinase receptors
c. G-protein coupled receptors
d. Guanylyl cyclase receptors
e. None of these
Steroid receptors
If there were a loss of function mutation in the protein Grb2, which of these steps of insulin signaling
would fail to occur?
1. Assembly and activation of a Ras signaling complex
2. Phosphorylation of Elk1 to initiate gene transcription
3. INSR activation
4. Initiation of the Raf-1-MEK-ERK signaling cascade
5. IRS-1 phosphorylation
a. 1, 2, 3, 4, 5
b. 2, 4
c. 1, 2, 4
d. 1, 2, 4, 5
e. 1, 2, 5
1, 2, 4
Assembly and activation of a Ras signaling complex
Phosphorylation of Elk1 to initiate gene transcription
Initiation of the Raf-1-MEK-ERK signaling cascade
You are working with a new hormone and are trying to understand the signaling pathway. When you
treat cells with your hormone, you observe that nitric oxide levels increase in the cytosol. Which of these
enzymes is your signal activating?
a. Adenylyl cyclase
b. phospholipase C
c. tyrosine kinase
d. protein kinase A
e. NO synthase
NO synthase
What is the molecule from which nitric oxide is produced?
a. Arginine
b. Asparagine
c. Nitrate
d. Citrulline
e. None of the above
Arginine
You also observe cGMP to increase in the cytoplasm after treatment with your hormone. Which type
of receptor might you hypothesize is detecting your hormone based on its enzymatic ability to make this
molecule?
a. Tyrosine kinase receptor
b. Guanylyl cyclase receptor
c. G-protein coupled receptor
d. Nuclear hormone receptor
e. Beta-adrenergic receptor
Guanylyl cyclase receptor
Your hormone stimulates activity of the kinase MAPKK. Which other kinase activity would you expect
to also be stimulated?
a. Protein kinase A
b. PI3K
c. MAP kinase
d. Protein kinase B
e. Beta adrenergic receptor kinase
MAP kinase
Which is TRUE about calmodulin proteins?
a. They contain EF hand motifs
b. They bind calcium ions
c. They change conformation
d. All of the above
e. None of the above
All of the above
The mechanism of action for cholera toxin A1 is:
a. Increased hydrolysis of the gamma phosphate in ARF6
b. Conjugation of an ADP ribose to the ARF6 active site
c. Constitutive activation of G-protein signaling
d. Both A and B
e. Both B and C
Conjugation of an ADP ribose to the ARF6 active site
Constitutive activation of G-protein signaling
