Abbreviations: RTK: Receptor Tyrosine Kinase
GPCR: G Protein Coupled Receptor
Rb: Retinoblastoma
MKP-1: Map Kinase Phosphatase
CDK: Cyclin Dependent Kinase
APC: Anaphase Promoting Complex
CAK: Cylcin Activating Kinase
PKA: Protein Kinase A
CDC: Cell Division Cycle
MPF: Maturation Promoting Factor
MCC: Mitotic Checkpoint Complex
ORC: Origin Recognition Complex
1. Ras is activated when
a. It binds to GRB
b. It is phosphorylated by the RTK
c. It is phosphorylated by the MAP Kinase cascade
d. The GEF Raf acts on it
e. SOS causes it to bind a GTP
2. Which of these functions as an adaptor molecule between the RTK and downstream signaling components?
a. GRB
b. Arrestin
c. ERK
d. Ras
e. CBL
3. _____ binds directly to a phosphorylated RTK
a. SOS
b. RAS
c. CBL
d. A&B
e. All of these
4. Which of these proteins moves into the nucleus?
a. SOS
b. Ras
c. RAF
d. CBL
e. ERK
5. RTK-mediated growth factor signaling is terminated by
a. MKP-1
b. ERK being dephosphorylated by Cyclin D
c. Hydrolysis of the GTP bound to SOS
d. Removal of the phosphates bound to the RTK by RTK Phosphatase
e. Arya Stark's cool little "drop the knife" trick
6. Which phenotype would be most likely to occur if STAT acquired a point mutation that prevented it from dimerizing?
a. JAK could not bind to the receptor
b. JAK could not phosphorylate the receptor
c. STAT could not enter the nucleus
d. STAT could not utilize its SH2 domain
e. STAT could not be phosphorylated
7. Which of these happens FIRST after an RTK binds a ligand?
a. The cytoplasmic domain binds GTP
b. The cytoplasmic domain autophosphorylates
c. A conformational change exposes a binding site for an SH2 protein
d. Receptors dimerize
e. It posts photos of itself on instagram bound to new ligand with the intention of making all of the other receptors jealous
8. Which is true of Cyclin/CDK combos?
a. Cyclins are active after they are phosphorylated by the CDK
b. Cyclins are active after they bind a GTP
c. Cyclins are kinases that phosphorylate a target
d. Cyclins directly bind to substrates that will be phosphorylated by CDK
e. In the absence of the correct cyclin, CDKs can phosphorylate incorrect substrates
9. Which of these statements explains why only one round of DNA replication can occur?
a. MCM helicase can only bind to DNA in its unphosphorylated form
b. ORC complex ubiquitination coincides with initiation of DNA replication
c. Chk1 activity prevents activation of MCM helicase later in the cell cycle
d. The p21 inhibitor that is produced as part of entry into S phase inhibits MCM helicase binding to DNA e. Aurora kinases are necessary for MCM activation, and they are not present when a second round of DNA replication could occur
10. How is cell cycle repression by p27 removed?
a. It is phosphorylated by E2F
b. It is degraded by APC
c. It is phosphorylated by CDK2/CycE
d. P27 is phosphorylated by DDK
e. CDC25 removes a phosphate from CDK2, which prevents P27 from binding
11. After a cell passes the ____________ checkpoint, it has comitted to either division or apoptosis.
a. G1
b. S
c. DNA Damage
d. Entry into M Phase
e. Spindle formation (Metaphase)
12. When in possession of all of its components, the MCC complex
a. inhibits APC
b. activates APC
c. binds to and degrades cohesin
d. phosphorylates Cyclin B
e. phosphorylates Retinoblastoma (Rb)
13. How does the cell activate Cyclin B/CDK1?
a. Phosphorylation blocks a nuclear export signal on Cyclin B
b. Phosphorylation activates a nuclear localization signal on Cyclin B
c. P21 is degraded by APC
d. P27 is degraded by APC
e. CyclinB/CDK1 are phosphorylated by CDC25
14. Which of the following is a target of APC?
a. Ink4
b. Cyclin B
c. Retinoblastoma
d. P21
e. MCM Helicase
15. CyclinB/CDK1 combo activates
a. CDC20
b. CDC25
c. Chk1
d. E2F
e. Condensin
16. A knockout mutation in _______________ would inhibit a cell's ability to pause the cell cycle in response to double-stranded DNA breaks
a. CHK2
b. ATM
c. P53
d. A&B
e. All of these
17. Which Cyclin/CDK combo is responsible for activating transcription of proteins required for DNA replication?
a. CDK1/CycB
b. CDK1/CycA
c. CDK4/CycD
d. CDK2/CycE
e. CDK2/CycA
18. How does APC prevent DNA replication?
a. It degrades p21
b. It phosphorylates the DNA binding site of MCM helicase
c. It degrades DDK
d. It degrades cdc25
e. It functions as the chaperone of the cell cycle by making sure Cyclin and CDK don't dance too close
19. A mutation in which of the following would be likely to make the cell cycle proceed faster?
a. Retinoblastoma
b. Ink4
c. P27
d. Chk1
e. All of these
20. What would be the difference in phenotype between a cell with a WEE1 knockout mutation and a cell with a mutation in both WEE1 and CDC25?
a. The double mutant will show slower cell division
b. MPF will remain completely unphosphorylated in both mutants
c. MPF will be phosphorylated at Tyr 15 in the WEE1 mutant, but not in the double mutant
d. The double mutant will be unable to move through the Mitosis checkpoint, but the single mutant will e. Both the double and single mutants will have the same phenotype
21. What mechanism does Chk1 use to pause the cell cycle?
a. It degrades APC
b. It activates APC
c. It phosphorylates CDC25
d. It degrades CyclinB
e. It activates Ink4
22. If a cell made more _______ you would expect it to have longer microfilaments.
a. Profilin
b. Spectrin
c. Formin
d. CapZ
e. Cofilin
23. If a microfilament is treadmilling, but NOT at steady state, which of the following is true?
a. ATP actin is adding to both the + and - end
b. ATP actin is dissociating from both the + and - end
c. The amount of actin that adds to the + end is equal to the amount of actin that dissociates from the - end
d. More actin is dissociating from the - end than is adding to the + end
e. Without the comfort of steady state, the actin is really worried it will not do well on the 319 exam
24. If you used recombinant DNA technology to generate a version of Formin without the Rho Binding Domain (RBD), which of these phenotypes would you expect?
a. Nucleation of less microfilaments than normal
b. Nucleation of more microfilaments than normal
c. Microfilaments grow more slowly after nucleation
d. Microfilaments grow more quickly after nucleation
e. Microfilaments have less branches than normal
25. Which of the following have dynamics (when considering critical concentration) that most closely resemble microtubules?
a. Intermediate filaments
b. ATP-Actin
c. ADP-Actin
d. B&C, because they have identical dynamics
e. Jon Snow and Danerys Targaryan, because they have dynamic instability
26. Cofilin binds to
a. ATP G-Actin
b. ADP G-Actin
c. ADP F-Actin
d. ATP F-Actin
e. Profilin
27. Which is true of myosin?
a. Mammalian cells have only one myosin isoform
b. Mysosin moves to the + end of microfilaments
c. Myosin utilizes GTP hydrolysis to move one step
d. A&B
e. All of these
28. Profilin's function is to
a. Cause actin to hydrolyze ATP
b. Cause actin to add a phosphate to ADP
c. Cause actin to bind ATP
d. Cause actin to release ADP
e. None of these
29. The energy for assembly of Intermediate Filaments comes from
a. ATP hydrolysis
b. GTP hydrolysis
c. Binding ATP
d. Binding GTP
e. None of these
30. What role does ATP play in the polymerization of microfilaments?
a. ATP is hydrolyzed, but not immediately after incorporation into a filament
b. ATP must be bound to an actin monomer prior to incorporation into a microfilament
c. ATP is hydrolyzed as the actin monomer binds to the actin filament
d. A&B
e. B&C
31. Which of these proteins would you expect to associate with the "-" end of G or F Actin?
a. Tropomodulin
b. Arp2/3
c. Formin
d. A&B
e. All of these
32. A knockout mutation in ______________ would lead to longer microfilaments with less branches
a. Wasp
b. CapZ
c. Rho
d. A&B
e. All of these
33. Which of these typically shows the fastest dissociation from an actin filament?
a. ATP-Actin from the - end
b. ADP-Actin from the - end
c. ATP-Actin from the + end
d. A&B are equal
e. The red viper of Dorne
34. Below is the graph we discussed in class for actin dynamics. Which of these would you expect to happen in a cell that has a current ATP-Actin concentration of 65uM?
a. ATP-actin will add to both ends
b. ATP-actin will dissociate from both ends
c. ATP-actin will add to the + end faster than monomers will dissociate from the - end
d. ATP-actin will add to the + end more slowly than monomers will dissociate from the - end
e. ATP and ADP-actin will associate with both the + and - end
35. This figure shows what happens when fluorescently-labeled intermediate filaments are injected into a cell. What can be concluded from this experiment?
a. Intermediate Filament building blocks integrate into the "+" end of the microfilament
b. Intermediate filament building blocks can associate with the interior of existing intermediate filament polymers
c. Intermediate filament monomers always associate into tetramers before addition to an existing filament
d. GTP hydrolysis is required for incorporation of intermediate filament building blocks into an existing filament
e. Fluorescently-labeled intermediate filaments cannot associate with existing intermediate filaments
36. _____________ is a molecule with polarity
a. Intermediate Filament monomer
b. Intermediate Filament dimer
c. Intermediate Filament tetramer
d. A&B
e. All of these
37. The CC of the + end of a microfilament is 1.5uM ATP-Actin. The CC of the - end of a microfilament is 4uM. Which cellular concentration of actin will lead to treadmilling?
a. 1uM
b. 3uM
c. 4.1uM
d. 8uM
e. 5uM
38. What is the function of spectrin?
a. Cap the + end of actin filaments
b. Cap the - end of actin filaments
c. Provide structure for the cell
d. Act as a scaffold protein to connect tropomodulin, long actin filaments, and the plasma membrane
e. Bind to the tail of myosin to mediate interactions between myosin and its cargo
39. Which of the following would you expect to interact with a GPCR at a similar location as a heterotrimeric G Protein?
a. Epinephrine
b. GPCR Kinase
c. Adenylyl Cyclase
d. Glycogen Phosphorylase
e. All of the terrible songs Darron plays before class
40. Which is true of Adenylyl Cyclase?
a. It is inactivated when RGS (Regulator of G-protein Signaling) binds to it
b. It dissociates from the plasma membrane after activation
c. It binds PKA
d. It binds to ATP
e. It has the worst, most confusing name in the history of proteins
41. Which of these events occurs as part of GPCR signaling?
a. GPCR Kinase binds to the alpha subunit of the heterotrimeric G protein
b. The GPCR binds to PKA
c. PKA binds to and is activated by adenylyl cyclase
d. The heterotrimeric G-Protein beta subunit binds to adenylyl cyclase
e. RGS binds to the alpha subunit of the heterotrimeric G-Protein
42. How is PKA activated?
a. Phosphorylation exposes a Nuclear Localization Signal to allow its entry into the nucleus
b. cAMP binds to inhibitory subunits of PKA
c. cAMP binding causes a conformational change that exposes the kinase domain
d. cAMP binding causes the PKA to bind an activating ATP
e. cAMP binding causes the PKA to bind an activating GTP
43. Which of these proteins enters the nucleus?
a. Heterotrimeric G-Protein Alpha subunit
b. PKA
c. Phosphodiesterase
d. All of these
e. None of these
44. Which of these events will occur if a cell acquired a knockout mutation in Adenylyl Cyclase?
a. All PKA is localized to the nucleus
b. Heterotrimeric G-Protein Alpha subunit binds GTP
c. Heterotrimeric G-Protein Beta/Gamma binds GTP
d. Heterotrimeric G-Protein Alpha subunit will be unable to hydrolyze its bound GTP
e. Arrestin will continually ubiquitinate PKA
45. How does Arrestin binding desensitize the cell to GPCR signaling?
a. It blocks the site of Heterotrimeric G-Protein binding
b. It catalyzes clathrin binding and endocytosis
c. It induces hydrolysis of a GTP
d. A&B
e. All of these
46. Which of the following is a GAP?
a. RGS
b. Arrestin
c. GPCR
d. Heterotrimeric G Protein Alpha subunit
e. All of these
47. What is the most immediate cellular impact of phosphorylating Glycogen Phosphorylase?
a. Inactivation of PKA
b. Phosphorylation of Glycogen Synthase
c. DNA is unwound to expose cAMP Response Elements (CREs)
d. Dephosphorylation of Phosphorylase Kinase
e. Glycogen Breakdown
48. If a cell acquires a knockout mutation in Protein Phosphatase 1 (which targets the same substrates as PKA), which of these phenotypes would you expect?
a. More glucose will be incorporated into glycogen molecules
b. The duration of PKA signaling will be extended
c. CREB protein will not be phosphorylated
d. CREB proteins will not be able to enter the nucleus
e. Glycogen will interact with CREB proteins for a longer time
49. Which of the following is a direct function of PKA?
a. Phosphorylate CRE Binding Proteins
b. Phosphorylate Glycogen Synthase
c. Phosphorylate Glycogen Phosphorylase
d. A&B
e. all of these
50. How are the two GPCR pathways we discussed (glucose release pathway and the Rhodopsin-mediated pathway) the same?
a. They use the same GPCR
b. They use the same Heterotrimeric G Protein alpha subunit
c. They use the same effector
d. They use the same MAP kinase cascade
e. None of these are the same between the pathways