Page 1 of 89
MCB 450 - Exam 3 Complete Accurate Actual
Questions And Verified Answers (100%
correct verified solutions) Brand new
Version. Graded A+
1. A growth factor binds to a receptor tyrosine kinase (RTK).
Which event occurs immediately after autophosphorylation?
A. Activation of Ras via Grb2/SOS
B. Dimerization of the receptor
C. Internalization of the receptor
D. Activation of PI3K
E. Phosphorylation of PLCγ
Correct Answer: A
Rationale: After autophosphorylation, adaptor proteins
(Grb2/SOS) bind to phosphorylated tyrosines to activate Ras.
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Dimerization (B) occurs before autophosphorylation.
Internalization (C) is later. PI3K (D) and PLCγ (E) are
downstream but not immediate—they require prior RTK
activation.
2. Which second messenger is generated by phospholipase C
(PLC)?
A. cAMP
B. cGMP
C. IP₃ and DAG
D. PIP₂
E. Ca²⁺
Correct Answer: C
Rationale: PLC cleaves PIP₂ into IP₃ (releases Ca²⁺ from ER)
and DAG (activates PKC). cAMP (A) is from adenylyl cyclase.
cGMP (B) from guanylyl cyclase. PIP₂ (D) is the substrate. Ca²⁺
(E) is downstream of IP₃.
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3. S#1: A patient has a mutation that prevents the GTPase
activity of Ras. What is the most likely consequence?
A. Constitutively inactive MAPK pathway
B. Uncontrolled cell proliferation
C. Increased apoptosis
D. Failure to dimerize RTKs
E. Decreased PI3K signaling
Correct Answer: B
Rationale: Ras GTPase activity hydrolyzes GTP to GDP,
inactivating Ras. Loss of GTPase activity locks Ras in active
(GTP-bound) state, leading to persistent MAPK signaling and
uncontrolled proliferation. (A, C, D, E are opposite or
unrelated.)
4. Which drug targets a kinase in the BCR-Abl fusion protein?
A. Cetuximab
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B. Imatinib
C. Rapamycin
D. Forskolin
E. LY294002
Correct Answer: B
Rationale: Imatinib (Gleevec) inhibits BCR-Abl tyrosine kinase.
Cetuximab (A) is anti-EGFR antibody. Rapamycin (C) inhibits
mTOR. Forskolin (D) activates adenylyl cyclase. LY294002 (E)
inhibits PI3K.
5. Which G protein subunit binds GTP and activates adenylyl
cyclase?
A. Gαs
B. Gαi
C. Gαq
D. Gβγ
E. Gα12
MCB 450 - Exam 3 Complete Accurate Actual
Questions And Verified Answers (100%
correct verified solutions) Brand new
Version. Graded A+
1. A growth factor binds to a receptor tyrosine kinase (RTK).
Which event occurs immediately after autophosphorylation?
A. Activation of Ras via Grb2/SOS
B. Dimerization of the receptor
C. Internalization of the receptor
D. Activation of PI3K
E. Phosphorylation of PLCγ
Correct Answer: A
Rationale: After autophosphorylation, adaptor proteins
(Grb2/SOS) bind to phosphorylated tyrosines to activate Ras.
,Page 2 of 89
Dimerization (B) occurs before autophosphorylation.
Internalization (C) is later. PI3K (D) and PLCγ (E) are
downstream but not immediate—they require prior RTK
activation.
2. Which second messenger is generated by phospholipase C
(PLC)?
A. cAMP
B. cGMP
C. IP₃ and DAG
D. PIP₂
E. Ca²⁺
Correct Answer: C
Rationale: PLC cleaves PIP₂ into IP₃ (releases Ca²⁺ from ER)
and DAG (activates PKC). cAMP (A) is from adenylyl cyclase.
cGMP (B) from guanylyl cyclase. PIP₂ (D) is the substrate. Ca²⁺
(E) is downstream of IP₃.
,Page 3 of 89
3. S#1: A patient has a mutation that prevents the GTPase
activity of Ras. What is the most likely consequence?
A. Constitutively inactive MAPK pathway
B. Uncontrolled cell proliferation
C. Increased apoptosis
D. Failure to dimerize RTKs
E. Decreased PI3K signaling
Correct Answer: B
Rationale: Ras GTPase activity hydrolyzes GTP to GDP,
inactivating Ras. Loss of GTPase activity locks Ras in active
(GTP-bound) state, leading to persistent MAPK signaling and
uncontrolled proliferation. (A, C, D, E are opposite or
unrelated.)
4. Which drug targets a kinase in the BCR-Abl fusion protein?
A. Cetuximab
, Page 4 of 89
B. Imatinib
C. Rapamycin
D. Forskolin
E. LY294002
Correct Answer: B
Rationale: Imatinib (Gleevec) inhibits BCR-Abl tyrosine kinase.
Cetuximab (A) is anti-EGFR antibody. Rapamycin (C) inhibits
mTOR. Forskolin (D) activates adenylyl cyclase. LY294002 (E)
inhibits PI3K.
5. Which G protein subunit binds GTP and activates adenylyl
cyclase?
A. Gαs
B. Gαi
C. Gαq
D. Gβγ
E. Gα12
