Pre-Exam Quiz Flashcards
(20 cards)
Signaling by the steroid hormone estrogen is an example of _______ signaling.
A) autocrine
B) paracrine
C) direct cell-to-cell
D) endocrine
D) endocrine
Steroid hormones usually act via receptors that
A) are coupled to G proteins that activate adenylyl cyclase
B) activate phospholipase C
C) activate tyrosine kinases
D) bind to DNA
D) bind to DNA
The alpha subunit of the G protein that is associated with the epinephrine receptor, Gs,
A) inhibits adenylate cyclase
B) opens Ca2+ channels
C) closes Na+ channels
D) activates adenylate cyclase
D) activates adenylase cyclase
Binding of cAMP to the _______ subunits of protein kinase A (PKA) leads to _______ of that protein kinase
A) regulatory; activation
B) regulatory; inactivation
C) catalytic; activation
D) catalytic; inactivation
A) regulatory; activation
A mutation that causes a G-protein to lose its ability to hydrolyze bound GTP would be expected to have constitutively
A) bound alpha/beta/gamma subunits
B) inactive alpha subunits
C) inactive beta/gamma subunits
D) active alpha subunits
D) active alpha subunits
Protein kinase A regulates glycogen metabolism by phosphorylating glycogen synthase and
A) glucokinase
B) glycogen phosphorylase
C) phosphorylase kinase
D) glycogen phosphatase
C) phosphorylase kinase
Mutated oncogenic Ras proteins usually
A) fail to bind Raf
B) cleave GTP more rapidly than normal
C) cleave GTP less rapidly than normal
D) bind GAP more tightly than normal
C) cleave GTP less rapidly than normal
MPF is a
A) dimer of Cdk1 and cyclin B
B) monomeric protein kinase
C) dimer of Cdk1 and cyclin A
D) dimer of two molecules of Cdk1
A) dimer of Cdk1 and cyclin B
Cdks bind to cyclin and are activated by
A) phosphorylation by Wee1
B) the binding of Cip
C) the binding of Ink4
D) dephosphorylation by Cdc25 protein phosphatase
D) dephosphorylation by Cdc25 protein phosphatase
During the spindle assembly checkpoint, degradation of _______ allows for separation of the sister chromatids
A) kinetochore
B) cohesin
C) cyclin B
D) separase
B) cohesin
Most cells in adult animals are in the _______ stage of the cell cycle
A) S
B) G2
C) G1
D) G0
D) G0
What set of events take place in the nucleus of the cell during glucocorticoid signaling?
A) exposed nuclear localization signals on receptor allows nuclear import as receptor tetramers; (ii) activated receptors bind recognition sites in sRNA; (iii) Histone Acetyltransferase binds receptor tetramer complex; (iv) translation activated
B) exposed nuclear localization signals on receptor allows nuclear import as receptor tetramers; (ii) activated receptors bind recognition sites in RNA; (iii) Histone Acetyltransferase binds receptor tetramer complex; (iv) transcription activated
C) exposed nuclear localization signals on receptor allows nuclear import as receptor dimers; (ii) activated receptors bind recognition sites in DNA; (iii) Histone Acetyltransferase binds receptor dimer complex; (iv) transcription activated
D) exposed nuclear localization signals on receptor allows nuclear import as receptor tetramers; (ii) activated receptors bind recognition sites in DNA; (iii) Histone Acetyltransferase binds receptor tetramer complex; (iv) translation activated
C) exposed nuclear localization signals on receptor allows nuclear import as receptor dimers; (ii) activated receptors bind recognition sites in DNA; (iii) Histone Acetyltransferase binds receptor dimer complex; (iv) transcription activated
What role do ‘GTPase activating proteins’ (GAP) have in regulating G-protein signaling?
A) GAP is required to hydrolyze the bg subunit, leading to activation of Adenylyl Cyclase
B) GAP is required to hydrolyze the Adenylyl Cyclase receptor, leading to the deactivation of the bg subunit of the G-protein
C) G-proteins can strongly hydrolyze GTP, therefore GTPase activity is not required to fully terminate the activity of the a subunit
D) G-proteins can only weakly hydrolyze GTP, therefore GTPase activity is required to fully terminate the activity of the a subunit
D) G-proteins can only weakly hydrolyze GTP, therefore GTPase activity is required to fully terminate the activity of the a subunit
From the point of adenylyl cyclase activation, what are the steps leading to cAMP-inducible gene expression?
A) cAMP activates Protein Kinase A; catalytic subunit releases regulatory subunit; enzymatically active regulatory subunit translocates to the nucleus; regulatory subunit dephosphorylates the transcription factor CREB; recruitment of coactivators; expression of cAMP-inducible genes
B) cAMP activates Protein Kinase A; regulator subunit releases catalytic subunit; enzymatically active catalytic subunit translocates to the nucleus; catalytic subunit phosphorylates the transcription factor CREB; recruitment of coactivators; expression of cAMP-inducible genes
C) cGMP activates Protein Kinase A; catalytic subunit releases regulatory subunit; enzymatically active regulatory subunit translocates to the cytoplasm; regulatory subunit dephosphorylates the transcription factor KRAB; recruitment of coactivators; expression of cGMP-inducible genes
D) cGMP activates Protein Kinase B; regulator subunit releases catalytic subunit; enzymatically active catalytic subunit translocates to the cytoplasm; catalytic subunit; phosphorylates the transcription factor CRAB; recruitment of coactivators; expression of cGMP-inducible genes
B) cAMP activates Protein Kinase A; regulator subunit releases catalytic subunit; enzymatically active catalytic subunit translocates to the nucleus; catalytic subunit phosphorylates the transcription factor CREB; recruitment of coactivators; expression of cAMP-inducible genes
Nitric Oxide (NO) is a major paracrine signaling molecule in the nervous, immune, and circulatory systems. Which of the following best describes the role of NO in the regulation of transcription
A) NO diffuses across the plasma membrane; NO alters activity of guanylyl cyclase; guanylyl cyclase stimulates synthesis of cyclic GMP
B) NO diffuses across the plasma membrane; NO alters activity of guanylyl cyclase; guanylyl cyclase stimulates synthesis of ATP
C) NO binds cell surface receptor; NO alters activity of guanylyl cyclase; guanylyl cyclase stimulates synthesis of cyclic AMP
D) NO binds cell surface receptor; NO alters activity of guanylyl cyclase; guanylyl cyclase stimulates synthesis of cyclic GMP
A) NO diffuses across the plasma membrane; NO alters activity of guanylyl cyclase; guanylyl cyclase stimulates synthesis of cyclic GMP
Cholera toxin inhibits the ability of the a subunit of Gs to split GTP. If you treat cells with cholera toxin, the resulting effect would be ______________ of adenylyl cyclase
A) Molecular degradation
B) Increased synthesis
C) Inhibition
D) Stimulation
D) Stimulation
What is the main difference between receptor tyrosine kinases and nonreceptor tyrosine kinases?
A) Receptor tyrosine kinases must be activated by the binding of a ligand (hormone), whereas nonreceptor tyrosine kinases do not need to be activated
B) Receptor tyrosine kinases contain an intrinsic kinase activity, whereas nonreceptor tyrosine kinases recruit separate kinase enzymes
C) Receptor tyrosine kinases can be phosphorylated and nonreceptor tyrosine kinases cannot
D) Receptor tyrosine kinases undergo ligand-induced dimerization and nonreceptor tyrosine kinases do not
B) Receptor tyrosine kinases contain an intrinsic kinase activity, whereas nonreceptor tyrosine kinases recruit separate kinase enzymes
Activation of the NF-κB pathway leads to what main step?
A) A kinase is activated, which phosphorylates a target protein.
B) A protein is phosphorylated, which inactivates the pathway
C) A protein is degraded, which inactivates the pathway
D) An inhibitory protein is phosphorylated and marked for degradation
D) An inhibitory protein is phosphorylated and marked for degradation
How would a mutated p53 gene lead to cancer?
A) p53 activity would be enhanced and lead to increased levels of DNA damage.
B) The mutated p53 protein would activate cell cycle proliferation
C) The loss of p53 activity would prevent cell cycle arrest due to DNA damage
D) The enzymes responsible for DNA damage would be activated
C) The loss of p53 activity would prevent cell cycle arrest due to DNA damage
SH2 domains bind to acetylated sites at the intracellular domain of receptor tyrosine kinases.
True
False
False
