cell and molecular biology 7e - university of colorado boulder
TRANSCRIPT
![Page 1: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/1.jpg)
What would you observe if you fused a G1 cell
with a S cell?
A. Mitotic and pulverized chromosomes.
B. Mitotic and compact G1 chromosomes.
C. Mostly non-compact G1 chromosomes.
D. Compact G1 and G2 chromosomes.
![Page 2: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/2.jpg)
What would you observe if you created a
transgenic mouse that over expressed p27
A. Normal size mouse with large thymus.
B. Normal size mouse with normal thymus.
C. Normal size mouse with small thymus.
D. Small size mouse with small thymus.
![Page 3: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/3.jpg)
Sister chromatids are held together by
A. Condensin and Cohesin.
B. Condensin.
C. Cohesin.
D. Smc4 and Smc2.
![Page 4: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/4.jpg)
The presence of the MAD2 checkpoint protein
on a chromatid occurs due to
A. Unattached Ndc80 proteins
B. An unassembled kinetochore
C. Unattached microtubules
D. Unattached microtubule depolymerase
![Page 5: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/5.jpg)
The separation of chromosomes during
telophase is driven by
A. Ndc80 motor proteins
B. Plus end depolymerization of microtubles
C. Minus end depolymerization of microtubules
D. Plus and minus end depolymerization of
microtubules
![Page 6: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/6.jpg)
Checkpoints in the cell cycle occur
A. In G1
B. In G1 and G2
C. In G1, G2 and M
D. In G1, G2, M and S
![Page 7: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/7.jpg)
Formation of the contractile ring and cleavage
furrow requires
A. Tubulin
B. ATP
C. Actin and Myosin
D. B and C
![Page 8: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/8.jpg)
EGF signaling is transmitted across the plasma
membrane by
A. Lipids.
B. Ras.
C. A heterotrimeric G protein.
D. A receptor tyrosine kinase.
E. An SH2 domain contain protein.
![Page 9: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/9.jpg)
Glucagon is a hormone secreted by the
pancreas. It then travels in the blood stream
and alters glucose metabolism in the liver.
What type of signaling is this?
A.Endocrine signaling.
B.Paracrine signaling.
C.Autocrine signaling.
D.Signaling via cell-cell contact.
![Page 10: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/10.jpg)
What protein-protein interaction is missing?
A. RasGEF
B. RasGAP
C. ERK
D. MAPKK
Ras
GAP
![Page 11: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/11.jpg)
What protein-protein interaction is missing?
A. RAF
B. RTK
C. ERK
D. MAPKK
Ras
GAP
Raf
![Page 12: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/12.jpg)
What would cause the same phenotype as inactivation of SOS,
the Ras GEF?
A. Ras that is stuck in a GTP bound state.
B. Grb2 (the SH2 containing protein) can bind to EGFR even
when EGFR is not phosphorylated.
C. An EGF receptor that dimerizes even in the absence of
ligand.
D. Raf is inactive.
E. A drug that mimics the effect of EGF on EGFR.
![Page 13: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/13.jpg)
Which feature is found in the Insulin receptor,
but NOT in EGF receptor?
A. Trans-autophosphorylation.
B. Generation of phosphotyrosine residues.
C. A disulfide linked receptor dimer.
D. Recruitment of downstream signaling
molecules.
![Page 14: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/14.jpg)
You have created a muscle cell line in which PKB
is locked in a phosphorylated state. What would
you likely observe in this cell line?
A. Increased PI3Kinase activity.
B. Glycogen synthesis is arrested.
C. Increased glucose uptake.
D. Decreased fusion of Glut4 vesicles with the PM.
![Page 15: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/15.jpg)
Insulin receptors are found on
A. Liver cells.
B. Muscles cells.
C. Fat cells.
D. All of the above.
![Page 16: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/16.jpg)
Type I diabetes is an autoimmune disease that
results in loss of the beta cells of the pancreas.
These patients could be treated by
A. Insulin injection
B. Drugs that phosphorylate IR
C. Drugs that phosphorylate PKB
D. All of the above.
![Page 17: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/17.jpg)
Type II diabetes is gradual resistance to insulin.
These patients could be treated by
A. Insulin injection
B. Glucagon injection
C. Drugs that dephosphorylate PKB
D. A and C.
![Page 18: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/18.jpg)
The insulin receptor activates
A. PKB
B. RAF
C. PI3K
D. All of the above
![Page 19: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/19.jpg)
PKB increases cellular glucose uptake by
upregulating
A. Glycogen synthesis
B. Glucose transporter activity
C. Fusion of transporter vesicles
D. A and C.
![Page 20: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/20.jpg)
G proteins are turned off by?
A. The production of cAMP.
B. Hydrolysis of bound GTP.
C. The dissociation of the Beta and Gamma
subunits.
D. Ligand binding to receptor.
E. phosphorylation.
![Page 21: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/21.jpg)
GPCRs are turned off by?
A. Binding of cAMP.
B. Hydrolysis of bound GTP.
C. Arrestin binding
D. Ligand binding to receptor.
E. Phosphorylation
![Page 22: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/22.jpg)
G protein alpha most tightly binds
A. GPCRs
B. Ligand bound GPCRs
C. Ligand bound GPCRs when they are in the GDP
state
D. Ligand bound GPCRs when they are in the GTP
state
![Page 23: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/23.jpg)
GPCRs and G protein alpha function together like
A. RAS and RAF
B. RTK and SH2
C. RasGEF and RAS
D. MAPKK and MAPK
E. PI3K and PI(4,5)P2
![Page 24: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/24.jpg)
Adenylate cyclases are?
A. soluble proteins.
B. usually membrane bound.
C. can be directly activated.
D. Are activated by GPCRs.
E. B and C.
![Page 25: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/25.jpg)
G proteins are turned off by?
A. The production of cAMP.
B. Hydrolysis of bound GTP.
C. The dissociation of the Beta and Gamma
subunits.
D. Ligand binding to receptor.
E. phosphorylation.
![Page 26: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/26.jpg)
Glucagon and Epinephrine do not share this
feature?
A. Bind and activate a GPCR.
B. Cause a G protein to exchange GDP for GTP.
C. Binding results in glycogen breakdown.
D. Made by the pancreas.
E. Leads to an increase in cAMP.
![Page 27: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/27.jpg)
PKB/AKT activates the Rab protein involved in GLUT4
exocytosis. If you use a chemical to inhibit PKB
activity, what would you likely observe in insulin-
treated cells?
A. PI3 kinase is activated.
B. GLUT4 vesicles tether to the plasma membrane.
C. GLUT4 vesicles fuse with the plasma membrane.
D. Increased glucose uptake into the cells.
![Page 28: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/28.jpg)
PKA cellular specificity is determined by?
A. PI3 kinase
B. GPCRs
C. PLCs
D. AKAPs
E. A and D
![Page 29: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/29.jpg)
Arrestin regulates GPCR signaling by?
A. Inactivation
B. Promoting GPCR endocytosis
C. Intracellular signaling
D. All of the above
E. None of the above
![Page 30: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/30.jpg)
All of the following are second messengers except
A. cAMP
B. Nitric Oxide
C. GTP
D. DAG
E. IP3
![Page 31: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/31.jpg)
The action of PI-PLCb can
A. hydrolyze PI(4,5)P2
B. be activated by Ga
C. produce IP3
D. produce DAG
E. all of the above
![Page 32: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/32.jpg)
Inhibition of PI-PLCb will
A. produce more DAG
B. decrease cystosolic Ca++
C. increase IP3 receptor activity
D. produce more IP3
E. all of the above
![Page 33: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/33.jpg)
GPCRs can activate ERK
A. When bound to arrestin
B. When bound to arrestin if endocytosed
C. Via PI3K
D. Via RAS
E. B and D
![Page 34: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/34.jpg)
GPCRs can inhibit RTK signaling
A. by activating RAS
B. by inhibiting RAS
C. by inhibiting RAF
D. by inhibiting ERK
![Page 35: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/35.jpg)
Divergent signaling occurs
A. when receptors activate the same pathway
B. when receptors inhibit the same pathway
C. when a receptor activates different pathways
D. any of the above
![Page 36: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/36.jpg)
You are studying the effect of 2 recently discovered
growth factors that bind to different receptors and
activate PKA. It is likely that
A. the two signaling pathways are the same
B. the two signaling pathways are convergent
C. the two signaling pathways are divergent
D. the two signaling pathways experience cross talk
E. none of the above
![Page 37: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/37.jpg)
Apoptosis occurs during
A. Embryo development
B. Cell turnover in adult tissue
C. T-cell clonal selection
D. Tissue atrophy
E. All of the above
![Page 38: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/38.jpg)
Apoptosis causes the following
A. RNA fragmentation
B. DNA fragmentation
C. Mitochondrial division
D. Membrane blebs
E. B and D
![Page 39: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/39.jpg)
During development apoptotic cells are phagocytosed
by
A.Immune cells
B. Macrophages
C. Microphages
D. B cells
E. A and B
![Page 40: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/40.jpg)
Apoptotic release of cytochrome c occurs
A. via the Bcl-2 MOMP complex
B. during extrinsic apoptosis
C. after caspase 9 activation
D. After caspase 8 activation
E. A and D
![Page 41: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/41.jpg)
Both extrinsic and intrinsic apoptosis require
A. caspase 8 activation
B. caspase 9 activation
C. cytochrome c release
D. caspase 3 activation
E. B and D
![Page 42: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/42.jpg)
You have isolated a mutant human cell line that
releases cytochrome c from the mitochondria but does
not undergo apoptosis. You could conclude that
A. caspase 8 activation is defective
B. caspase 9 activation is defective
C. Bcl-2 is defective
D. caspase 3 activation is defective
E. either B or D
![Page 43: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/43.jpg)
You have isolated a mutant human cell line that
undergoes apoptosis but cannot be phagocytosed.
Treating these cells with GFP annexin V will
A. highlight the nuclear membrane
B. show a diffuse cytochrome c distribution
C. show nothing
D. highlight the plasma membrane
E. either B or D
![Page 44: Cell and Molecular Biology 7e - University of Colorado Boulder](https://reader031.vdocument.in/reader031/viewer/2022011820/61d590ccd829ae5a51010c2c/html5/thumbnails/44.jpg)
Apoptotic cells show a loss of phosphotidylserine
asymmetry at the plasma membrane. This most likely
occurs due to
A. activation of a flippase
B. inactivation of a flippase
C. activation of a lipid transferase
D. inactivation of a lipid transferase
E. either A or D