Chapter 18: Apoptosis ch 4
Killer lymphocytes can elicit self-destruct mechanisms in target cells by interacting with A) Fas ligand. B) Fas receptors. C) Ras ligand. D) adaptor protein
B) Fas receptors
Mice lacking the ability to make caspase-9 die as the result of numerous defects. During the necropsy (animal autopsy) of the animal you note that the brains of these mice are A) unregulated growth of the nerve cells. B) lack of apoptosis of some cells. C) overstimulation of G-protein-mediated transduction. D) overproduction of G
B) lack of apoptosis of some cells.
Apoptosis differs from necrosis in that necrosis ________________. (a)requires the reception of an extracellular signal (b)causes DNA to fragment (c)causes cells to swell and burst, whereas apoptotic cells shrink and condense (d)involves a caspase cascade
C) causes cells to swell and burst, whereas apoptotic cells shrink and condense
Which of the following statements about apoptosis is true? (a)Cells that constitutively express Bcl2 will be more prone to undergo apoptosis. (b)The prodomain of procaspases contains the catalytic activity necessary for procaspase activation. (c)Bax and Bak promote apoptosis by binding to procaspases in the apoptosome. (d)Apoptosis is promoted by the release of cytochrome c into the cytosol from mitochondria.
D) Apoptosis is promoted by the release of cytochrome c into the cytosol from mitochondria.
All of the following participate in apoptosis except A) caspases. B) death-promoting proteins. C) mitochondria. D) Bcl-2
D) Bcl-2
Protein whose elimination in a cancer cell inhibit apoptosis. a. BH3 b. BH123 c.Bax d. anti-IAP e.all of them
D) all of them
Protein whose overexpression in a cancer cell inhibit apoptosis are: a.IAP b. Bcl-2 c.Akt kinase active-c d.all of them
D) all of them
Which of the following mutations in proteins involved in apoptosis will be expected to have dominant-negative phenotype (to cause a defect in apoptosis even in cells that also contain the normal protein): A.Deletion of death domain of Fas death receptor. B.Mutation of the catalytic cysteine of caspase-8 to serine. C.Mutational change to IAP that increases its affinity for caspases. D.all of them
D) all of them
High activity of the initiator caspase-8 &-9 are required to be incorporated into the splisosome.
FALSE
IAP proteins bind and inhibit active caspases and/or ubiquitylate and promote the degradation of caspases by transporting them to the ECM.
FALSE
IAP proteins inactivate or degrade caspases that normailly degrade targets like ECM.
FALSE
If a cell goes under necrosis the cytochrome-c will be concentrated in the mitochondria as they swell and burst.
FALSE
Necrotic cells keep the integrity of their plasma membranes, so a dye such as ethidium bromide can enter the cells to bind to DNA in the nucleus.
FALSE
Apoptotic cells flip phosphatidylserine from the inner to the outer leaflet of the plasma membrane as an "eat me" signal to other cells.
TRUE
Apoptotic cells will show a DNA ladder electrophoresis caused when cellular endonuclease activated in apoptotic cells cuts at some linker DNA in between the nucleosomes in the chromatin. Each band will be in multiples of 180 base pairs which is the length of the linker DNA and the core nucleosome.
TRUE
Each procaspases has an adaptor domain (which enables it to assemble with other proteins), a dimerization domain, and a catalytic domain.
TRUE
Effector procaspases acquire high proteolytic activity only after they have been cleaved by active initiator caspases.
TRUE
If a cell goes under apoptosis, the cytochrome c is rapidly be released from the mitochondria into the cytosol and will appear diffuse.
TRUE
In non apoptotic cells, cytochrome-c is localized in the mitochondrial intermembrane space.
TRUE
When a cell gets deprivaded of survival signals it may trigger a pathway that causes increased expression of BH3. BH3 in turn may cause BH123 proteins to release cytochrome-c from the mitochondrial to activateapoptosomes, which activate caspase-9.
TRUE
Protein whose elimination in a cancer cell inhibit apoptosis. a.Fas receptor b.procaspase c.Apaf-1 d.all of them
all of them
Cancer cells often exhibit abnormal regulation of the apoptotic program. Mutations that prevent the regulation of apoptosis not only contribute to _1_and affect the response to anticancer therapies. Apoptosis normally acts as a _2_mechanism that eliminates cells that are not needed or have become abnormal or suffered damage. If, for example, cells that have acquired a mutation are not killed, they may proliferate and accumulate additional mutations that allow them _3_from normal growth and social controls to become cancer cells. Many anticancer drugs and radiation treatments act by damaging _4_ or other cellular components, thereby triggering apoptosis. If cancer cells cannot undergo apoptosis, then they will be to these drugs and will continue to proliferate and acquire further mutations. a.quality control b. carcinogenesis c. to escape d.resistant e. DNA
1. B 2. A 3. C 4. E
There is some evidence in other tissues and organisms that the number of nerve cells is controlled by limited amounts of _1_that are secreted by the target cells with which the nerve cells connect. When there are _2_ nerve cells than normal, the competition for the same limited amount of factors will be increased. Perhaps very _3_ of the nerve cells can get enough survival factor to _4_ apoptosis, causing a catastrophic loss of the nerve cells. a. more b. few c.inhibit d.survival factors
1. D 2. A 3. B 4. C
Which of the following statements regarding Fas-mediated programmed cell death is false? A) Fas ligand binding with Fas receptor stimulates a specific G protein. B) Fas ligand and receptor interaction results in the recruitment of adaptor proteins in the target cell. C) Capases are activated in the process. D) The caspase cascade results in the cleavage of the proteins within the target cell.
A) Fas ligand binding with Fas receptor stimulates a specific G protein.
Programmed cell death occurs ________________. (a)by means of an intracellular suicide program (b)rarely and during plant development (c)only in unhealthy or abnormal cells (d)only during embryonic development
A) by means of an intracellular suicide program
