Upon learning about the mechanism of apoptosis, the question asked was; Is cytochrome c being released from mitochondria or is it being expressed by an induced nuclear gene and being produced in the cytosol. Which one of the following observations would provide the best evidence that it was being released from the mitochondria? Bcl2 blocks release of cytochrome c from mitochondria and also inhibits apoptosis Active Fas receptors trigger release of cytochrome c from mitochondria. Extracellular signals that block apoptosis do not produce cytosolic cytochrome c Caspase inhibitors block release of cytochrome c from the mitochondria

Upon learning about the mechanism of apoptosis, the question asked was; Is cytochrome c being released from mitochondria or is it being expressed by an induced nuclear gene and being produced in the cytosol. Which one of the following observations would provide the best evidence that it was being released from the mitochondria? Bcl2 blocks release of cytochrome c from mitochondria and also inhibits apoptosis Active Fas receptors trigger release of cytochrome c from mitochondria. Extracellular signals that block apoptosis do not produce cytosolic cytochrome c Caspase inhibitors block release of cytochrome c from the mitochondria

Biology: The Dynamic Science (MindTap Course List)

4th Edition

ISBN:9781305389892

Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Publisher:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Chapter9: Cell Communication

Section: Chapter Questions

Problem 2ITD

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Artificially induced apoptosis (controlled cellular death) is found to be an effective treat- ment for some forms of cancer. Which of the following describes the most likely mechanism by which apoptosis might be induced? A B с D by causing ribosomes to increase the rate of protein synthesis by triggering the division of mitochondria in the cell to increase ATP production by increasing the expression of membrane-bound glucose protein channels by causing lysosomes to release digestive enzymes into the cytosol
What from mitosis is triggered by mitotic CDK inactivationmainly brought about by mitotic cyclin degradation.
Stathmin is phosphorylated by cyclin dependent kinases in response to extracellular signals such as growth factors. To further understand the role of phosphorylation in stathmin function, you decide to treat cells with growth factors in the presence or absence of phosphatase and observe microtubule dynamics. Based on the known function of stathmin, and phosphorylation of stathmin, how would you expect phosphatase treatment to affect microtubule dynamics? A. Decreased frequency of catastrophe in the presence of phosphatase, compared to untreated control B. Increased frequency of catastrophe in the presence of phosphatase, compared to untreated control C. Rapid microtubule polymerization in the presence of phosphatase, compared to untreated control D. Catastrophe frequency is the same in phosphatase treated and control cells
Predict the effects of the following mutations on the ability of a cell to undergo apoptosis:a. Mutation in Bad such that it cannot be phosphorylated by protein kinase B (PKB)b. Overexpression of Bcl-2c. Mutation in Bax such that it cannot form homodimersOne common characteristic of cancer cells is a loss of function in the apoptotic pathway. Which of the mutations listed above might you expect to find in some cancer cells?
Virtually all cancer treatments are designed to killcancer cells, usually by inducing apoptosis. However, oneparticular cancer—acute promyelocytic leukemia (APL)—has been successfully treated with all-trans-retinoic acid, which causes the promyelocytes to differentiate into neu-trophils. How might a change in the state of differentiation of APL cancer cells help the patient?
Fighting Cancer by Disrupting Mitosis Scientists have identified a number of toxins that disrupt mitosis. These toxins can be used in many different ways – some of them are used during scientific research to arrest the cell cycle at specific points so that the cells can be studied. Others have clinical applications as chemotherapeutic drugs that are useful in the treatment of cancer, as well as other types of disease. Study the list of toxins below, and use the information provided and your understanding of mitosis to answer the questions below. Note: some of these drugs are currently approved for clinical use, while others are still in development. For the purposes of this exercise, assume that all of them are available for use. Drug How it affects mitosis Status of drug Vincristine Prevents polymerization of tubulin Approved Paclitaxel Prevents depolymerization of tubulin and can result in multipolar spindle formation Approved Flavopiridol Blocks Cdk-1. Cdk-1 is a kinase that helps…
You are studying the function of Bax as a positive regulator of apoptosis. You've engineered a version of the Bax protein that is functional, but is mislocalized to the plasma membrane rather than the mitochondria. You expect that this will block the intrinsic pathway of apoptosis. When you activate the intrinsic pathway of apoptosis, you are surprised to find that the cells still die. You then do a cell fractionation experiment and verify that Bax is. indeed being sent to the plasma membrane, rather than the mitochondria. In one sentence, what is the most likely hypothesis for what is happening?
If you wanted to engineer the initiator caspase from the Fas/FasL extrinsic apoptosis pathway to function in the intrinsic pathway (e.g. in response to DNA damage), which of the following would be the most likely approach to succeed? O Replace the extrinsic pathway's initiator caspase Death Effector Domain with a CARD domain O Replace the Fas Death Domain with a cytochrome C binding domain O Generate a version of the Fas receptor that localizes to the mitochondrial intermembrane space 80 O Replace the intrinsic pathway's initiator caspase CARD domain with a Death Effector Domain F3 0 $ 4 DOD DOO R F4 S % 5 T No new data to save. Last checked at 3:01pm Submit Qu B4 ♫ 8 tv A F5 < 6 MacBook Air F6 Y & 7 F7 * 8 X F8 ( 9
Progression through the cell cycledepends on the phosphorylationof hundreds of different proteins bycyclin–Cdk complexes. What are themolecular mechanisms ensuring thatthese proteins are phosphorylated atprecisely the right time and place?
Heparan sulfate proteoglycans appertain to which of the following processes?*a. transport by argosomesb. transport by cytonemesc. restricted diffusiond. simple diffusion The model for planar transcytosis is characterized by which of the following?* a. Morphogen-receiving cells employ long actin-based filopodia. b. Morphogens interact with cell surface receptors and coreceptors. c. Lipid-modified morphogens are transported in lipoprotein vesicles. d. Morphogens are transported by repeated rounds of endocytosis and re-secretion. Metamerism is NOT observed in which of the following structures?* a. acron b. rhombomeres c. somites d. vertebral column The anterior structure of the Drosophila is promoted by which of the following events?* a. nanos proteins block the transcription of the caudal gene. b. caudal proteins promote the transcription of the bicoid gene. c. bicoid proteins promote transcription of the…
Figure 28.11 depicts the eukaryotic cell cycle. Many cell types â€œexitâ€� the cell cycle and donâ€™t divide for prolonged periods, a state termedG0; some, for example neurons, never divide again. a. In what stage of the cell cycle do you suppose a cell might be when it exits the cell cycle and enters G0? b. The cell cycle is controlled by checkpoints, cyclins, and CDKs. Describe how biochemical events involving cyclins and CDKs might control passage of a dividing cell through the cell cycle.
Biologists have long been interested in the effects of radiation on cells. In one experiment, researchers examined the effect of radium on mitosis of chick embryo cells growing in culture. A population of experimental cells was examined under the microscope for the number of cells in telophase (as a measure of mitosis occurring) before, during, and after exposure to radium. The results are shown in the Figure. What is the effect of radium exposure on mitosis? Source: R. G. Canti and M. Donaldson. 1926. The effect of radium on mitosis in vitro. Proceedings of the Royal Society of London, Series B, Containing Papers of a Biological Character 100:413419.