Which of the following types of mutations would be most likely to cause cells to undergo apoptosis (programmed cell death)? One that increases the affinity of p21 for Cdks One that decreases the affinity of Rb for the transcription factor E2F One that decreases the ability of p53 to bind to DNA One that causes p53 to be constitutively phosphorylated
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Which of the following types of mutations would be most likely to cause cells to undergo apoptosis (programmed cell death)?
One that increases the affinity of p21 for Cdks
One that decreases the affinity of Rb for the transcription factor E2F
One that decreases the ability of p53 to bind to DNA
One that causes p53 to be constitutively phosphorylated
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- A growth factor Fsh3 stimulates the proliferation of culture fish cells. The receptor that binds Fsh3 is a receptor tyrosine kinase (RTK) and there are numerous fish tumor cell lines that have a mutation for the gen for this receptor. Which of the following mutations would be expected to promote uncontrolled cell proliferation. a mutation that inactivates the protein tyrosine phosphatase that acts on the receptor a mutation that prevents the binding of the normal extracellular signal to the receptor a mutation that inhibits the Ras GEF a mutation that destroys the kinase activity of the receptor a mutation that prevents dimerization of the receptorWhich of the following must occur for programmed cell death (apoptosis): 1. p53 must be stabilized 2. M-Cdk must be active 3. Caspases must be inactivated 4. There must be local inflammationHuman cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice. State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth. the mitogenic signaling pathway controlled by Ras. the cell cycle checkpoint controlled by pRb. the alarm pathway controlled by p53. the telomere maintenance pathway controlled by hTERT. the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.
- See figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. Cyclin Serine Lysine Aspartic "Acid Lysine -OH NH3t -Coo NH3+ NH3 + -OH Aspartic Aad Aspartic Acid /Lysine Serine сокSee figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. A Explain what a kinase does and how the cyclin controls the activity of the Cdk.After DNA damage (e.g. caused by X-ray exposure) in eukaryotic cells, the cell cycle can be arrested by the stabilisation of the protein which drives the transcription of the gene, whose protein product interacts with the G1/S-Cdk and S-Cdk complexes. O PDGF, acetyltransferase O phenylalanine hydraxylase, PDGF O p53, acetyltransferase O p53, p21 O p21. p53
- Match the following changes with the correct responses. (Some answers may be used more than once. Some answers may not be used.) Deacetylation of histones Methylation of cytosines a single nucleotide polymorphism, where adenine may be present instead of cytosine phosphorylation of cytosines is an epigenetic change that is an epigenetic change that [Choose ] is an epigenetic change that results in decreased gene transcription is not an epigenetic change ✓ is an epigenetic change that results in increased gene transcription is an epigenetic change that could either increase or decrease gene transcriptionIndividuals with the hereditary disorder ataxia telangiectasia suffer from neurodegeneration, immunodeficiency, and an increased incidence of cancer. The genetic basis for ataxia telangiectasia is a loss-of-function mutation in the gene encoding ATM (ATM; ataxia telangiectasia mutated). Besides p53, what other substrate is phosphorylated by ATM? How does the phosphorylation of this substrate lead to inactivation of CDKs to enforce cell cycle arrest?Nucleation of straight, single line microfilaments is mediated by which of the following? Rho GTPase and Formin Rho GTPase and Arp 2/3 Cdc42 GTPase and Arp2/3 OCdc42 GTPase and Formin 14 < Previous
- which of the following correctly describes how protein kinase A can activate genes? A: nuclear protein kinase A is activated by cAMP to phosphorylate general transcription factors B: cytosolic protein kinase A is activated by cAMP to release the catalytic subunits, which move into the nucleus and phosphorylate CREB C: cytosolic protein kinase A is activated by cAMP to release the catalytic subunits, which move into the nucleus and phosphorylate general transcription factors D: G protein-coupled receptors may be desensitized by serine phosphorylationWhy is it advantageous for p53 to be activated by factors such as ER stress, light, and hypoxia (low oxygen concentration)?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