Principles of Biology
2nd Edition
ISBN: 9781259875120
Author: Robert Brooker, Eric P. Widmaier Dr., Linda Graham Dr. Ph.D., Peter Stiling Dr. Ph.D.
Publisher: McGraw-Hill Education
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Textbook Question
Chapter 8.5, Problem 1BC
Look ahead to Figures 13.9 and, in particular, 13.10. Certain mutations alter the structure of the Ras protein so if will not hydrolyze GTR Such mutations cause cancer. Explain why.
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Describe the common signal transduction event that is perturbed by cancer-promoting mutations in the genes encoding RAS and NF-1. Why are mutations in RAS more commonly found in cancers than mutations in NF-1?
Mutations that inactivate p53 have a recessive phenotype, whereas mutations affecting Ras are dominant. Explain the difference.
We saw that most cancer mutations in the ras/mapk pathway occur upstream of mapk rather than in mapk itself. what might be a reason for that?
Chapter 8 Solutions
Principles of Biology
Ch. 8.1 - What is the signaling molecule in this example?Ch. 8.1 - Prob. 2CCCh. 8.1 - Prob. 3CCCh. 8.1 - A general reason for cell signaling is to respond...Ch. 8.1 - Prob. 2TYKCh. 8.1 - Prob. 3TYKCh. 8.2 - Prob. 1BCCh. 8.2 - Prob. 1TYKCh. 8.2 - Prob. 2TYKCh. 8.3 - Prob. 1CC
Ch. 8.3 - What has to happen for the a and subunits of the...Ch. 8.3 - Prob. 1TYKCh. 8.3 - After a G-protein-coupled receptor is activated,...Ch. 8.4 - Prob. 1TYKCh. 8.5 - Look ahead to Figures 13.9 and, in particular,...Ch. 8.5 - Prob. 1TYKCh. 8.5 - Prob. 2TYKCh. 8.6 - Prob. 1CCCh. 8.6 - Prob. 2CCCh. 8.6 - Prob. 3CCCh. 8.6 - Prob. 1TYKCh. 8.6 - Prob. 2TYKCh. 8 - Prob. 1TYCh. 8 - Prob. 2TYCh. 8 - Prob. 3TYCh. 8 - Prob. 4TYCh. 8 - Which of the following is not an example of a cell...Ch. 8 - Prob. 6TYCh. 8 - The EGF receptor functions as a receptor tyrosine...Ch. 8 - Prob. 8TYCh. 8 - Prob. 9TYCh. 8 - The benefit of second messengers in signal...Ch. 8 - Prob. 1CCQCh. 8 - Prob. 2CCQCh. 8 - Prob. 3CCQCh. 8 - Discuss and compare several different types of...Ch. 8 - Prob. 2CBQ
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- what are the rolls that the p53 gene and RAS protein take on when trying to stop a cancer cell from further replicating. Also, what would happen if a mutation were to occur in both genes?arrow_forwardWe have studied Ras signal transduction pathway. In an experiment, two different mutations were produced using different chemicals. The proteins with mutation are listed below. State what will be the effect of each mutation and explain whether it will result in cell proliferation or not. GEF protein GTPasearrow_forwardHow would a mutation that prevents the Ras proteinfrom hydrolyzing GTP affect the cell-signaling pathway in 25.11?arrow_forward
- Do you think there are more unique alleles of p53 that lead to cancer or more unique alleles of Ras that lead to cancer? Please explain.arrow_forwardWhich of the following defects in RAS would be tumorigenic? multiple answers A. Deletion of nucleotide binding domain B. Inactivation of Guanine Exchange Factor (GEF) C. Mutation at amino acid 61 that prevents hydrolysis of bound GTP D. Inactivation of GTPase Protein (GAPS) E. Mutation that prevents binding of GTParrow_forwardWhich of the following mutations would produce a form of the Ras protein that would be more difficult to inactivate than normal Ras? Briefly explain your reasoning.(i) A mutation that allows Ras to cleave (hydrolyze) GTP more rapidly than usual(ii) A mutation that causes Ras to bind Ras-GAP more tightly than usual(iii) A mutation that causes Ras to cleave (hydrolyze) GTP more slowly than usualarrow_forward
- A mutation in the Ras protein renders Ras constitutively active (RasD). What is constitutive activation?arrow_forwardIntitial analysis of a human colon cancer tumor indicates mutations/defects in APC, B-Raf and p53. Which of the genes below is also most likely mutated in this tumor (select one)? A. Beta-catenin B. K-RAS C. SMAD4 D. MDM2 E. p14 ARFarrow_forwardBased on Figure 17-35, write a sentence stating howtranslocation can lead to cancer. Can you think of another genetic cause of cancer?arrow_forward
- A second hit might occur through epigenetic modification. There is a CpG island in the RB1 promoter. What epigenetic modification is associated with CpG islands? What does this type of modification usually do to gene expression? How could this CpG island/this epigenetic modification be related toRB1 expression and retinoblastoma?arrow_forwardwhat protein is phosphorylated by Raf in the Ras/MAP kinase signal transduction cascade? I put ERK2 and ERK1 but was partially incorrect, what was the part I messed up on that would be correct? I know that one of the two is there but correct me if i'm wrongarrow_forwardThis data shows the efficacy of different treatments on the survival rates of patients with glioblastomas, as well as methylated, and on methylated MGMT promoters. A. Explain the trends in the figure B. Relate MGMT methylation to the central dogma/flow of genetic information, and how genes are expressed. arrow_forward
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