EBK ESSENTIALS OF GENETICS
9th Edition
ISBN: 8220102741614
Author: Palladino
Publisher: YUZU
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Chapter 16, Problem 10PDQ
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Chapter 16 Solutions
EBK ESSENTIALS OF GENETICS
Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 - HOW DO WE KNOW? In this chapter, we focused on...Ch. 16 -
2. Review the Chapter Concepts list on page 307....Ch. 16 - What is the relationship between signal...Ch. 16 - Where are the major regulatory points in the cell...Ch. 16 -
5. Describe kinases and cyclins. How do they...Ch. 16 - (a) How does pRB function to keep cells at the G1...Ch. 16 - What is the difference between saying that cancer...
Ch. 16 -
8. What is apoptosis, and under what...Ch. 16 - Define tumor-suppressor genes. Why is a mutation...Ch. 16 - A genetic variant of the retinoblastoma protein,...Ch. 16 -
11. Part of the Ras protein is associated with...Ch. 16 - If a cell suffers damage to its DNA while in S...Ch. 16 - Prob. 13PDQCh. 16 - Prob. 14PDQCh. 16 - Prob. 15PDQCh. 16 - Prob. 16PDQCh. 16 - Prob. 17PDQCh. 16 - How do normal cells protect themselves from...Ch. 16 - Prob. 19PDQCh. 16 - Explain how environmental agents such as chemicals...Ch. 16 - Radiotherapy (treatment with ionizing radiation)...Ch. 16 - Genetic tests that detect mutations in the BRCA1...Ch. 16 - Prob. 23PDQCh. 16 - Prob. 24PDQCh. 16 - Prob. 25PDQCh. 16 - Prob. 26PDQCh. 16 - Prob. 27PDQCh. 16 - Prob. 28PDQ
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- why are Rb ans other negatively protiens that regulate the cell cycle called tumar supressors?arrow_forwardThe expression patterns as well as activation of different types of CDKs happen at different stages of the cell cycle. Explain why.arrow_forwardWhat is the effect of having fluctuating cyclin levels throughout the cell cycle, while the levels of its corresponding cyclin dependent kinase stay relatively constant? Explain.arrow_forward
- The tumor suppressor pRB also binds to and suppresses theactivity of retinoblastoma binding protein 2 (RBP2), ahistone demethylase that removes methyl groups from diand trimethylated lysines in histone 3. What is the possibleconsequence of an inactivating mutation in RB1 that causesan inability of pRB to bind RBP2?arrow_forwardThe retinoblastoma tumor suppressor gene Rb (RB1) codes forthe retinoblastoma protein (pRB). pRB prevents the progression of the cell cycle through G1 if DNA has been damaged. Itdoes so in part because it binds a transcription-activatingdimer referred to as E2F-DP. The pRB-E2F/DP complex recruits a histone deacetylase to chromatin. Explain.arrow_forwardWhy doesn't Cdk1 active immediately upon binding to cyclin B? What other components of the cell’s regulatory machinery could explain the delay in activation of the kinase activity?arrow_forward
- Cancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.arrow_forwardThe destruction of the various cyclins is commonly used to inactivate the Cdk/cyclin complexes. Why is it advantageous to inactivate these complexes via protein destruction instead of some other method that does not require the re-synthesis of a cyclin protein the next time the cell divides?arrow_forwardMaturation promoting factor, MPF, is a cyclin-CDK complex that catalyzes the phosphorylation of other proteins to start mitosis. The activity level of MPF is dependent on the relative concentrations of the cyclin and CDK components of MPF (Figure 1). Based on Figure 1, which of the following describes the role of cyclin in the regulation of the cell cycle? a.During S phase, the cyclin level remains the same because DNA replication is occurring. b.During G2 phase, the cyclin level remains low, causing MPF activity to decrease, which leads cells to initiate mitosis. c.During G1 phase, the cyclin level decreases to signal the start of the resting phase of the cell cycle. d.During M phase, the cyclin level peaks, resulting in an increased binding frequency with CDK.arrow_forward
- Overexpression of the Myc protein is a common feature of many types of cancer cells, contributing to their excessive cell growth and proliferation. By contrast, when Myc is overexpressed in most normal cells, the result is not excessive proliferation, but cell-cycle arrest or apoptosis.Which one of the following statements provides the most likely explanation for why overexpression of Myc can have such different outcomes in normal cells and in cancer cells? A. Normal cells contain checks and balances that prevent Myc-induced proliferation. B. In normal cells, Myc protein acts as a mediator in cell-cycle arrest and apoptosis. C. The target protein for Myc-induced proliferation is missing from most normal cells. D. In normal cells, when Myc is overexpressed, the excess Myc protein precipitates.arrow_forwardAfter the initial Actualization of the Cit+ phenotype, there was another alteration to the A-3 genome that resulted in increased growth (e.g. Refinement). What explained the increase in growth rate in response to Refinement? A. Increase number of transporters localized to the plasma membrane. B. Increased ability to metabolize glucose. C. Increased citric acid cycle activity. D. Altered promoter activity resulting in constitutive gene expression.arrow_forward(a) the cell cycle is divided into different phases (referred to as M, G0, G1, S and G2); Can you account for what happens during the different parts of the cycle and out of it is checked? ( b) What is the difference between apoptosis and necrosis? ( c) What are caspases and what is their function in the cell?arrow_forward
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