Essentials of Genetics (9th Edition) - Standalone book
9th Edition
ISBN: 9780134047799
Author: William S. Klug, Michael R. Cummings, Charlotte A. Spencer, Michael A. Palladino
Publisher: PEARSON
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Chapter 16, Problem 10PDQ
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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.
The 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.
The output of RTK pathways is often the activation of MAP Kinase. Explain how MAPK
can lead to activation of a specific subset of proteins, leading to distinct effects in different
cell types in response to the same growth signal.
Chapter 16 Solutions
Essentials of Genetics (9th Edition) - Standalone book
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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Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- Drug A323 inhibits the activity of the cyclin-dependent kinase (CDK) - G1 cyclin complex. Consider possible effects of the drug on the cell cycle of normal and malignant cells. Predict what is likely to happen if the drug is added to the cell types described in A). Motivate your answers and describe the role of cycle-regulatory pathways that are relevant with respect to the action. of drug A323. A) Carcinoma cells in which both allels of the Rb gene carries loss of function mutation.arrow_forwardI just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.arrow_forwardThe expression patterns as well as activation of different types of CDKs happen at different stages of the cell cycle. Explain why.arrow_forward
- Describe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.arrow_forwardCell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.arrow_forwardThe retinoblastoma protein (RB) suppresses human cell division by arresting cells in the G₁ phase of the cell cycle and preventing progression to the next phase. It accomplishes this task by binding to another protein, E2F, a transcription factor needed for further progression through the cell cycle. Normal progression through the cell cycle is accomplished when cyclin-dependent kinases (CDKs) phosphorylate RB, preventing its binding to E2F. Many viruses can induce abnormal exit from G, using viral proteins that bind to RB at a motif at the N-terminal called LXCXE. An example is the E7 papilloma protein, which causes the excessive proliferation of cells in warts. The site at which LXCXE proteins bind is called the pocket domain and is highly conserved on RB and related proteins in plants and animals. The configuration of the pocket domain is well established. Mutant experimental RB proteins are available with alterations in the conserved amino acids of the pocket domain. A simple…arrow_forward
- The retinoblastoma protein (RB) suppresses human cell division by arresting cells in the G₁ phase of the cell cycle and preventing progression to the next phase. It accomplishes this task by binding to another protein, E2F, a transcription factor needed for further progression through the cell cycle. Normal progression through the cell cycle is accomplished when cyclin-dependent kinases (CDKs) phosphorylate RB, preventing its binding to E2F. Many viruses can induce abnormal exit from G, using viral proteins that bind to RB at a motif at the N-terminal called LXCXE. An example is the E7 papilloma protein, which causes the excessive proliferation of cells in warts. The site at which LXCXE proteins bind is called the pocket domain and is highly conserved on RB and related proteins in plants and animals. The configuration of the pocket domain is well established. Mutant experimental RB proteins are available with alterations in the conserved amino acids of the pocket domain. A simple…arrow_forwardAlthough numerous treatments are available for advanced hormone receptor- positive (HR+) and human epidermal growth factor receptor 2 negative (HER2-) breast cancers, they are rarely curable. Drugs such as palbociclib that inhibit cyclin-dependent kinase 4 and 6 (CDK4/6) are rapidly altering this therapeutic environment. Discuss the function of CDK4 and CDK6 in promoting cell growth as well as the overall effects of their inhibition by palbociclib on the progression of the cell cycle.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
- Notch signaling orchestrates transition from G1 to S phase of cell cycle by multiple other interactions that target the G1/S checkpoint machinery. This is a highly conserved pathway that is seen across multiple kingdoms of life and the ligands involved in notch signaling are typically membrane-bound proteins. This suggests that: -This pathway relies on hormone interactions via endocrine pathways -This pathway relies on signal propagation via paracrine molecules -This pathway relies on direct signaling across gap junctions -This pathway relies on cell binding via autocrine signalingarrow_forwardAfter a cell "clears" the G₁ restriction checkpoint, it can proceed into S phase. This S phase entry is achieved by a cyclin dependent kinase (Cdk2) and its cyclin (Cyclin E), but additionally requires the action of a protein kinase (CDC2) as well as a phosphatase (CDC25) enzyme. Explain how these 4 proteins work together to orchestrate S phase entry.arrow_forwardCancer cells typically lose cell cycle entry control. Explain how the following mutations, which are found in some cancer cells, lead to a bypass of these controls: (a) overexpression of cyclin D, (b) loss of Rb function, (c) loss of p16 function, (d) hyperactive E2F.arrow_forward
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