Becker's World of the Cell (9th Edition)
9th Edition
ISBN: 9780321934925
Author: Jeff Hardin, Gregory Paul Bertoni
Publisher: PEARSON
expand_more
expand_more
format_list_bulleted
Videos
Textbook Question
Chapter 24, Problem 24.3CC
Cyclin D is part of the G1 Cdk-cyclin complex. Cyclin D is often overexpressed in cancers. Why would overexpression of cyclin D tend to cause cancer?
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solution
Students have asked these similar questions
The expression patterns as well as activation of different types of CDKs happen at different stages of the cell cycle. Explain why.
Changes in the activity of a variety of Cdks are essential for accurate progression through the cell cycle, and yet the levels of Cdk expression are fairly constant during the cell cycle. Briefly describe three mechanisms by which the activity of Cdks is regulated.
Explain why the continually active CDK will most likely change the normal cells into cancer cells.
Chapter 24 Solutions
Becker's World of the Cell (9th Edition)
Ch. 24 - Prob. 1QCh. 24 - Which DNA sequences are more alike: a pair of...Ch. 24 - Suppose you treat rapidly dividing tissue culture...Ch. 24 - Cyclin D is part of the G1 Cdk-cyclin complex....Ch. 24 - Both EGF (a mitogen) and TGF (when acting as an...Ch. 24 - A knockout mouse has been produced using the...Ch. 24 - Cell Cycle Phases. Indicate whether each of the...Ch. 24 - QUANTITATIVE The Mitotic Index and the Cell Cycle....Ch. 24 - Chromosome Movement in Mitosis. It is possible to...Ch. 24 - Cytokinesis. Predict what will happen in each of...
Knowledge Booster
Learn more about
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
- Relatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.arrow_forwardCancer-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_forwardWhat would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?arrow_forward
- (46) A mutated form of protein p5x is found in patients with squamous cell carcinoma. In vitro studies show that the normal p5x molecule binds to DNA, and neoplastic cells accumulate in the G0 phase of the cell cycle. In contrast, the mutated form of p5x does not bin d to DNA. These finding are most characteristics of which of the following? (A) Growht factor receptors (B) GTP-binding protein (C) Nonreceptor tyrosine kinases (D) Oncogene proteins (E) Tumor suppressor gene proteinsarrow_forwardWhat are cyclins and cyclin-dependent kinases for? Describe how do these factors affect cell proliferation.arrow_forward(46) A mutated form of protein pox is found in patients with squamous cell carcinoma. In vitro studies show that the normal p5x molecule binds to DNA, and neoplastic cells accumulate in the G0 phase of the cell cycle. In contrast, the mutated form of p5x does not bind to DNA. These finding are most characteristics of which of the following? (A) Growht factor receptors (B) GTP-binding protein (C) Nonreceptor tyrosine kinases (D) Oncogene proteins (E) Tumor suppressor gene proteinsarrow_forward
- 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?arrow_forwardSee 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 сокarrow_forwardSee 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.arrow_forward
- 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?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_forwardDescribe the roles of p53 and NFAT and their nuclear import. How does the phosphorylation regulate the nuclear import/export of Pho4? Propose an experiment to test this mechanismarrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSON
Biology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStax
Anatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education
Human Anatomy & Physiology (11th Edition)
Biology
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:PEARSON
Biology 2e
Biology
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:OpenStax
Anatomy & Physiology
Biology
ISBN:9781259398629
Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa Stouter
Publisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)
Biology
ISBN:9780815344322
Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter
Publisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & Physiology
Biology
ISBN:9781260159363
Author:Martin, Terry R., Prentice-craver, Cynthia
Publisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)
Biology
ISBN:9781260231700
Author:Sylvia S. Mader, Michael Windelspecht
Publisher:McGraw Hill Education
Cell Differentiation | Genetics | Biology | FuseSchool; Author: FuseSchool - Global Education;https://www.youtube.com/watch?v=gwAz_BtVuLA;License: Standard YouTube License, CC-BY