Campbell Biology in Focus
3rd Edition
ISBN: 9780134710679
Author: Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Rebecca Orr
Publisher: PEARSON
expand_more
expand_more
format_list_bulleted
Videos
Question
Chapter 16.3, Problem 1CC
Summary Introduction
To discuss:
How mutation in protein coding genes functioning in apoptosis can lead to cancer.
Introduction:
Apoptosis is defined as the programmed cell death (PCD). It is a process, which only occurs in multi-cellular organisms. The cells undergoing PCD include blebbing, fragmentation of DNA (deoxyribonucleic acid), cell shrinkage, and engulfment by the phagocytes.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solution
Students have asked these similar questions
Explain how p53 functions as a tumor suppressor gene. How can mutations in p53 lead to cancer, and how might gene therapy or other drug interventions inhibit the growth of a tumor?
. MAKE CONNECTIONS The p53 protein can activategenes involved in apoptosis. Review Concept 11.5, anddiscuss how mutations in genes coding for proteins thatfunction in apoptosis could contribute to cancer.
D)
The level of carbon dioxide increases with the level of available oxygen.
60)
The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome,
this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing
t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches
directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self-
destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be
repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis.
Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice
correctly predict if the cell will become cancerous and why?
No, the cell will not…
Chapter 16 Solutions
Campbell Biology in Focus
Ch. 16.1 - Prob. 1CCCh. 16.1 - MAKE CONNECTIONS Explain how the signaling...Ch. 16.1 - How do fruit fly maternal effect genes determine...Ch. 16.2 - Prob. 1CCCh. 16.2 - Deitys egg donor and surrogate mother were...Ch. 16.2 - Prob. 3CCCh. 16.3 - Prob. 1CCCh. 16.3 - Prob. 2CCCh. 16.3 - Prob. 3CCCh. 16 - Muscle cells differ from nerve cells mainly...
Ch. 16 - Cell differentiation always involves A. the...Ch. 16 - Prob. 3TYUCh. 16 - Absence of bicoid mRNA from a Drosophila egg leads...Ch. 16 - Prob. 5TYUCh. 16 - Prob. 6TYUCh. 16 - Prob. 7TYUCh. 16 - FOCUS ON ORGANIZA-ION The property of life emerges...Ch. 16 - SYNTHESIZE YOUR K\IOWLEDGE Recently, new...
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
- Describe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?arrow_forwardTumor suppressor proteins can assist in slowing down the cell cycle under appropriate conditions. In humans, the TP53 gene encodes a tumor suppressor called p53. Most mutations in the TP53 gene result in a mutant form of p53 that can no longer function to slow down the cell cycle, which can lead to a cell becoming cancerous. However, some mutant forms of p53 actually possess the ability to increase a cell's resistance to anticancer treatments. Which of the following BEST describes the latter type of mutation? loss-of-function mutation gain-of-function mutation suppressor mutation reverse mutationarrow_forwardDescribe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.arrow_forward
- Describe how Ras and p53 can alter the simplified genetic pathway controlling cell division shown below. For each of the two genes, would uncontrolled cell division result from a loss-of-function or a gain-of-function mutation? growth factors - receptors - cyclins - cyclin-dependent kinases - cell divisionarrow_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. eg Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will…arrow_forwardDiscuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle. Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.arrow_forward
- List the regulatory mechanisms that might be lost in a cell producing faulty p53.arrow_forwardThe p53 gene encodes a tumor-suppressor protein, p53, which acts as a transcription factor for several genes. Discuss an example of a specific gene that is activated by p53 and how this gene activation will lead to a pause in the cell cycle for DNA repair to take place.arrow_forward#9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #2) When cancer cells have not spread beyond its original site, the term used to describe it is benign growth intraepithelial neoplasia carcinoma stage 3 carcinoma in sit #10) Single or double stranded breaks in DNA activate Chk 1 and 2 kinases, which phosphorylates p53. This results in --- in the level of p53 in the cell. increase decrease please answer them all. they are very short and won't take your time. Thank you in advance.arrow_forward
- How can a defect in p53 gene contribute to cancer development?arrow_forwardExplain the role of p53 protein in protecting normal cells against cancer. With respect to this protein and its function, explain how a normal cell turns cancerous.arrow_forwardHow can the role of epigenetics in cancer be reconciled with the idea that cancer is caused by the accumulation of genetic mutations in tumor-suppressor genes and proto-oncogenes?arrow_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
What are Mutations and what are the different types of Mutations?; Author: Science ABC;https://www.youtube.com/watch?v=I16YlE8qTBU;License: Standard youtube license