Campbell Biology (10th Edition)
10th Edition
ISBN: 9780321775658
Author: Jane B. Reece, Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Robert B. Jackson
Publisher: PEARSON
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Chapter 18.5, Problem 1CC
MAKE CONNECTIONS Ø The p53 protein can activate genes involved in apoptosis. Review Concept 11.5, and discuss how mutations in genes coding for proteins that function in apoptosis could contribute to cancer.
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Describe the molecular mechanisms involved in P53’s role as a tumor repressor protein.
illustrate some of the molecular mechanisms leading from loss-of-function mutations in tumor-suppressor genes to increased predispositions to cancer?
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?
Chapter 18 Solutions
Campbell Biology (10th Edition)
Ch. 18.1 - How does binding of the trp corepressor to the trp...Ch. 18.1 - Describe the binding of RNA Polymerase,...Ch. 18.1 - WHAT IF? A certain mutation in E. coli changes...Ch. 18.2 - In general, what are the effects of histone...Ch. 18.2 - Compare the roles of general and specific...Ch. 18.2 - WHAT IF? Suppose you compared the nucleotide...Ch. 18.2 - Once mRNA encoding a particular protein reaches...Ch. 18.3 - Compare miRNAs and siRNAs, including their...Ch. 18.3 - WH AT IF? Suppose the mRNA being degraded in...Ch. 18.4 - MAKE CONNECTIONS As you learned in Chapter 12,...
Ch. 18.4 - MAKE CONNECTIONS Explain how the signaling...Ch. 18.4 - How do fruit fly maternal effect genes determine...Ch. 18.4 - Prob. 4CCCh. 18.5 - MAKE CONNECTIONS The p53 protein can activate...Ch. 18.5 - Under what circumstances is cancer considered to...Ch. 18.5 - Prob. 3CCCh. 18 - Compare and contrast the roles of a corepressor...Ch. 18 - Describe what must happen in a cell for a gene...Ch. 18 - Why are miRNAs called noncoding RNAs? Explsin how...Ch. 18 - Describe the two main processes that cause...Ch. 18 - Compare the usual functions of proteins encoded by...Ch. 18 - If a particular operon encodes enzymes for making...Ch. 18 - Muscle cells differ from nerve cells mainly...Ch. 18 - The functioning of enhancers is an example of (A)...Ch. 18 - Cell differentiation always involves (A)...Ch. 18 - Which of the following is an example of...Ch. 18 - What would occur if the repressor of an inducible...Ch. 18 - Absence of bicoid in mRNA from a Drosophila egg...Ch. 18 - Which of the following statements about the DNA in...Ch. 18 - Within a cell, the amount of protein made using a...Ch. 18 - Prob. 10TYUCh. 18 - Prob. 11TYUCh. 18 - Prob. 12TYUCh. 18 - Prob. 13TYUCh. 18 - Prob. 14TYUCh. 18 - WRITE ABOUT A THEME: INTERACTIONS In a Short essay...Ch. 18 - SYNTHESIZE YOUR KNOWLEDGE The flashlight fish has...
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- 1. True or Flase: Cells must only divide when they receive a signal to divide. 2. BRCA1 is a gene that codes for a tumor suppressor protein. If a person inherits a mutation in BRCA1, it greatly increases his or her risk of developing breast cancer. Are the cancer-causing mutations in the BRCA1 gene more likely to: a) increase expression of the gene b)decrease expression of the gene c)not affect the expression of the genearrow_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_forwardDescribe 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_forward
- p53 iš an important tumor suppressor gene that is activated in response to a variety of stress signals. Upon activation it induces a cell cycle arrest or cell death. Hence, loss-of-function mutations in the p53 gene are found in almost every type of cancer. How do you predict loss-of-function mutations in the DNA binding domain of the p53 protein affect its function? OIt no longer will act as activator of gene expression O It no longer will act as repressor of gene expression O It no longer will act as activator or repressor of gene expression O It no longer will act as coactivator or corepressorarrow_forwardDescribe error prone polymerases and the process of translesion synthesis (TLS). In regards to tumor biology, what is the mutator phenotype hypothesis? What are some ways in which error-prone polymerases could be targeted for potential anti-cancer treatments?arrow_forwardFBBS 2 Worksheet 2 Name HINT: when you are explaining mechanisms affected by mutations, think about molecular interactions, or enzymatic functions, or conformational changes that are involved in the normal pathways, since these are the aspects most likely to be affected by mutations or drugs, or viral proteins. If a consequence of a mutation/drug/virus results in a cdk being more frequently active, then the cell cycle will proceed at the given checkpoint. If the consequence of a mutation/drug/virus results in a cdk being inactivated or inhibited, then the cell cycle is stopped at the given checkpoint. cdc2 kinase Inactive 1) Given the following diagram of a mechanism regulating the cell cycle of the fission yeast S. pombe. Interphase (G₂) CAK Wee1 Cyclin Thr161-P Tyr15-P cdc2 kinase Cyclin Inactive Thr161-P cdc25 G₂ fission yeast cell cdc2 kinase Cyclin Active Interphase (G₁) Post-mitotic fission yeast cells Date cdc2 kinase Dr. Milani Inactive Cyclin Degradation A) Predict the…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_forwardexamine the process of gene expression. Include the following: Explain the regulation of gene expression in eukaryotic cells. Discuss mechanisms by which gene expression may be altered. How do these alterations induce cancer-causing mutations in cell DNA? Explain how cancer is formed. Describe genetic changes found in cancer cells and how these changes lead to alterations in cell behavior. Determine whether proteome data can be utilized in genetic disorder diagnosis. Relate the Human Genome Project data to the analysis of cancer genes. Relates the Human Genome Project's utility in pharmacogenomics and personalized medicine to diagnose and treat cancerarrow_forwardEssay: Relate the structure of the DNA to its role as a molecule for inheritance. Elaborate on the significance of DNA Describe the molecular mechanisms involved in P53’srole as a tumor repressor protein packaging in the inheritance and transmission of traits.arrow_forward
- Why is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.arrow_forwardD) 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…arrow_forwardExplain 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?arrow_forward
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