We have studied Ras signal transduction pathway. In an experiment, two different mutations were produced using different chemicals. The proteins with mutation are listed below. State what will be the effect of each mutation and explain whether it will result in cell proliferation or not. GEF protein GTPase

We have studied Ras signal transduction pathway. In an experiment, two different mutations were produced using different chemicals. The proteins with mutation are listed below. State what will be the effect of each mutation and explain whether it will result in cell proliferation or not. GEF protein GTPase

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 2VCQ: Figure 9.10 In certain cancers, the GTPase activity of the RAS G-protein is inhibited. This means...

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Cancers are often caused by overactive growth factor receptor signaling (remember growth factor receptors are enzyme-linked receptor pathways). If you were able to use gene therapy to overexpress a particular protein in a cancer cell, which of the following might be useful to overexpress in order to combatt cancer? a GAP that acts on Ras a phosphatase that acts on GPCR a protein that enhances the activity of Akt a ubiqtuin ligase that acts on the MAPK phophatase
5) Briefly explain why the formation of a tumour can pose a risk to a person's homeostasis. 6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug "vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief…
Part of the Ras protein is associated with the plasma membrane, and part extends into the cytoplasm. How does the Ras protein transmit a signal from outside the cell into the cytoplasm? What happens in cases where the ras gene is mutated?
See 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 сок
siRNAs are used to “knockdown” gene expression in research. Imagine you are a scientist who hopes to study several genes related to cancer. Select all the scenarios you will be able to successfully use RNA interference with the use of siRNAs (select all that apply): Group of answer choices Regulate transcript levels by targeting the siRNA to core promoter regions (e.g. TATA box) of tumor suppressor genes Regulate transcript levels by targeting the siRNA to the regulatory promoter regions (e.g. enhancers) of tumor suppressor genes Regulate transcript levels by targeting the siRNA to any region of the processed mRNA Regulate transcript levels by targeting the siRNA to the 5’ UTR of the processed mRNA Regulate transcript levels by targeting the siRNA to the 3’ UTR of the processed mRNA Regulate transcript levels by targeting the siRNA to sites where the histone acetyl transferase will acetylate the histones Regulate transcript levels by targeting the siRNA to where the start…
See 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.
6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. - In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug “vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief explanation: 19
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Describe the common signal transduction event that is perturbed by cancer-promoting mutations in the genes encoding RAS and NF-1. Why are mutations in RAS more commonly found in cancers than mutations in NF-1?
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