Given what you have learned about tumor suppressors and proto-oncogenes, predict whether the following genes are likely to be tumor suppressors or proto-oncogenes. An inhibitory protein of a Cdk is likely to be a [Select] Ras is likely to be a [Select] The RTK in the MAP kinase pathway is likely to be a [Select] the MAP kinase pathway covered in Topic 6]. Protein A is a transcription factor that normally activates the expression of genes needed for S- phase. The inhibitor of protein A is likely to be a [Select] [Hint: review

Given what you have learned about tumor suppressors and proto-oncogenes, predict whether the following genes are likely to be tumor suppressors or proto-oncogenes. An inhibitory protein of a Cdk is likely to be a [Select] Ras is likely to be a [Select] The RTK in the MAP kinase pathway is likely to be a [Select] the MAP kinase pathway covered in Topic 6]. Protein A is a transcription factor that normally activates the expression of genes needed for S- phase. The inhibitor of protein A is likely to be a [Select] [Hint: review

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 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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Figure 9.10 In certain cancers, the GTPase activity of the RAS G-protein is inhibited. This means that the RAS protein can no longer hydrolyze GTP into GDP What effect would this have on downstream cellular events?
I 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.
A temperature-sensitive mutant yeast strain stops dividing when shifted from 25°C to 37°C. These cells are analyzed at different temperatures by a machine that measures the amount of DNA they contain, and the following graphs are obtained. number of cells number of cells [ Select] [Select] [Select] 25°C [Select] مل Cells in G1 phase should have [Select] Which of the following would explain the behavior of your mutant? Mark yes or no for each of the following choices. 2 amount of DNA/cell (arbitrary units) 37°C 1 2 amount of DNA/cell (arbitrary units) unit(s) amount of DNA. ✓ Inability to initiate DNA replication Defect in chromosome condensation ✓Defect in centrosome duplication ✓Defect in cytokinesis
Signaling pathways often require receptor dimers to become active. What would be an advantage of the extrinsic apoptosis pathway requiring a trimer? I note from the article "Nature Reviews, Cancer 16:539, 2016" the following: The extrinsic apoptotic pathway, upon binding to their cognate ligand, death receptors such as tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor (TRAILR) and FAS can activate initiator caspases (caspase-8 and caspase-10) through dimerization mediated by adaptor proteins such as FAS-associated death domain protein (FADD). Active caspase-8 and caspase-10 then cleave and activate the effector caspase-3 and caspase-7, leading to apoptosis. I can't think of any other pathway that uses a trimer, so there must be a reason. Glad an exprt can help.
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
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…
In a patient with a constitutively active receptor tyrosine kinase that increases the activity of PI3K, the administration of a drug that increases PTEN expression will likely inhibit tumorigenesis because; Group of answer choices PTEN prevents growth factor binding to RTK PTEN competitively inhibits the catalytic subunit of PI3K PTEN dephosphorylates PIP3 PTEN inhibits the dimerization of the regulatory subunit of RTKs
You established two cell lines (Cell line X and Cell line Y) from colon cancer patients and both of them can proliferate without the Wnt ligand. When you analyze the tumor suppressor APC (Adenomatous Polyposis Coli) protein in these lines, X does not express functional APC but Y expresses functional APC. How can Y keep proliferating without Wnt? Which function (protein) within the Wnt signaling pathway might be defective in Y?
The best strategy for treating a specific type of human tumor can depend on identifying the type of cell that became cancerous to give rise to the tumor. For some tumors that have colonized a distant location (metastasized), identifying the parental cell type can be difficult. Because the type of IF protein expressed is cell-type-specific, using monoclonal antibodies that react with only one type of IF protein can help in this identification. What IF proteins would you produce monoclonal antibodies against to identify (a) a sarcoma of muscle cell origin, (b) an epithelial cell carcinoma, and (c) an astrocytoma (glial cell tumor)?
BCL2 binds to and inactivates BAX and other pro-apoptotic proteins, thereby inhibiting apoptosis. Venetoclax has been approved for marketing in patients with chronic lymphocytic leukemia (CLL) Venetoclax is a highly selective BCL2 inhibitor that disrupts the interaction of this protein with BH3 domain proteins thereby permitting apoptosis. Proapoptotic Proapoptotic proteins protein binds to BCL2 BCL2 Venetoclax Venetoclax displaces proapoptotic proteins BCL2 Venetoclax Proapoptotic proteins No venetoclax binding BCL2 Glys01Val mutation Which of the following can you conclude from this information? Select all that apply Bcl2- mutations that prevent Ventoclax binding promote cell survival Venetoclax binding to Bcl2 promotes cell survival . Venetoclax binding to Bcl2 promotes cell death Proapoptotic protein binding to Bcl2 promotes cell survival
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.
What is the most likely outcome is we lose the tumor suppressor proteins, cyclin- dependent kinase inhibitors. Select one: o a. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will not proceed. o b. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will not proceed. o c. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will proceed. o d. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will proceed.