Two mechanisms inducing Apoptosis, Extrinsic pathway and Intrinsic pathway, have difference and similarity. a What is the key protein that both pathway uses? b How can intrinsic pathway be initiated and what molecule is critical for that?
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A: To answer this question we should have knowledge about Cell biology.
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- 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?Imagine that you created a cell that over-expresses a truncated version of its extrinsic pathway initiator caspase. This protein contains the caspase's DED, but none of the caspase's protease domains. This truncated version is present as an extra copy in addition to the WT copy. In 1-2 sentences, explain what the outcome would be on extrinsic apoptosis (i.e. would it be a positive/negative regulator/have no effect) and why.A current focus of molecular medicine is to trigger or promote apoptosis of specific cells. several components of the apoptotic pathways are being targeted using this approach. for each of the following, state specifically how the treatment would be expected to stimulate or inhbit apoptosis. b. exposing cells to recombinant TRAIL protein, a ligand for thr tumor necrosis factor family of receptors
- A current focus of molecular medicine is to trigger or promote apoptosis of specific cells. several components of the apoptotic pathways are being targeted using this approach. for following, state specifically how the treatment would be expected to stimulate or inhibit apoptosis. c. Treatment of cells with organic compounds that enter the cell and bind with high affinity to the active site of Caspase-3Overexpression of the Myc protein is a common feature of many types of cancer cells, contributing to their excessive cell growth and proliferation. By contrast, when Myc is overexpressed in most normal cells, the result is not excessive proliferation, but cell-cycle arrest or apoptosis.Which one of the following statements provides the most likely explanation for why overexpression of Myc can have such different outcomes in normal cells and in cancer cells? A. Normal cells contain checks and balances that prevent Myc-induced proliferation. B. In normal cells, Myc protein acts as a mediator in cell-cycle arrest and apoptosis. C. The target protein for Myc-induced proliferation is missing from most normal cells. D. In normal cells, when Myc is overexpressed, the excess Myc protein precipitates.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?
- Compare and contrast the intrinsic and extrinsic apoptosis pathways. Please keep brief - 3 sentences/dot points each.Which component of cell division machinery is frequently targeted by anti-cancer drugs? Can you explain the common side-effects of chemotherapy (e.g. hair loss, mucositis) based on this information?If somatic tumors cause local regions in their vicinity to have an increased pOH, how is this strategic for the survival of the tumor? Select one: a. It allows the increased hydroxide concentrations to cause a conformational change in nearby hemoglobin to the R state so that ample oxygen is deposited for tumor growth. b. It allows the increased proton concentrations to cause a conformational change in nearby hemoglobin to the R state so that ample oxygen is deposited for tumor growth. c. It allows the increased proton concentrations to cause a conformational change in nearby hemoglobin to the T state so that ample oxygen is deposited for tumor growth. d. It allows the increased hydroxide concentrations to cause a conformational change in nearby hemoglobin to the T state so that ample oxygen is deposited for tumor growth. e. None of these.
- 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…Dr. Jace is a research officer in a laboratory that studies anticancer treatment. She is interested to test a plant extract for its apoptosis-inducing effect on colon cancer cells. After incubating the cells with the extracts, she is using the FITC Annexin V Apoptosis Detection Kit I by BD Biosciences for her apoptotic assay. Discuss the detection of apoptosis using this kit and include the utilization of flow cytometry in her experiment.How does p53 induce apoptosis? How does the cell determine what "too much" damage is? Meaning, how can it tell if the damage to the DNA is too severe to fix in order for the cell to move on to S phase? Thank you.