Which of the following must occur for programmed cell death (apoptosis): 1. p53 must be stabilized 2. M-Cdk must be active 3. Caspases must be inactivated 4. There must be local inflammation
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Which of the following must occur for programmed cell death (apoptosis):
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- Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.# 3 You've engineered a mutant cell where the FADD adapter was truncated. The mutant FADD only contains the Death Domain, and lacks the Death Effector Domain. What is the most likely phenotypic outcome for this mutant cell when presented with the Fas ligand? 20 E O The Fas/FasL oligomer is formed, but apoptosis is blocked O The Fas/FasL oligomer is formed, and apoptosis is hyperactivated O The Fas/FasL oligomer is not formed, and apoptosis is blocked O The Fas/FasL oligomer is not formed, but apoptosis is hyperactivated F3 $ 4 DOD 000 R F4 % 5 F5 T BARAT 6 tv @ MacBook Air F6 Y & 7 F7 U * ➤11 8 F8 · 9 F9I 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.
- Nucleation of straight, single line microfilaments is mediated by which of the following? Rho GTPase and Formin Rho GTPase and Arp 2/3 Cdc42 GTPase and Arp2/3 OCdc42 GTPase and Formin 14 < PreviousTumor necrosis factor alpha (TNF-α) is an important cytokine used by immune cells to initiate and coordinate inflammatory responses. Inflammation is a key response to cell damage or infection, but can, in some diseases, spiral out of control and become more of a problem than the original cause (COVID-19 lung damage is a relevant example...). TNF-α receptors exist on many cell types. Let’s study the interaction between TNF-α (T) and its receptor (R), to form an activated complex C: T + R ↔ C A macrophage is measured to have ~105 TNF-α receptors on its surface. If the macrophage is immersed in a high concentration of TNF-α molecules (i.e. L0 ≅ L), how will the number of activated receptors change over time? Plot this trend for the case L0 =10 nM, kf=106 M-1 min-1, kr=0.1 min-1. There is constant ligand concentration and an initial condition of C0 = 0. We are given the constants needed to model the number of activated receptors over time and can use the following equation:You have two patients with pancreatic cancer. Patient 1 has a KRAS oncogenic mutation; a myc oncogenic mutation and has normal levels of P53. Patient 2 has normal KRAS expression: a myc oncogenic mutation and a tumor suppressor mutation in P53. You have the following therapeutics available Flavopiradol (a CDK inhibitor); CBP-93872 (a G2/M checkpoint inhibitor); Rigosertib; Oncorine; Nutlin a. Which patient would CBP-93872 be the most effective? Explain your answer. b. Which therapeutic(s) would not be expected to be effective in patient 2? For each, explain your answer
- 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 cytokinesisA cell begins to undergo apoptosis due to stress. Which of the following are true about this cell? (select all that apply) The cell can exit apoptosis if the stressful factor is removed The cell has high levels of p53. The cell's DNA will inevitably degrade The cell may undergo mitosis before completing apoptosisWhich of the following could be classified as an oncogene? None are possible oncogenes A mutant of MAP kinase that was active with or without being phosphorylated All are possible oncogenes A mutant of MEK with significantly reduced enzyme activity A mutant cAMP phosphodiesterase that made it super-active
- The P63 and P53 have similar functionalities in the cell, however, p53 is rarely associated directly with p63, suggesting that p63 may indirectly act as an oncogene by blocking p53 function. This hypothesis may also explain why p63 is associated with other indications of misinterpretation. I do understand the above statement, however once piece not clear – why would p63 block p53 function? Have these genes been shown to have opposing functions? From the background information provided above, it seems like they would have seminar functions. Explain.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…Genistein is a compound found in soybeans that is known to increase the expression of a protein called Bax in certain breast cancer cells. Outside of Cell Toxins TNF DNA Damage Tradd TraF2 p53 Fadd Bax Caspases Bd-2 IKB NF-KB Apoptosis Inside of Cell Based on the above diagram, would you expect ingestion of soybeans to promote, suppress or have no effect on the progression of breast cancer cells. Suppress progression of breast cancer cells Have no effect on progression of breast cancer cells Promote progression of breast cancer cells TNFR