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- 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.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…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.
- 1) One cell-signaling pathway implicated in the regulation of cell division is the mTOR/Akt pathway. mTOR is a protein that stimulates the translation of other proteins, which is an important requirement for cell division. In the absence of growth factor signals from the cell's environment, the proteins TSC1 and TSC2 will physically bind to each other, which allows them to inhibit mTOR from functioning. However, when membrane receptors do encounter certain growth factors from the environment, they will result in the activation of a protein called Akt. Once activated, Akt will phosphorylate TSC2, preventing it from being able to physically bind to TSC1. a) In the description of the cellular signaling pathway above, four genes and their respective encoded proteins were mentioned: TSC1, TSC2, mTOR, and Akt, In the table below, identify which of these is/are acting as proto-oncogene (s), and which is/are acting as tumour suppressor(s) by writing the appropriate names in the correct column.…14)How does a compound that inhibits the GTPase activity of ras affect cell responses to growth factors? It would increase proliferation. It would increase glucose production. It would decrease glucose production. It would decrease proliferation.Tumor 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:
- 1a. Contrast the activation of cytokine receptors to the activation of receptor threonine kinases. b. We discovered a new cytokine that stimulates cancer cell growth. Now we want to determine if the JAK/STAT pathway is activated after stimulation. In the lab we have a small molecule that can competitively bind to SH2 domains. Explain where and how in the pathway this inhibitor would be effective.3) The “Met" receptor is a membrane receptor protein responsible for initiating signal transduction pathways that cause cells to divide, among other things. After the Met receptor has been stimulated by its specific growth factor, another protein called c- Cbl will bind to the Met receptor. C-Cbl will then attach a chain of small proteins called ubiquitin to the Met receptor. These chains of ubiquitin help the cell recognize that the Met receptor should undergo receptor-mediated endocytosis, which eventually leads to the destruction of the Met receptor. Circle any answer or answers that include mutations that could cause the cell to potentially become a cancer cell. A) a mutation causing there to be too much ubiquitin protein produced. B) a mutation causing c-Cbl to be inactivated. C) a mutation causing ubiquitin to be inactivated. D) a mutation causing there to be too few Met receptors produced. E) a mutation causing the Met receptor to no longer be able to bind to its growth factor.…(46) A mutated form of protein pox is found in patients with squamous cell carcinoma. In vitro studies show that the normal p5x molecule binds to DNA, and neoplastic cells accumulate in the G0 phase of the cell cycle. In contrast, the mutated form of p5x does not bind to DNA. These finding are most characteristics of which of the following? (A) Growht factor receptors (B) GTP-binding protein (C) Nonreceptor tyrosine kinases (D) Oncogene proteins (E) Tumor suppressor gene proteins
- For each of the following situations, provide a plausible explanation for how it could lead to unrestricted cell division.(a) Colon cancer cells often contain mutations in the gene encoding the prostaglandin E2 receptor. PGE2 is a growth factor required for the division of cells in the gastrointestinal tract.(b) Kaposi sarcoma, a common tumor in people with untreated AIDS, is caused by a virus carrying a gene for a protein similar to the chemokine receptors CXCR1 and CXCR2. Chemokines are cell-specific growth factors.(c) Adenovirus, a tumor virus, carries a gene for the protein E1A, which binds to the retinoblastoma protein, pRb. (d) An important feature of many oncogenes and tumor suppressor genes is their celltype specificity. For example, mutations in the PGE2 receptor are not typically found in lung tumors. Explain this observation. (Note that PGE2 acts through a GPCR in the plasma membrane.)Non-canonical Hedgehog signaling results in actin cytoskeleton rearrangements, leading to cellmovement and changes in cell shape. Describe how changes to the actin cytoskeleton lead to cellmovement and changes in cell shape.You do not need to draw out the signaling pathway again (#1b). Your answer should focus onthe changes to the actin cytoskeleton. Drawings will be helpful!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