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Hedgehog - Cell signaling pathway
1) describe its normal function and mechanism, and 2) predict what may happen if certain proteins in the pathway become mutated to be constitutively active (activated even in the absence of the preceding step in the pathway) or inactivated. It will be clearest to include a drawing of the pathway.
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- 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.), create a simple flowchart depicting the MC1R pathway. There should be a minimum of five steps in the pathway. Be sure to include reception (protein binding to its ligand), a portion of the transduction pathway (what’s the intracellular reaction? What molecule works intracellularly?), and the cellular response (What’s produced from the cell?).Part A (Short Response): You are developing a TGF-β agonist, but you don’t yet know which specific proteins it is signaling through. You want to do a single Western blot to measure changes in signaling activity, regardless of which pathway is being activated. For which protein involved in these pathways could you measure the levels in the nucleus of cells and be confident in your results? Why? This part was already posted on chegg, but I didn't understand the answer. I need a thorough explanation, so I can fully understand. Part B (Short Response): There have been many attempts to block TGF-β signaling in cancer through many different mechanisms, but none of been very successful. Why do you think this is? I know they have gotten close to being successful, but I don't know what preventing their success.
- 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.The PYK gene codes for the expression of pyruvate kinase, which is one of the enzymestargeted for anti-cancer drug design. You have identified an RNAi that targets the mRNAof PYK gene. To study the effect of the RNAi towards pyruvate kinase, the respected RNAiis expressed in Saccharomyces cerevisiae. The level of pyruvate kinase can be detectedwith a fluorescent antibody.(a). Predict the result that you will obtain in recombinant S. cerevisiae that expresses therespected RNAi.(b). Compare the result in Q3a(i) with the wild-type S. cerevisiae.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…
- 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-3Describe 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.The MARCH-1 E3-ubiquitin ligase is expressed in B cells, dendritic cells, and macrophages. The pathway regulated by MARCH-1 is targeted by some pathogens in an immune evasion strategy. In this strategy, the pathogens encode: A protein that induces degradation of MARCH-1 A protein that mimics MARCH-1 and functions similarly A protein that binds to MARCH-1 and inhibits its function A protein that is induced by IL-10 in macrophages and dendritic cells A protein that induces degradation of CD86
- A mutant B cell line is examined by confocal microscopy after incubation with a microbial pathogen recognized by the BCR on these B cells. The B cells have been stained with antibodies to visualize the localization of polymerized actin and microtubules. As a control, wild-type B cells are examined. The results are shown in the figure below, with the numbers indicating the proportion of cells examined that show each pattern of staining. To identify the specific signaling defect in these mutant B cells, a reasonable biochemical assay would be to: Determine if BCR stimulation of mutant B cells produces enhanced binding of the B cell to the microbe Determine whether the mutant B cells have reduced levels of the enzyme Protein kinase C-q Determine whether the mutant B cells are overexpressing the enzyme Vav Determine whether BCR stimulation of mutant B cells promotes exchange of GDP for GTP on cdc42 Determine whether BCR stimulation of mutant B cells produces increased levels of DAGi) For serotonin receptor associated with the G protein class of subtype Gs, list the various ways how cell signalling can be terminated at stage 0 and 2 shown in Figure 1. 1 Reception ExtracellularA Hama Membra ely Malecle 2 Transduction 3 Response At Select by putting an arrow at the end of the correct choice(s). 2 a) - ) CytoplaseUse the SGF-signaling pathway image as a reference, to answer the following questions. Use the data provided to EXPLAIN if the cell will get to the response step or not. Keep in mind the purpose of this pathway is to cause skin cell division Growth Factor (GF-signal) Activation of GF Receptor (RTK-receptor) To cause Cell proliferation/cell division (Response) Plasma membrane Sos Grb2 (Ras GEF) (adapter) Raf МАРКK Mek МАРКK Activation of target genes that stimulate proliferation Erk МАРК You have a skin cell in a dish and have added Neural Growth Factor (NGF) to the cell media (the liquid the cell needs to live).