Are any of the following feasibly linked to COVID-19 susceptibility? . Leucine zipper transcription factor-like protein 2. C-C chemokine receptor type 9 3. FYVE and coiled-coil domain-containing protein 1 4. C-X-C chemokine receptor type 6 5. Chemokine XC receptor 1
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Are any of the following feasibly linked to COVID-19 susceptibility?
. Leucine zipper transcription factor-like protein
2. C-C chemokine receptor type 9
3. FYVE and coiled-coil domain-containing protein 1
4. C-X-C chemokine receptor type 6
5. Chemokine XC receptor 1
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- COVID-19 MRNA vaccines have the potential to stimulate the following types of immune attack against COVID-19 except: O production of antibodies against the COVID-19 spike proteins O none of these choices O proliferation of CD8 cytotoxic killer T cells that recognize epitopes of the COVID-19 spike protein O proliferation of NK cells that will destroy cells lacking MHC-1 (COVID-19 inhibits MHC1 expressionI 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.What is the function of each of the following genes 1. Leucine zipper transcription factor-like protein 2. C-C chemokine receptor type 9 3. FYVE and coiled-coil domain-containing protein 1 4. C-X-C chemokine receptor type 6 5. Chemokine XC receptor 1
- a.What would happen if IKKbeta did not phosphorylate IkappaB? b.Why is it so hard to make cytokine therapies? c.Why would you use the MyD88 independent pathway versus the MyD88 dependent pathway?You are given a project to characterize the effect of mutation on two newly discovered G protein coupled-receptors, GPCR-UCI and GPCR-UC2, both of which bind to the same ligand. For the cell signalling assay, you have the UMR-106 cell line that expresses both GPCR-UC1, CPCR- UC2, the corresponding G proteins, and adenyl-cyclase. A basal adenylyl cyclase activity, and thus, a baseline cAMP concentration, is detected in the cell line. (i) You found that, upon binding to the ligand, the mutation in GPCR-UC1 results in increased CAMP level but the mutation in GPCR-UC2 results in a low cAMP concentration. Based on these results, identify the subclass of G protein isoforms that the GPCRs activate. Explain your answer. (ii) If the mutation affects the G protein from GDP release, how would this affect the CAMP production after ligand binding? Explain your answer.Draw a cell signaling pathway following EGFR activation in host cells with the possible downstream activities. The new covid-19 strain acts on other cells in the body such as the lungs and kidney via ACE2. (we will say that EGFR is a receptor for the new variant).
- Match the letter in the diagram with the accumulation or localization of active (or about to be active) protein in a given cellular context, which is wild-type unless specified. AD5CES5) 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…Binding of a ligand (like TGFA) to a receptor tyrosine kinase (RTK) causes all of the following except (can use cell): OA. Dimerization of the receptor B. Auto-phosphorylation of the receptor O C. Activation of Ras through an interction with GRB2 (an adaptor) and SOS (a GEF) proteins. O D. Activation of heterotrimeric G proteins
- 1.Describe in detail the signal transduction pathway that leads to activation of either PKA, Kinase or PC. 2. Describe in detail the signal transduction pathway that leads to activation of MAPKinase or Akt/PKB. 3.Describe the similarities and differences in the structures of GPCRs specific for various ligands including the extracellular , transmembrane , and intracellular domains.do you have any clues? GAP protein helps hydrolyze the GTP to GDP in RAS protein. Argenine 789 residue in GAP protein interacts with GTP in RAS protein. However, Arg 789 is mutated to Alanine. which are true or false? ____We expect Ala789 GAP to have no consequence for cell growth or survival signaling. ____Arg789 stabilizes the T-loop of GAP in the outward (active) position, so we expect Ala789 GAP to have no kinase activity. ___Arg789 participates in the GTP hydrolysis reaction carried out by RAS, so we expect RAS to be catalytically inactive when partnered with Ala789 GAP. ____Arg789 binds in the major groove of the DNA double helix, so we expect Ala789 GAP to be inactive as a transcriptional regulator. __Arg789 interacts with RAS switch 1 and switch 2 regions, so we expect the RAS switch to fail with Ala789 GAP. ____The RAS switch would be locked in the OFF position by Ala789 GAP, so we expect no constitutive RAS signaling and hence no risk of this tumor metastasizing. ____The…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: