Please outline the general steps you would take to test your hypothesis that SIN-47 works by disrupting the interaction between LEK2 and JAK4. You have: -several dishes of cancer cells -antibodies to LEK2 and JAK 4 -lots of the SIN-47 drug
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- Cyclosporin A and rapamycin are each used as T cell immunosuppressants. They share the property of binding to immunophilin molecules in T cells as the initial step in their mechanisms of action. However, in the case of cyclosporin A, the drug:immunophilin complex binds to and inhibits the protein phosphatase calcineurin, whereas the rapamycin:immunophilin complex binds to and inhibitors mTOR. As a consequence, Cyclosporin A, but not rapamycin, blocks cytokine production by T cells. Both cyclosporin A and rapamycin block cytokine production by T cells. Rapamycin, but not cyclosporin A, blocks T cell proliferation. Neither rapamycin nor cyclosporin A block T cell proliferation. Both cyclosporin A and rapamycin inhibit co-stimulatory signaling through CD28 on T cells.To study the immune responses that provide protection against tumor growth in mice, some investigations have used the EL4 mouse thymoma line. This tumor cell line was derived from a C57BL/6 mouse, and represents a type of T cell lymphoma. When transplanted into Rag-deficient mice, the mice rapidly succumb to the tumor. This is also the case when the mice receive wild-type C57BL/6 T cells the day before tumor cell injection. However, Rag-deficient mice were protected when the transferred T cells came from mice that lacked expression of one cytokine receptor, as shown in the fugure below. Name one likely candidate for the cytokine receptor that is knocked out in the T cells that are able to protect the mice.Based on these data, where would you MOST likely find toll-like receptor-XX (TLR-XX) among the following options? Justify WHY you selected that option.Your justification must be based on the data that are presented here, not the type of bacteria. A. On the cell surface B. In the endosome/ lysosome C. In the nucleus D. In the mitochondria E. In the endoplasmic reticulum
- Several vaccines against viral infections are made by isolating purified surface proteins of the viral particle, mixing them with an adjuvant to stimulate an innate immune response, and injecting the mixture into people. Two examples of this are the vaccine against Hepatitis B virus, and the vaccine against Human Papilloma Virus (the ‘cervical cancer’ vaccine). One interesting property of vaccines of this type (known as ‘subunit vaccines’) is that there is a requirement for a CD4 T cell response to the vaccine antigen in order to generate antibodies to the innocuous protein in the vaccine. In the case of the Hepatitis B vaccine, the viral protein included in the vaccine is the Hepatitis B surface antigen (HepB-SAg), a protein that is approximately 200 amino acids in length. The graph in Figure Q4.27 shows the data from immunizing individuals with this vaccine, and monitoring their production of protective antibody responses to the viral protein. a) What results would be predicted if…Why is it important to measure the pharmacokinetics(PK) and metabolism of an antibody drugIf antibody responses are not elicited by a Covid-19 vaccine, are there other types of immune response that could provide protection from the SARS-Co-V2 virus following vaccination? Explain why or why not.
- Describe in detail the effect of loss or mutation of LAT & Blk of the following molecules/proteins/genes/domains in immune signaling. Be sure to include the normal function and the function effected by the mutation. Include all relevant players and their roles. You may use diagrams if needed.Several classes of LDLreceptor mutations have been identified as causes of this disease. Suppose that you have been given cells from patients with different mutations, an antibody specific for the LDL receptor that can be seen with an electron microscope, and access to an electron microscope. What differences in antibody distribution might you expect to find in the cells from different patients?G-protein-coupled receptors on phagocytes link microbe recognition with increased efficiency of intracellular killing. The NBT (Nitro Blue Tetrazolium) test is used to diagnose the genetic disorder Chronic Granulomatous Disease (CGD). To perform this test, peripheral blood cells from the patient are stimulated with bacterial extracts, and then incubated with the NBT compound. Normal neutrophils turn blue in this test due to cleavage of the compound, while patient neutrophils remain uncolored, as shown in Figure below. Name a neutrophil receptor that is likely to be stimulated by the bacterial extract in this assay, and describe how this receptor regulates the activity of the enzyme that cleaves NBT.
- Which of the following statements is true? O Streptolysin-O is a growth factor for white blood cells. O Anti-streptolysin-O antibodies peak several months after initial symptoms. O Currently, the main method for detecting anti-streptoryan-G antibodies in radal immansattfo O Streptolysin-O does not induce an immune response. In the classical method of testing for anti-streptolysin-O antibodies, a positive reaction is indica intact red blood cellsExperiments are performed to analyze protein tyrosine phosphorylation in response to TCR stimulation. For these experiments, T cells are stimulated with anti-CD3 antibody, and then lysates are prepared and run on a protein (SDS-PAGE) gel to separate the proteins by molecular weight. The proteins are transferred from the gel to a membrane for immunoblotting using an antibody that binds to all phosphorylated tyrosine residues in any protein; this antibody is called ‘anti-phospho-tyrosine antibody,’ and is abbreviated as anti-P-Y. The results are shown in the figure below. You confirm that the mutant T cells express normal levels of all the proteins detected in the WT cells, including PLC-g, SLP-76, ITK, ZAP-70, LCK, LAT, and the CD3 and TCRz proteins. Based on these data, which of the following proteins (biotin, hygromycin, and streptavidin) can rule out its presence? Briefly explain your answer. What protein is most likely defective in the mutant cells and why? For the protein you…a major cause of septic shock is the presence of lipopolysaccharide (LPS) from bacteria in the blood. suppose you have available purified LPS and several strain of mice, each with a mutation that inactivates a particular TLR gene. How might you use these mice to test the feasibility of treating septic shock with a drug that blocks TLR signaling?