Molec Exam 1 (1)

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Clemson University *

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Biology

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Apr 3, 2024

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Short Answer Questions. (5 pts each blank) 1. A gene mutation that replaces one base pair in the genome with another is called _____. Point mutation 2. The immunoglobulin protein responsible for initiating the defense against microbial infections in the circulatory system is ________. IgM 3. The latest technique that can ACCURATELY quantify gene expression profiling between two different samples is called ______. Rna Sequencing (Rna-Seq) 4. Imagine you are working in a lab to quantify the expression of a gene in different samples using quantitative PCR. The CT value of Sample 1 is 15, and the CT value of Sample 2 is 17. Assuming you loaded the same amount of RNA for both samples, Sample _1__ has more RNA, and the fold change is _4_ -fold. 5. The receptor on human cells for the HIV virus is _CD4___ , and the co-receptor is named Chemokine . CD4 Chemokine Essay Questions. 6. In 2080, an outbreak of the X virus leads to a significant increase in the mortality rate among the human population. To combat this, scientists develop a drug called Xterminatormab. Given the name, what category does this drug belong to? When Xterminatormab is injected into the patient's circulatory system, it effectively reduces symptoms. What is this type of therapy called? (10 pts) This drug belongs to the monoclonal antibody category because it ends with the “mab” indicating that it is a monoclonal antibody. After being injected, it results in an effective reduction of symptoms indicating that it can be classified as antiviral therapy. 7. What’s triple negative breast cancer (TNBC)? Why is TNBC thought to be the hardest breast cancer type for therapeutic treatment? Provide a strategy for the treatment of the TNBC. (15 pts)
TNBC is a malignancy that arises due to the lack of three different receptors on breast cancer cells. These receptors include the Estrogen receptor (ER), HER2 and progesterone receptors. This is the hardest to treat because it lacks all three important receptors making it harder to treat or target. To treat this disease, parp inhibitors and heavy metals are applied to the patient. Heavy metals induce breakage in DNA to induce apoptosis. The wild-type cells have the BRCA gene and the Parp1 gene to induce a repair mechanism however, cancer cells lack the BRCA gene. Applying the inhibitor will disable the cancer genes from repairing the DNA which will lead to cell death in the cancer cells only. 8. List three GENERAL molecular strategies to cure cancer and describe the basic principles for each strategy. Hints: these strategies are based on specific molecular targets. (15 pts) Three molecular strategies to cure cancer include, the use of monoclonal antibodies, kinase inhibitors, and programmed death receptors. Monoclonal antibodies could be used to bind to the cell receptors so that the growth factors are unable to stimulate proliferative activities and result in eventual cell death. Kinase inhibitors can also be applied to prevent the phosphorylation of kinases which would result in the activation of downstream effects often resulting in uncontrolled proliferation. Lastly, by disrupting the pd1 and pdl1 connection. By doing this, the T cells will be unable to recognize the tumor cells and will pursue killing them. 9. Explain why flu vaccine has to be immunized annually and the scientific basis for this? (10pts) The flu vaccine must be immunized annually because the flu virus has fragmented DNA which causes high DNA mutation. The flu virus has the ability to do antigenic drift and shift. Antigenic drift causes the flu virus to have a replication mutation. The Antigenic shift causes the flu to shuffle the DNA every time it mutates causing a variation of many different genome combinations. 10.Compare and contrast the direct and indirect ELISA assay and their applications. (15 pts) The enzyme-linked immunosorbent assay (ELISA) is commonly used to detect viruses. Both processes are used as an immunity-based way of detecting viruses. For the Direct ELISA method, it used to directly detect the viral protein. This is done by generating antibodies against the surface protein. The well contains antibodies and then the sample is added to the well to test for the virus. The sample’s initial antigens will bind to the antibody. After, the virus’ second antibody connected to a substrate and enzyme is added to the well. This will bind to the antigen on the initial antibody in the well, causing the structure to connect with the antigen in the middle. Once bound, the enzyme will
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