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You performed a whole genome CRISPR screen in cancer cells to identify regulators of T cell killing. One of your hits leads to increased killing of your cancer cells in presence of T cells but it represents an uncharacterised protein. What is your hypothesis and which three experiments would you carry out to elucidate the function of your hit?


keeping track of which arrows you click, advance time until the display on the face of the machine reads complete. which arrows did you click to advance time far enough


Imagine that you are working in the cell and molecular biology laboratory. You are examining the components of the DNA replication complex. If you wanted to disrupt or interfere with the enzyme that functions to relieve the stress of unwinding the DNA double helix during the DNA replication process, which of the following would you disrupt?

A. ligase B. helicase C. single stranded binding proteins D. Topoisomerase II


what supplies the energy to form phosphodiester bonds as DNA is replicated?


If you want to transcribe (express) a gene in E. coli, which necessary regulatory genetic elements must be present in vector and why?


Question 6: From the video describe the phenotype of the SCA1 mouse. Is it similar to symptoms observed in SCA1 patients?



I have to make LB plate with 50mg per ml adenine hemisulfate I’m trying to figure how much adenine sulfate to add to the the LB plate I make 700 ml LB plate and I have to make 100mg per L adenine hemisulfate LB plate I need help figuring out how to make this do I make a stock solution and how much how do I start I want all the explanation from start to finish so I can understand the calculations and the process of making this thank you very much 


A sample from the planet Mars has yielded a new eukaryotic organism, the MARS Amoeba (MARSA). Initial studies have determined it contains a nucleus with 3 distinct DNA based chromosomes. You have been assigned the task to study this new creature.

 

Using your knowledge, you are expected to: (25 points each)

 

1)   Generate both MARSA genomic and cDNA libraries while testing your libraries for completeness and titer by using many techniques discussed in our lectures such as Southern and Northern Blotting, mRNA to cDNA techniques, genomic DNA isolation via Principle of pulse-field gel electrophoresis (PFGE) followed by partial restriction digestions, and ligations into lambda phage vectors (expression-based Lambda gt11.). Include in your written journey all need steps and controls.


Reduction vs oxidation


Judy did a little research on skin cancer on the Internet before the visiting her doctor next morning. She found out what happened with other people, that were significantly older than she. It didn’t make sense that this would happen to her - she was only 20 years old!

The articles talked about how the sun’s ultraviolet light can be cause of DNA mutations. Accumulated DNA mutations over the years can cause genes super-activation. Judy was really grateful for the college biology course she attended. She knew that DNA was hereditary material that acted as a “plan” for everything our cells did, and that the gene was a piece of DNA that contained instructions for synthesizing a single protein. However, she should ask the doctor about these genes.

During the examination Dr. O'Brien was silent, looking at the mole on her leg. Finally, he said kindly: “I want to do a biopsy. All this means that we will remove your mole and look at the cells under a microscope and determine if they look abnormal. "

Judy said with tears: “You mean you can tell me that I have a tumor just by looking at some cells?”

 “It is very possible that your cells will look completely normal. A tumor is not necessarily the same as cancer. ” She looked embarrassed, so he continued: “A tumor means that the cells divide and gather in the same mass. But not all tumors automatically become malignant and life-threatening. A benign tumor is a mass of normal cells. These tumors are not considered as a cancer, and they are usually easily treated - we just remove them”, Dr. O'Brien replied.

The doctor smiled and seemed pleased that Judy read about it herself. “Let's remember! You see, we have tens of thousands of genes in our cells, but this does not mean that mutations in just any of them will lead to cancer. Genes that become mutated and can cause cancer have a specific type called cell cycle genes. Each person has a set of cell cycle genes in each of his cells that encode cell cycle proteins.  In normal healthy cells, cell cycle protein formation is tightly controlled, activating proteins are produced only when we really need more cells, and inhibitory proteins appear only when we don't need more cells. However, mutations in these genes can eliminate this tight regulation and lead to uncontrolled cell division. This is what happens in many types of cancer: the normal cell process, cell division, that is no longer properly controlled. ”

Judy thought for a second. “Okay, but you still haven't said what proto-oncogenes are.”

 

Issues for discussion:

1. What genes is Judy talking about? What are these genes called?

2. What are the functions of these genes in the cell? Explain.

3. List several genes that belong to this group.

4. In addition to these genes, mutation of what other genes leads to cell transformation?

5. Explain the mechanisms of conversion of proto-oncogenes into an oncogene.

6. What properties are characteristic of benign and malignant tumors.  Describe.

7. What stages of malignant transformation of cells do you know? Describe each stage.

 

 



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