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- A cell inherits a mutation in a gene that results in a transcription factor, called NF-kB, constantly being in its active conformation. When active, NF-kB stimulates the expression of cyclins that promote progression of the cell cycle, regardless of other conditions. As a result of this mutation, how would this cell's phenotype be affected by this mutation? A) This cell would have a cancer phenotype B) This cell would grow larger in size, but would never divide C) This cell would likely undergo apoptosis D) This cell would not duplicate its chromosomes .What is the effect of having fluctuating cyclin levels throughout the cell cycle, while the levels of its corresponding cyclin dependent kinase stay relatively constant? Explain.What would be the effect on the cell cycle if a cell acquired a mutation that rendered each of the following domains inactive? Explain your reasoning. The PSTAIR region of an M-phase Cdk The Wee1 Kinase The kinase that normally phosphorylates Sic 1 The Sic1 cyclin-Cdk inhibitor
- This phosphatase removes an inhibitory phosphotyrosine phosphate from serine protein kinase, mentioned in question 6, which activates kinase. What phosphatase is it? This is what question 6 says....This is the serine protein kinase that when activated in a complex cyclin, controls onset of mitosis and M-phase of the cell cycle. 1. Cyclin A/B 2. Wee 1 3. TOR (Target of Rapmycin) 4. Cdk1 5. none of the these ***I believe the answer is Cdk1 for number 6, but I could be wrongDescribe how Ras and p53 can alter the simplified genetic pathway controlling cell division shown below. For each of the two genes, would uncontrolled cell division result from a loss-of-function or a gain-of-function mutation? growth factors - receptors - cyclins - cyclin-dependent kinases - cell divisionRegulation of the cell cycle is very complex and involves multiple proteins. In yeast, a complex of cdc2 and a mitotic cyclin is responsible for moving the cell past the G2/M checkpoint. The activity of the cyclin-dependent kinase cdc2 is inhibited when it is phosphorylated by the kinase, Wee-1. What would you predict would be the phenotype of a Wee-1 mutant yeast? What other genes could be altered in a Wee-1 deficient mutant strain that would make the cells act normally?
- What role do aurora kinase play in the cell cycle and how would using these kinases as target for cancer treated work?A researcher studying a line of cancer cells noticed that cellular content of RhoBTB3 and Cyclin E1 increase and decrease through the cell cycle. a. He hypothesizes that RhoBTB3 signaling regulates the production of Cyclin E1 and the entry of the cell into mitosis. Based on the data below, explain why his results do not support this hypothesis. Identify what conclusions are supported by this data. b. Suppose that the researcher can engineer a cell line in which RhoBTB3 expression can be induced by the addition of a drug. Design an experiment using this cell line to test whether RhoBTB3 regulates the production of Cyclin E1. Describe what results he can expect if his hypothesis is correct.The p53 gene encodes a tumor-suppressor protein, p53, which acts as a transcription factor for several genes. Discuss an example of a specific gene that is activated by p53 and how this gene activation will lead to a pause in the cell cycle for DNA repair to take place.
- Explain Cyclin-dependent kinases (CDKs) control the cell cycle by phosphorylating other proteins?In attempting to design a drug that will impede cell cycle progression in ovarian cancers cells. you will want the drug to have this effect on the cells; Group of answer choices Increase expression of CDK7 Increase the phosphorylation of the ATP-binding pocket of CDK1 Increase expression of CDC25A All of theseWhich of the following is the primary method by which cyclin proteins are regulated to influence entry into the cell cycle or transition from one stage to the next? A. Transcriptional upregulation and translation followed by targeted ubiquitin-mediated degradation by a proteasome. B. Phosphorylation to regulate the activity of the kinase site. C. An activating phosphorylation and an inactivating phosphorylation. D. All of these are mechanisms that can be used to regulate cyclins.