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1.identify and describe the normal function of the cdc25 gene responsible for the observed cdc9-50
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- After a cell "clears" the G₁ restriction checkpoint, it can proceed into S phase. This S phase entry is achieved by a cyclin dependent kinase (Cdk2) and its cyclin (Cyclin E), but additionally requires the action of a protein kinase (CDC2) as well as a phosphatase (CDC25) enzyme. Explain how these 4 proteins work together to orchestrate S phase entry.There is now significant evidence to support the existence of cytoneme-mediated delivery of signaling ligands. What is their mechanism of action, and what is the relevance of this discovery to embryonic development?The output of RTK pathways is often the activation of MAP Kinase. Explain how MAPK can lead to activation of a specific subset of proteins, leading to distinct effects in different cell types in response to the same growth signal.
- Drug A323 inhibits the activity of the cyclin-dependent kinase (CDK) - G1 cyclin complex. Consider possible effects of the drug on the cell cycle of normal and malignant cells. Predict what is likely to happen if the drug is added to the cell types described in A). Motivate your answers and describe the role of cycle-regulatory pathways that are relevant with respect to the action. of drug A323. A) Carcinoma cells in which both allels of the Rb gene carries loss of function mutation.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.Cell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.
- Changes in the activity of a variety of Cdks are essential for accurate progression through the cell cycle, and yet the levels of Cdk expression are fairly constant during the cell cycle. Briefly describe three mechanisms by which the activity of Cdks is regulated.The destruction of the various cyclins is commonly used to inactivate the Cdk/cyclin complexes. Why is it advantageous to inactivate these complexes via protein destruction instead of some other method that does not require the re-synthesis of a cyclin protein the next time the cell divides?Which of the following is false about cyclin-cdk complexes? OCdk's do not have to bind to cyclin proteins for complex to be active. OCdk/cyclin complexes phosphorylates proteins required to trigger next cell cycle phase. Process acts as molecular brakes to ensure cell is ready to continue with cell cycle. O Cyclin concentrations increase gradually, but cdk must be phosphorylated by specific kinase for complex to be active
- Select all the true statements about cyclins: (select all that applies) Group of answer choices They have functionally important regions called cyclin boxes that show high levels of homology They contain a cyclin destruction box with a conserved consensus sequence of RXXLXXIXD/N They regulate the activity of cyclin-dependent kinases (Cdks) by promoting phosphorylation of a single Thr side chain They bind protein partners with high specificity in regions called cyclin boxes..TNF-alpha treatment of prostate carcinoma, LNCAP cells decreases cell survival as shown in the graph below. Which of the following would you observe in these cells treated with TNF- alpha? Select all that apply TNF-a 120 100 80 - 60 40 20 0. 24 72 (hrs) Control + TNF-a 100 ng TNFA 10 ng O Activation of extrinsic pathway of apoptosis O Activation of intrinsic pathway of apoptosis Activation of executioner caspases Recruitment of adapter protein FADD to the TNF-alpha receptor LNCAP cell viability (% of control)Describe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.