Photodynamic therapy results in induction of WAF1 or CIP1 or P21 leading to cell cycle arrest and apoptosis. Justify.
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Photodynamic therapy results in induction of WAF1 or CIP1 or P21 leading to cell cycle arrest and apoptosis. Justify.
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- MPF plays an important role during the regulation of the cell cycle. give examples that will support this statement.You are studying a drug that leads to cell cycle arrest during mitosis. You examine levels of cyclin and cdk proteins in the cells treated with the drug, and untreated cells as control. Shown below are the Western blot results of protein expression. Drug No Drug Time (minutes) 15 30 45 60 75 0. 15 30 45 60 75 CDK Cydin Which of the following could be a mechanism by which the drug leads to cell cycle, arrest?could you explain a bit more what this sentences mean: The information displayed demonstrates a significant increase in cell proliferation inside the dentate gyrus of mice that were locked in voluntary exercise compared to the control group. The use of 5-Bromo-2'-deoxyuridine (BrdU), a thymidine analog, permits the following of recently formed cells because it is incorporated into the DNA of dividing cells amid the S stage of the cell cycle. The immunocytochemical examination uncovered a 67% increase in BrdU-labeled cells within the running group, meaning upgraded neurogenesis, which is factually noteworthy as shown by the p-value of 0.0001. The observation that the runner group effectively utilized the running wheels given in their cages relates to the increment in BrdU-labeled cells.
- Discuss/explain, in details, the relationship between cell viability and cell vitality and cell apoptosis as suggested by neutral red uptake,“Disruption in the pathway of apoptosis & autophagy can lead to different diseases”- explain brieflyDescribe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.
- 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)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.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.
- Dr. Jace is a research officer in a laboratory that studies anticancer treatment. She is interested to test a plant extract for its apoptosis-inducing effect on colon cancer cells. After incubating the cells with the extracts, she is using the FITC Annexin V Apoptosis Detection Kit I by BD Biosciences for her apoptotic assay. Discuss the detection of apoptosis using this kit and include the utilization of flow cytometry in her experiment.cells undergo programmed cell death. Write out the pathway(s), noting the changes (e.g., localization, phosphorylation, activation) When mammalian cells are irradiated, they stop dividing by arresting at cell cycle checkpoint. If the damage persists, the kinase (CdK), Cdk inhibitor, cytochrome c, DNA damage, mitochondria, p53, phosphorylation, transcription. each step. Include: apoptosis, apoptosome, ATM, pro-apoptotic proteins, caspase, Checkpoint Kinase (Chk), cyclin, cyclin-dependeExplain the concept of loss of heterozygosity (LOH). Why do most cancer cells exhibit LOH of one or more genes? How does failure of the spindle assembly checkpoint lead to loss of heterozygosity?