T7-MDM2 Myc-RYBP p53-(His-Ub), MDM2 p53 Myc-RYBP B-Actin QUESTION 12 In the RYBP case study paper, in Figure 3C, What happens to p53 in lane 6, and why? Ubiquitylated levels of p53 increase because mdm2 is inhibited Ubiquitylated levels of p53 increase because mdm2 is mutated Ubiquitylated levels of p53 increase because mdm2 is absent Ubiquitylated levels of p53 decrease because mdm2 is mutated Ubiquitylated levels of p53 decrease because mdm2 is inhibited Ubiquitylated levels of p53 decrease because mdm2 is absent + + I EO O 0 O OO

T7-MDM2 Myc-RYBP p53-(His-Ub), MDM2 p53 Myc-RYBP B-Actin QUESTION 12 In the RYBP case study paper, in Figure 3C, What happens to p53 in lane 6, and why? Ubiquitylated levels of p53 increase because mdm2 is inhibited Ubiquitylated levels of p53 increase because mdm2 is mutated Ubiquitylated levels of p53 increase because mdm2 is absent Ubiquitylated levels of p53 decrease because mdm2 is mutated Ubiquitylated levels of p53 decrease because mdm2 is inhibited Ubiquitylated levels of p53 decrease because mdm2 is absent + + I EO O 0 O OO

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter10: Cell Reproduction

Section: Chapter Questions

Problem 3VCQ: Figure 10.14 Human papillomavirus can cause cervical cancer. The virus encodes E6, a protein that...

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You are analyzing the activity of the protein p53 in two different cell types. You notice that p53 has the same primary structure in both cells, but has a different function in each cell. What could be the reason for the functional difference in this case? A. p53 mRNA has been spliced differently in each cell type. B. p53 is phosphorylated on some amino acid residues in its transactivation domain in one cell type but not in the other cell type. C. The tetramerization domain of p53 is acetylated at the same amino acid residues in both cell types. D. All of the above E. B and C only
"Changes to the p53 protein structure can be caused by differences in DNA and can affect protein function." Can you give detailed explanation why this is causation and not correlation? The explanation should be related with mutation, structure changes during protein synthesis, chemical property changes in amino acids, and functions of p53 protein.
In addition, when ARF is artificially expressed in normal cells, a rapid increase in p53 levels is observed. Studies have demonstrated that ARF, when expressed, is associated with Mdm2. When associated, the two proteins display a particular pattern of localization restricted to the nucleolus. Suggest a mechanism by which ARF leads to p53 build-up.
MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side. She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer. Past Medical History Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up. Past Surgical History: Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago. Medications: Glyburide, 5mg PO BID Verapamil SR, 240mg PO daily Furosemide, 40mg PO daily Allergies: NKDA Physical Examination: GEN: Well-developed, obese woman in no…
Name four downstream effects of p53 activation.
The P63 and P53 have similar functionalities in the cell, however, p53 is rarely associated directly with p63, suggesting that p63 may indirectly act as an oncogene by blocking p53 function. This hypothesis may also explain why p63 is associated with other indications of misinterpretation. I do understand the above statement, however once piece not clear – why would p63 block p53 function? Have these genes been shown to have opposing functions? From the background information provided above, it seems like they would have seminar functions. Explain.
Why is it advantageous for p53 to be activated by factors such as ER stress, light, and hypoxia (low oxygen concentration)?
In a few sentences, describe how p53 guards the genome. Include at least two specific ways that p53 guards the genome. In a few more sentences, describe the structure and function of the p53 protein. Structure: what domains are present in the p53 protein? Do p53 work as a single protein or as part of a complex? Function: what do the different domains do? How can p53 do so many different things?
List the regulatory mechanisms that might be lost in a cell producing faulty p53.
Figure 10.14 Human papillomavirus can cause cervical cancer. The virus encodes E6, a protein that binds p53. Based on this fact and what you know about p53, what effect do you think E6 binding has on p53 activity? E6 activates p53 E6 inactivates p53 E6 mutates p53 E6 binding marks p53 for degradation
How does the activity of human p53 get regulated through the interaction of the transactivation domains with its corresponding macromolecules when the cell is under stress vs unstressed conditions? based on this articles Primary paper: Lee, C. W., Martinez-Yamout, M. A., Dyson, H. J., & Wright, P. E. (2010). Structure of the p53 Transactivation Domain in Complex with the Nuclear Receptor Coactivator Binding Domain of CREB Binding Protein. Biochemistry, 49(46), 9964–9971. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982890/#SD1 https://www.rcsb.org/structure/2L14 PDB file for TAD domain
Why is it advantageous for p53 to be activated by factorssuch as ER stress, UV light, and hypoxia (low oxygenconcentrations)?