Protein P, normally stimulates apoptosis or cell death when activated. Consider a cell with a mutation in one allele such that protein P is always expressed and active, while the other allele of gene P is deleted. Which of the following is true for this cell?
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- Human cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice. State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth. the mitogenic signaling pathway controlled by Ras. the cell cycle checkpoint controlled by pRb. the alarm pathway controlled by p53. the telomere maintenance pathway controlled by hTERT. the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.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.Protein N, normally inactivates a tumor suppressor protein. Consider a cell with a mutation in one allele such that protein N is nonfunctional, while the other allele of gene N is wild-type. Which of the following is true for this cell? Gene N is a tumor suppressor gene, and the phenotype of the cell is not transformed. Gene N is a proto-oncogene, and the phenotype of the cell is transformed. Gene N is a tumor suppressor gene, and the phenotype of the cell is transformed. Gene N is a proto-oncogene, and the phenotype of the cell is not transformed.
- 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.The expression patterns as well as activation of different types of CDKs happen at different stages of the cell cycle. Explain why.Isothiocyanates arè compounds found in vegetables such as broccoli. Such compounds have been shown to induce the expression of proteins called caspases in cervical cancer cells. Outside of Cell Toxins DNA Damage p53 Apoptosis Inside of Cell Based on the above diagram, would you expect ingestion of broccoli to promote, suppress or have no effect on the progression or survival of cervical cancer cells? Promote progression of cervical cancer cells Suppress progression of cervical cancer cells O Have no effect on progression of cervical cancer cells
- 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.Relatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.Can you please help me by drawing a serie of schematic figures that demonstrates the information in the paragraph below? In addition to phosphorylation, the C-terminal domain of p53 can also be acetylated and sumolated in response to DNA damage. Acetylation and sumolation both result in an increase in the transactivation ability of p53 and may account for this finding. In vivo, IR induces the acetylation of p53 at Lys320 by PCAF and Lys382 by CBP/p300. Acetylation at these sites is dependent on N-terminal phosphorylation at Ser15 and to a lesser extent on phosphorylation at Ser6, Ser9, and Thr18 (Saito et al., 2002; Wahl and Carr, 2001). All of these phosphorylation events are ATM-dependent, although only Ser15 has been shown to be phosphorylated directly by ATM. Sumolation occurs at Lys386 after DNA damage (Muller et al., 2000). Sumolation refers to the covalent attachment of a small ubiquitin-like molecule (SUMO-1) to Lys residues, but in contrast to ubiquitination, does not result…
- Cancer cells typically lose cell cycle entry control. Explain how the following mutations, which are found in some cancer cells, lead to a bypass of these controls: (a) overexpression of cyclin D, (b) loss of Rb function, (c) loss of p16 function, (d) hyperactive E2F.Describe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.Lac operon: Put plus or minus in each box to show that the cell will make, or will not make, tunctional Beta galactosidase (product of LacZ gene) or functional permease (product of the lacY gene). Ignore the effects of glucose (pretend it is not present). Each of the 3 cells is a “partial diploid." Not induced (no lactose present) Beta galactosidase (Z) Induced (with lactose) Permease (Y) Permease (Y) Beta galactosidase (Z) LacI+ P- O° Z+ Y- LacI- P+ O+ Z- Y* LacIS P+ O Z+ Y- LacI+ P+ O+ Z- Y* LacI+ P+ O° Z+ Y- LacI- P+ O+ Z Y*