Please answer asap QUESTION 8Which of the following is true of the RAS proto-onoogene?O Mutations involving RAS are dominant in their effects.O Cancer cells typically show both alleles have loss of function mutations.OA gain of function mutation in just one allele would signal to the cell to proceed through the cell cycle.O A gain of function mutation in one allele would be hidden or masked by the presence of a normal, wild-type allele.Deletion of both alleles would signal to the cell to proceed through the cell cycle.QUESTION 9Which of the following is true regarding tumor suppressor genes?O Knudson's two-hit imodel applies to these genes.Typical cancer cells show gain of function of tumor suppressors.O Typical cancer cells show inactivating, loss of function mutation in these genes.Tumor suppressor mutations are recessive in their effects on the cell.

Mutations are alterations in the DNA sequence of an organism. Small changes, such as adding or…

QUESTION 8 Which of the following is true of the RAS proto-oncogene? O Mutations involving RAS are dominant in their effects. O Cancer cells typically show both alleles have loss of function mutations. OA gain of function mutation in just one allele would signal to the cell to proceed through the cell cycle. O A gain of function mutation in one allele would be hidden or masked by the presence of a normal, wild-type allele. O Deletion of both alleles would signal to the cell to proceed through the cell cycle. QUESTION 9 Which of the following is true regarding tumor suppressor genes? O Knudson's two-hit mutation model applies to these genes. O Typical cancer cells show gain of function of tumor suppressors. O Typical cancer cells show inactivating, loss of function mutation in these genes. O Tumor suppressor mutations are recessive in their effects on the cell.

QUESTION 8 Which of the following is true of the RAS proto-oncogene? O Mutations involving RAS are dominant in their effects. O Cancer cells typically show both alleles have loss of function mutations. OA gain of function mutation in just one allele would signal to the cell to proceed through the cell cycle. O A gain of function mutation in one allele would be hidden or masked by the presence of a normal, wild-type allele. O Deletion of both alleles would signal to the cell to proceed through the cell cycle. QUESTION 9 Which of the following is true regarding tumor suppressor genes? O Knudson's two-hit mutation model applies to these genes. O Typical cancer cells show gain of function of tumor suppressors. O Typical cancer cells show inactivating, loss of function mutation in these genes. O Tumor suppressor mutations are recessive in their effects on the cell.

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 42CTQ: List the regulatory mechanisms that might be lost in a cell producing faulty p53.

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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.
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.
Name the mutation at the protein level which is the basis for mutant A-1 Would a nonsense mutation in protein A be an enhancer or suppressor mutation of mutant B-1 Name the mutation at the phenotype level when a new function is acquired: ____morphic
The Wnt planar polarity signaling pathway nor-mally ensures that each wing cell in Drosophila has a sin-gle hair. Overexpression of the Frizzled gene from a heat-shock promoter (hs-Fz) causes multiple hairs to grow frommany cells (Figure Q15–5A). This phenotype is suppressedif hs-Fz is combined with a heterozygous deletion (DshΔ)of the Dishevelled gene (Figure Q15–5B). Do these resultsallow you to order the action of Frizzled and Dishevelledin the signaling pathway? If so, what is the order? Explainyour reasoning
Wilms tumor 1, or nephroblastoma, is caused by mutations in the WT1 gene, which encodes a transcription factor. You have identified a novel variant in WT1: Arg422Pro. You have control cells and cells that have been engineered to carry the homozygous WT1 p.Arg422Pro mutation. You want to assess effects of this mutation on a variety of endpoints. For each endpoint listed below, choose the one technique is best suited to answer the question. Choose from: array CGH, qRT-PCR, qPCR, RNA-seq, FISH, in situ hybridization, western blot, immunostaining, WT1 ChIP-seq, WT1 ChIP-PCR, ATAC-seq, 3C Endpoint Technique? WT1 protein amount (quantitative) Western blot WT1 protein binding to all enhancers, genome-wide Chip-seq WT1 mRNA amount (quantitative) WT1 protein subcellular localization Quantitative assessment of all mRNAs in these cells (genome-wide) RNAseq Chromatin interactions between a specific WT1 chromatin binding site (identified above)…
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…
The GA(T>C)A mutation in the Duffy promoter impacted expression of Duffy in the following cell types... O Blood cells O Endothelial cells O Purkinje cells O Purkinje, Endolthelial, and Blood cells.
27 of 41 Mutations in two important cancer-critical genes, encoding p53 and Rb, respectively, are commonly found in cancers. What type of mutations are these expected to be? O Gain-of-function mutation in p53 and loss-of-function mutation in Rb O Loss-of-function mutation in p53 and gain-of-function mutation in Rb O Loss-of-function mutations in both genes O Gain-of-function mutations in both genes
Name the mutation at the protein level which is the basis for mutant B-1 Would a nonsense mutation in protein A be an enhancer or suppressor mutation of mutant B-1 Name the mutation at the phenotype level when a new function is acquired: ____morphic Name one mutation which is a suppressor of bri1-5
Your friend sends you two cancerous cel| lines to examine and determine possible mutations. The results are shown below: Cell Line Mutation WT none (wild type DNA) 1 a deletion at the same region on both copies of chromosome 4 2 a point mutation in a gene on only one copy of chromosome 7 You learn that cell line 2 is a breast cancer cell line that expresses a mutant version of a receptor protein called KIT. Based on this data, which of the following is true ? Select all that apply Activation of KIT promotes progression through the cell cycle Activation of KIT releases an inhibition of a cyclin Activation of KIT causes cells to enter GO O Activation of KIT promotes cells to undergo apoptosis
3.3. Using your knowledge of the function of p53, discuss why targeting mutant p53 is promising for cancer therapy. 3.4. Using your knowledge of the function of Rb, discuss the consequences of a dysfunctional Rb protein on cell cycle progression. 4.1. Why is glucose consumed at a high rate in the absence of oxygen and at a low rate in its presence? Explain.
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.