for question 1, choose wheater each choice is either tumor suppressor or proto oncogene\for question 2, which behaviors are or are not responsible for the behavior of the strain of yeast You have isolated a strain of temperature-sensitive mutant yeast that divides normally at 25°C.However, at 37°C, the mutant pauses in the cell cycle right before M phase. You found that thegene for M-Cdk is not mutated. For each one of the following conditions, state whether or not itcould be responsible for the behavior of this strain of yeast.[Select]Inactivation of an enzyme that degrades M-Cyclin[Select]Inactivation of an inhibitor of M-Cdk Given what you have learned about tumor suppressors and proto-oncogenes, predict whether thefollowing genes are likely to be tumor suppressors or proto-oncogenes.An inhibitory protein of a Cdk is likely to be a [Select]Ras is likely to be a [Select]The RTK in the MAP kinase pathway is likely to be a [Select]the MAP kinase pathway covered in Topic 6].Protein A is a transcription factor that normally activates the expression of genes needed for S-phase. The inhibitor of protein A is likely to be a [Select]✓ [Hint: review

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Description: for question 1, choose wheater each choice is either tumor suppressor or proto oncogene\for question 2, which behaviors are or are not responsible for the behavior of the strain of yeast You have isolated a strain of temperature-sensitive mutant yeas

Proto-oncogenes and tumor suppressor genes are two types of genes that play important roles in the…

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for question 1, choose wheater each choice is either tumor suppressor or proto oncogene\ for question 2, which behaviors are or are not responsible for the behavior of the strain of yeast

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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Figure 9.10 In certain cancers, the GTPase activity of the RAS G-protein is inhibited. This means that the RAS protein can no longer hydrolyze GTP into GDP What effect would this have on downstream cellular events?
which of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTP
In a patient with a constitutively active receptor tyrosine kinase that increases the activity of PI3K, the administration of a drug that increases PTEN expression will likely inhibit tumorigenesis because; Group of answer choices PTEN prevents growth factor binding to RTK PTEN competitively inhibits the catalytic subunit of PI3K PTEN dephosphorylates PIP3 PTEN inhibits the dimerization of the regulatory subunit of RTKs
Which of the following statements are correct about cytoplasmic signaling in cancer cells? Multiple answers. A. Only minor modifications of cell control machinery are required for normal cells to become highly proliferating cancer cells B. Immediate early genes are induced in the presence of protein synthesis inhibitors C. Many immediate -early genes are oncogenes D. Delayed early genes are highly expressed in the presence of protein synthesis inhibitors E. Delayed early genes are highly expressed in normal cells in the absence of growth factors
In your own words: Describe the molecular mechanisms involved in P53’s role as a tumor repressor protein.
Cancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.
I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.
a. A typical cellular response of a mammary epithelial cell to EGF signal is proliferation. the Kd for the interaction between EGF and its receptor is 1x10^-10 M. Lets imagine that at least 25% of the receptors on a normal cell must be engaged by EGD in order to trigger the cellular proliferation response. What minimum concentration of EGF is required to reduce cell proliferation? (Show calculation). b. Mammary epithelial cancer cells have amplified levels of EGF receptors on their surface. If such a cell has 1000 EGF receptors, as compared to 200 receptors on a normal cell, what minimum concentration of EGF is required to induce cell proliferation in the cancer cell? [Show calculation]. Note that the same number of receptors (not percentage of receptors) must be activated to promote proliferation in normal cells and cancer cell. c. The ambient (unstimulated) concentration of EGF in mammary epithelial tissue is 1x10^-11 M. Will this level of EGF stimulate proliferation in normal…
Signaling pathways often require receptor dimers to become active. What would be an advantage of the extrinsic apoptosis pathway requiring a trimer? I note from the article "Nature Reviews, Cancer 16:539, 2016" the following: The extrinsic apoptotic pathway, upon binding to their cognate ligand, death receptors such as tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor (TRAILR) and FAS can activate initiator caspases (caspase-8 and caspase-10) through dimerization mediated by adaptor proteins such as FAS-associated death domain protein (FADD). Active caspase-8 and caspase-10 then cleave and activate the effector caspase-3 and caspase-7, leading to apoptosis. I can't think of any other pathway that uses a trimer, so there must be a reason. Glad an exprt can help.
Cancers are often caused by overactive growth factor receptor signaling (remember growth factor receptors are enzyme-linked receptor pathways). If you were able to use gene therapy to overexpress a particular protein in a cancer cell, which of the following might be useful to overexpress in order to combatt cancer? a GAP that acts on Ras a phosphatase that acts on GPCR a protein that enhances the activity of Akt a ubiqtuin ligase that acts on the MAPK phophatase
Distinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.
TGF-β1 is a protein that affects cell growth and differentiation. Scientists conducted an experiment where epithelial cells were treated with transforming growth factor beta 1 (TGF-β1) in the laboratory. At the end of the experiment, the epithelial cells had transformed through several stages from epithelial cells to embryonic stem cells (ESCs) to neural progenitor cells (NPCs), and finally to cortical neurons (CNs). The scientists observed the transformation of the cells by analyzing gene expression at certain stages (M1-M7) and determined the relative gene expression level, as shown in the graph. The graph shows the relative gene expression level for cells at different stages of differentiation. Which of the following claims could account for the differences in gene expression at each stage of cell differentiation, and how does this correlate with the distance of the genes on the chromosome? A - Cell differentiation is controlled by RNA translation, but there is no…