You are studying Protein X which plays a role in promoting the G1/S phase transition in eukaryotic cells. You design an experiment using wild-type yeast cells to measure the amount of Gene X MRNA and activity levels of Protein X during the cell cycle. The results from your experiment are shown in the graph below. From the data, which of the following could Protein X be? Protein X activity levels Gene X MRNA levels Relative Units G1 G2 O cyclin inhibitor protein O cyclin dependent kinase Helicase Cyclin
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- You are studying cancer progression in mice. Your results show the following pathway in which two proteins play important roles in how mouse cell division is regulated. nutrients cell division Prot 1 Prot 2 You isolate a mutant strain of mice that have a Prot 1 mutation (Prot 1-). These mutant mice frequently develop cancer as young adults. You isolate a mutant strain of mice that have a Prot 2 mutation (Prot 2-). These mutant mice frequently develop cancer as young adults. Which of the following can you conclude from these observations? Select all that apply O Function of wild-type Prot 2 is to promote cell division when nutrients are present Function of wild-type Prot 2 is to promote cell division when nutrients are absent Function of wild-type Prot 1 is to inhibit cell'division when nutrients are absent Function of wild-type Prot 1 is to inhibit cell division when nutrients are presentRegulation of the cell cycle is very complex and involves multiple proteins. In yeast, a complex of cdc2 and a mitotic cyclin is responsible for moving the cell past the G2/M checkpoint. The activity of the cyclin-dependent kinase cdc2 is inhibited when it is phosphorylated by the kinase, Wee-1. What would you predict would be the phenotype of a Wee-1 mutant yeast? What other genes could be altered in a Wee-1 deficient mutant strain that would make the cells act normally?You are studying the M-cyclin. You treat mitotic cells with an inhibitor of the proteasome and find that M-cyclin is no longer degraded and that this prolongs mitosis. You also find that in the presence of the inhibitor, M-cyclin is now running slower/larger in a Western than you have previously doserved. In 1-2 sentences, explain why this might be happening.
- You are studying the M-cyclin. You treat mitotic cells with an inhibitor of the proteasome and find that M-cyclin is no longer degraded and that this prolongs mitosis. You also find that in the presence of the inhibitor, M-cyclin is now running slower/larger in a Western than you have previously observed. In 1-2 sentences, explain why this might be happening. Edit View Insert Format Tools Table 12pt Paragraph B IU Αν S A C I AT²✓ #tv A MacBook Air X : GThe retinoblastoma protein (RB) suppresses human cell division by arresting cells in the G₁ phase of the cell cycle and preventing progression to the next phase. It accomplishes this task by binding to another protein, E2F, a transcription factor needed for further progression through the cell cycle. Normal progression through the cell cycle is accomplished when cyclin-dependent kinases (CDKs) phosphorylate RB, preventing its binding to E2F. Many viruses can induce abnormal exit from G, using viral proteins that bind to RB at a motif at the N-terminal called LXCXE. An example is the E7 papilloma protein, which causes the excessive proliferation of cells in warts. The site at which LXCXE proteins bind is called the pocket domain and is highly conserved on RB and related proteins in plants and animals. The configuration of the pocket domain is well established. Mutant experimental RB proteins are available with alterations in the conserved amino acids of the pocket domain. A simple…The retinoblastoma protein (RB) suppresses human cell division by arresting cells in the G₁ phase of the cell cycle and preventing progression to the next phase. It accomplishes this task by binding to another protein, E2F, a transcription factor needed for further progression through the cell cycle. Normal progression through the cell cycle is accomplished when cyclin-dependent kinases (CDKs) phosphorylate RB, preventing its binding to E2F. Many viruses can induce abnormal exit from G, using viral proteins that bind to RB at a motif at the N-terminal called LXCXE. An example is the E7 papilloma protein, which causes the excessive proliferation of cells in warts. The site at which LXCXE proteins bind is called the pocket domain and is highly conserved on RB and related proteins in plants and animals. The configuration of the pocket domain is well established. Mutant experimental RB proteins are available with alterations in the conserved amino acids of the pocket domain. A simple…
- Which of the following small GTP-binding proteins does NOT play a role in cell migration during chemotaxis? O Cap Z Rho Cdc42 O All of the listed GTPases play a role in cell migration O Rac ◆ PreviousIn attempting to design a drug that will impede cell cycle progression in ovarian cancers cells. you will want the drug to have this effect on the cells; Group of answer choices Increase expression of CDK7 Increase the phosphorylation of the ATP-binding pocket of CDK1 Increase expression of CDC25A All of theseControl of gene expression in eukaryotic cells occurs at which level(s)? a. only the transcriptional level b. epigenetic and transcriptional levels c. epigenetic, transcriptional, and translational levels d. epigenetic, transcriptional, post-transcriptional, translational, and post-translational levels
- You are studying cancer progression in mice. Your results show the following pathway in which two proteins play important roles in how mouse cell division is regulated. nutrients cell division Prot 1 Prot 2 You isolate a mutant strain of mice that have a Prot 1 mutation (Prot 1-). These mutant mice frequently develop cancer as young adults. Which of the following can you conclude from these observations? Select all that apply Prot 1- mutation can be classified as dominant Prot 1 can be classified as a proto-oncogene Prot 1- mutation can be classified as recessive Prot 1 can be classified as a tumor suppressor geneAfter DNA damage (e.g. caused by X-ray exposure) in eukaryotic cells, the cell cycle can be arrested by the stabilisation of the protein which drives the transcription of the gene, whose protein product interacts with the G1/S-Cdk and S-Cdk complexes. O PDGF, acetyltransferase O phenylalanine hydraxylase, PDGF O p53, acetyltransferase O p53, p21 O p21. p53Protein 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? Gene P is a proto-oncogene, and the phenotype of the cell is transformed. Gene P is a proto-oncogene, and the phenotype of the cell is not transformed. Gene P is a tumor suppressor gene, and the phenotype of the cell is not transformed Gene P is a tumor suppressor gene, and the phenotype of the cell is transformed 로