Complete the following statements by selecting one of the options provided. A mutation that inactivates the kinase activity of S-Cdk will lead to [Select] The inactivation of a cell cycle checkpoint will lead to [Select] A mutation that increases the activity of the monomeric GTPase Ras will lead to [Select] of cells. A mutation that [Select] V ✓the activity of MAP kinase will lead to <
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Chioces for each statement: hyperproliferation or cell cycle arrest; cell cycle arrest or accumulatio of dna; hyperproliferation or growth arrest; increase or decrease
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- 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 ◆ PreviousA temperature-sensitive mutant yeast strain stops dividing when shifted from 25°C to 37°C. These cells are analyzed at different temperatures by a machine that measures the amount of DNA they contain, and the following graphs are obtained. number of cells number of cells [ Select] [Select] [Select] 25°C [Select] مل Cells in G1 phase should have [Select] Which of the following would explain the behavior of your mutant? Mark yes or no for each of the following choices. 2 amount of DNA/cell (arbitrary units) 37°C 1 2 amount of DNA/cell (arbitrary units) unit(s) amount of DNA. ✓ Inability to initiate DNA replication Defect in chromosome condensation ✓Defect in centrosome duplication ✓Defect in cytokinesisFigure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.
- List the regulatory mechanisms that might be lost in a cell producing faulty p53.How does NF-kB induce gene expression? A small, hydrophobic ligand binds to NF-kB, activating it. Phosphorylation of the inhibitor Ik-B dissociates the complex between it and NF- kB, and allows NF-kB to enter the nucleus and stimulate transcription. NF-kB is phosphorylated and is then free to enter the nucleus and bind DNA. NF-kB is a kinase that phosphorylates a transcription factor that binds DNA and promotes protein production.E VG ✓H NA MATEN Match each letter (A through G) to its description. B A ya pada saat ada para a H F காலிமாம்ம் P S —— 1. Receptor 2. RNA 3. Lysosome 4. DNA 5. Ribosome 6. Ligand 7. Kinase domain 8. Nucleus 9. Mitochondria 10. Phosphorylated transcription factor 11. Dephosphorylated transcription factor 12. Plasma membrane
- S-Cdk is likely to be a [Select] The inhibitor of Ras is likely to be a [Select] The MAP kinase is likely to be a [Select] Q Search 14:31 Protein X is a transcription factor that normally activates the expression of genes needed for S- phase. The activator of protein X is likely to be a [Select] is 4 ******* > 21**113 ***** ****** V f6 99+ 1- Il app.honorlock.com is sharing your screen. **** 1 a hp Stop shaCan I get help on drawing a mechanism for the paragraph below? p53 stabilization by IR The signal upstream of p53 stabilization and activation after IR exposure most likely originate from DNA DSBs. This is supported by the fact that the kinases implicated in the phosphorylation of p53 are also implicated in DSB repair. These include two kinases that belong to the PI-3 kinase family, DNA-PK and ATM (see above), and indirectly, the checkpoint kinase 2 (Chk2). Ser15 of p53 was identified as a substrate for DNA-PK in vitro (Lees-Miller et al., 1992). Since DNA-PK is required for DSB repair in mammalian cells after IR exposure and since this residue falls within the MDM2-binding domain of the protein, this was an attractive model of p53 stabilization after IR. However, several recent reports have shown that Ser15 of p53 is phosphorylated in cells deficient in DNA-PK and that p53 accumulation in these cells is capable of generating cell cycle arrest or apoptosis after IR (Abraham et al.,…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.
- Dr. Jace is a research officer in a laboratory that studies anticancer treatment. She is interested to test a plant extract for its apoptosis-inducing effect on colon cancer cells. After incubating the cells with the extracts, she is using the FITC Annexin V Apoptosis Detection Kit I by BD Biosciences for her apoptotic assay. Discuss the detection of apoptosis using this kit and include the utilization of flow cytometry in her experiment.BCL2 binds to and inactivates BAX and other pro-apoptotic proteins, thereby inhibiting apoptosis. Venetoclax has been approved for marketing in patients with chronic lymphocytic leukemia (CLL) Venetoclax is a highly selective BCL2 inhibitor that disrupts the interaction of this protein with BH3 domain proteins thereby permitting apoptosis. Proapoptotic Proapoptotic proteins protein binds to BCL2 BCL2 Venetoclax Venetoclax displaces proapoptotic proteins BCL2 Venetoclax Proapoptotic proteins No venetoclax binding BCL2 Glys01Val mutation Which of the following can you conclude from this information? Select all that apply Bcl2- mutations that prevent Ventoclax binding promote cell survival Venetoclax binding to Bcl2 promotes cell survival . Venetoclax binding to Bcl2 promotes cell death Proapoptotic protein binding to Bcl2 promotes cell survivalI 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.