Complete the following statements by selecting one of the two options provided. A mutation that [Select] arrest. The [Select] the kinase activity of S-Cdk will lead to cell-cycle of a cell cycle checkpoint will lead to cell-cycle arrest. A mutation that [Select] the activity of the monomeric GTPase Ras will lead to hyper-proliferation of cells [Hint: review Ras and the MAP kinase pathway covered in Topic 6]. A mutation that [Select] proliferation of cells [Hint: review the MAP kinase pathway covered in Topic 6]. the activity of MEK 1/2 will lead to hyper-

Complete the following statements by selecting one of the two options provided. A mutation that [Select] arrest. The [Select] the kinase activity of S-Cdk will lead to cell-cycle of a cell cycle checkpoint will lead to cell-cycle arrest. A mutation that [Select] the activity of the monomeric GTPase Ras will lead to hyper-proliferation of cells [Hint: review Ras and the MAP kinase pathway covered in Topic 6]. A mutation that [Select] proliferation of cells [Hint: review the MAP kinase pathway covered in Topic 6]. the activity of MEK 1/2 will lead to hyper-

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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This phosphatase removes an inhibitory phosphotyrosine phosphate from serine protein kinase, mentioned in question 6, which activates kinase. What phosphatase is it? This is what question 6 says....This is the serine protein kinase that when activated in a complex cyclin, controls onset of mitosis and M-phase of the cell cycle. 1. Cyclin A/B 2. Wee 1 3. TOR (Target of Rapmycin) 4. Cdk1 5. none of the these ***I believe the answer is Cdk1 for number 6, but I could be wrong
(a) the cell cycle is divided into different phases (referred to as M, G0, G1, S and G2); Can you account for what happens during the different parts of the cycle and out of it is checked? ( b) What is the difference between apoptosis and necrosis? ( c) What are caspases and what is their function in the cell?
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
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.
What is the effect of having fluctuating cyclin levels throughout the cell cycle, while the levels of its corresponding cyclin dependent kinase stay relatively constant? Explain.
Which of the following could be classified as an oncogene? None are possible oncogenes A mutant of MAP kinase that was active with or without being phosphorylated All are possible oncogenes A mutant of MEK with significantly reduced enzyme activity A mutant cAMP phosphodiesterase that made it super-active
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
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…
Can 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.,…
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?
Why is the p53-meditated apoptosis pathway, and the GSK3 signaling pathway important for cancer therapy. Explain each of them in 3-5 sentences.
Stimulation of map kinase can help regulate cell division and cell mass. the following effects of map kinase activation explains an increase in cell mass. Phosphorylation of RSK (kinase and the subsequent phosphorylation of S6 ribosomal subunit. Phosphorylation of myosin light chain Phosphorylation of glyceraldehyde dehydrogenase phosphorylation of histone H1 none of these