that binds Fsh3 is a receptor tyrosine kinase (RTK) and there are numerous fish tumor cell lines that have a mutation for the gen for this receptor. Which of the following mutations would be expected to promote uncontrolled cell proliferation.
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- 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 GTPThe PYK gene codes for the expression of pyruvate kinase, which is one of the enzymestargeted for anti-cancer drug design. You have identified an RNAi that targets the mRNAof PYK gene. To study the effect of the RNAi towards pyruvate kinase, the respected RNAiis expressed in Saccharomyces cerevisiae. The level of pyruvate kinase can be detectedwith a fluorescent antibody.(a). Predict the result that you will obtain in recombinant S. cerevisiae that expresses therespected RNAi.(b). Compare the result in Q3a(i) with the wild-type S. cerevisiae.In the normal cycle of Ras activity, when Ras is bound to y activity that removes a phosphate to convert GTP back to GDP and this it is inactive. Activation of Ras involves exchanging GDP for The Ras protein has intrinsic Ras. inactivates activates ATP GTP «< Questic A Moving to another question will save this response. ADP GDP GTPase Clo nuclease
- The oscillatory clock that drives somite forma-tion in vertebrates involves three essential componentsHer7 (an unstable repressor of its own synthesis), Delta (atransmembrane signaling molecule), and Notch (a trans-membrane receptor for Delta). Notch is bound by Delta onneighboring cells, activating the Notch signaling pathway,which then activates Her7 transcription. Normally, thissystem works flawlessly to create sharply defined somites(Figure Q21–2A). In the absence of Delta, however, onlythe first five somites form normally, and the rest are poorlydefined (Figure Q21–2B). If a pulse of Delta is suppliedlater, somite formation returns to normal in the regionswhere Delta was present (Figure Q21–2C). A diagram ofthe connections between the components of the clockand how they interact in adjacent cells is shown in FigureQ21–2D. In the absence of Delta, why do the cells becomeunsynchronized? What is it about the presence of Deltathat keeps adjacent cells oscillating in synchrony?# 3 You've engineered a mutant cell where the FADD adapter was truncated. The mutant FADD only contains the Death Domain, and lacks the Death Effector Domain. What is the most likely phenotypic outcome for this mutant cell when presented with the Fas ligand? 20 E O The Fas/FasL oligomer is formed, but apoptosis is blocked O The Fas/FasL oligomer is formed, and apoptosis is hyperactivated O The Fas/FasL oligomer is not formed, and apoptosis is blocked O The Fas/FasL oligomer is not formed, but apoptosis is hyperactivated F3 $ 4 DOD 000 R F4 % 5 F5 T BARAT 6 tv @ MacBook Air F6 Y & 7 F7 U * ➤11 8 F8 · 9 F9Cell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.
- Proto-oncogenes can be converted to oncogenes in a numberof different ways. In some cases, the proto-oncogene itselfbecomes amplified up to hundreds of times in a cancer cell.An example is the cyclin D1 gene, which is amplified in somecancers. In other cases, the proto-oncogene may be mutatedin a limited number of specific ways, leading to alterations inthe gene product’s structure. The ras gene is an example of aproto-oncogene that becomes oncogenic after suffering pointmutations in specific regions of the gene. Explain why thesetwo proto-oncogenes (cyclin D1 and ras) undergo such differentalterations to convert them into oncogenesI 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.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 ◆ Previous
- Rous Sarcoma Virus can cause cancer in infected cells. The tumor causing nature of the virus is linked to it harbouring a gene that codes for a unique receptor tyrasine kinase (RTK). What is it about the tyrosine kinase that accounts for the tumor-causing nature of the virus? O It is unrelated to any human kinase and thus is able to act uncontrollably in causing cell division. O It cantain activate downstream effectors without binding to a SH2 domain. O It lacks the carboxy-terminal regulatory domain that is present in RTKS of non-cancerous cells.What factors called mitogens stim-ulate cultured mammalian cells to proliferate by inducing expression of early response genes. Many of these genesencode transcription factors that stimulate expression ofgenes encoding the G1/S phase cyclins and E2F transcriptionfactors.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