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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A: False statement about tumor suppressor genes.
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A: Proliferation is the cellular response.
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A: This pathway is receptor tyrosione kinase.
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A:
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- A human gene called theCFTR gene (for cystic fibrosis transmembrane regulator) encodes aprotein that functions in the transport of chloride ions across the cellmembrane. Most people have two copies of a functional CFTR geneand do not have cystic fibrosis. However, a mutant version of the CFTRgene is found in some people. If a person has two mutant copies ofthe gene, he or she develops the disease known as cystic fibrosis. Arethe following descriptions of this disease related to genetics at themolecular, cellular, organism, or population level?A. People with cystic fibrosis have lung problems due to a buildupof thick mucus in their lungs.B. The mutant CFTR gene encodes a defective chloride transporter.C. A defect in the chloride transporter causes a salt imbalance inlung cells.D. Scientists have wondered why the mutant CFTR gene is relativelycommon. In fact, it is the most common mutant gene that causesa severe disease in persons of Northern European descent. Onepossible explanation why…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 the cellular regulatory pathways that controlcell growth and proliferation, the products of oncogenesare stimulatory components and the products of tumorsuppressor genes are inhibitory components.'' 'Is this statement true? Explain why or why not.
- The retinoblastoma tumor suppressor gene Rb (RB1) codes forthe retinoblastoma protein (pRB). pRB prevents the progression of the cell cycle through G1 if DNA has been damaged. Itdoes so in part because it binds a transcription-activatingdimer referred to as E2F-DP. The pRB-E2F/DP complex recruits a histone deacetylase to chromatin. Explain.Cell 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.Predict the effects of the following mutations on the ability of a cell to undergo apoptosis:a. Mutation in Bad such that it cannot be phosphorylated by protein kinase B (PKB)b. Overexpression of Bcl-2c. Mutation in Bax such that it cannot form homodimersOne common characteristic of cancer cells is a loss of function in the apoptotic pathway. Which of the mutations listed above might you expect to find in some cancer cells?
- A researcher studying a line of cancer cells noticed that cellular content of RhoBTB3 and Cyclin E1 increase and decrease through the cell cycle. a. He hypothesizes that RhoBTB3 signaling regulates the production of Cyclin E1 and the entry of the cell into mitosis. Based on the data below, explain why his results do not support this hypothesis. Identify what conclusions are supported by this data. b. Suppose that the researcher can engineer a cell line in which RhoBTB3 expression can be induced by the addition of a drug. Design an experiment using this cell line to test whether RhoBTB3 regulates the production of Cyclin E1. Describe what results he can expect if his hypothesis is correct.Certain hormones, such as epinephrine, can increase the levels ofcAMP within cells. Let’s suppose you pretreat cells with or withoutepinephrine and then prepare a cell extract that contains theCREB protein.You then use an electrophoretic mobility shift assay to analyzethe ability of the CREB protein to bind to a DNA fragmentcontaining a cAMP response element (CRE). Describe what theexpected results would be.Tumor-suppressor genes are normal human genes that prevent uncontrollable cell growth. Starting with a normal laboratory humancell line, describe how you could use transposon tagging to identifytumor-suppressor genes. (Note: When a TE hops into a tumorsuppressorgene, it may cause uncontrolled cell growth. This is detected as a large clump of cells among a normal monolayer of cells.)
- 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…I. The retinoic acid receptor (RAR) is a transcription factor that is similar to steroid hormone receptors. Thesubstance (ligand) that binds to this receptor is retinoicacid. One of the genes whose transcription is activatedby retinoic acid binding to the receptor is myoD. Thediagram that follows shows a schematic view of theRAR proteins produced by genes into which one oftwo different 12-base double-stranded oligonucleotides had been inserted in the ORF. The insertion site(a–m) associated with each mutant protein is indicatedwith the appropriate letter on the polypeptide map.For constructs encoding proteins a–e, oligonucleotide 1(5′ TTAATTAATTAA 3′ read off either strand) wasinserted into the RAR gene. For constructs encoding proteins f–m, oligonucleotide 2 (5′ CCGGCCGGCCGG 3′)was inserted into the gene.NH2 f g h i j k l m COOHa b c d eThe wild-type RAR protein can both bind DNA and activate transcription weakly in the absence of retinoic acid(RA) and strongly in RA’s presence. Each…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.