A knockout mouse with an ablated PRNP gene is injected with exogenous prions. Which of the following is expected to occur? Select one: a. Detection of P.PC in neuronal cell lysosomes O b. Apoptosis of neuronal cells O c. Appearance of PrPSc on the surface of the neuronal cell membrane O d. Enhanced conversion to PrPSc in the central nervous system O e. Spongiform transformation of the brain
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- A current focus of molecular medicine is to trigger or promote apoptosis of specific cells. several components of the apoptotic pathways are being targeted using this approach. for each of the following, state specifically how the treatment would be expected to stimulate or inhbit apoptosis. b. exposing cells to recombinant TRAIL protein, a ligand for thr tumor necrosis factor family of receptorsWhich of the following defects in RAS would be tumorigenic? multiple answers A. Deletion of nucleotide binding domain B. Inactivation of Guanine Exchange Factor (GEF) C. Mutation at amino acid 61 that prevents hydrolysis of bound GTP D. Inactivation of GTPase Protein (GAPS) E. Mutation that prevents binding of GTP1) Are NGN2-induced neurons (NGN2-iNs) the same as the cells in neural organoids? If not, how are they different? 2) Forced expression of the transcription factor neurogenin 2 (NGN2) induces human neurons, but to mature into electrophysiologically active neurons the require the presence of another cell type: what is that? 3)What kind of expression of NGN2 is associated with a central nervous system (CNS)-like cell? How do you know this?
- The transcription factor Pax6 is required continuallyduring the life of a mouse (or a human) for the development and maintenance of the retina. HomozygousPax6 knockout mice die soon after birth because Pax6protein is also required in essential organs, such as thepancreas.a. In order to study the role of Pax6 in eye development, a researcher wants to generate a mouse thatexpresses Pax6 everywhere except in its eyes.Describe how you could construct such a mouse.b. Suppose the scientist wants to create a mousesimilar to that in part (a), but in which the eye cellsfrom which Pax6 function has been removed nowexpress GFP. Marking the cells in this way willallow the investigator to see the shapes of the Pax6−eye cells more easily than if they did not expressGFP. Diagram a Pax6 gene construct that wouldenable her to do this experiment.You have treated undifferentiated embryonic stem cells (ESCs) with sonic hedgehog (Shh)for several days. This should induce a neural fate in your ESCs and you hope that you havebeen successful in differentiating the ESCs into NSCs. What is one assay you could use to testwhether your cells had differentiated into NSC-like cells? Name and shortly describe the assay?Which of the following statements are correct about the drug Gleevec (select all that apply)? A. Only inhibits activity of transit amplifying cells B. Gleevec is a natural product that was identified in a rare plant C. Negative side effects of drug are inhibition of PDGF and KIT D. Mutations in ABL gene cause resistance to Gleevec E. Inhibits the phosphorylation activity of tyrosine kinase
- a.What would happen if IKKbeta did not phosphorylate IkappaB? b.Why is it so hard to make cytokine therapies? c.Why would you use the MyD88 independent pathway versus the MyD88 dependent pathway?Binding of a ligand (like TGFA) to a receptor tyrosine kinase (RTK) causes all of the following except (can use cell): OA. Dimerization of the receptor B. Auto-phosphorylation of the receptor O C. Activation of Ras through an interction with GRB2 (an adaptor) and SOS (a GEF) proteins. O D. Activation of heterotrimeric G proteinsTumor cells from a person with leukemia have been analyzed to determine which oncogene is involved in the transformation. After partial sequencing of the gene, the predicted gene product is identified as a tyrosine kinase. Which of the following proteins would most likely be encoded by an oncogene and exhibit tyrosine kinase activity? A. Nuclear transcriptional activator B. Epidermal growth factor C. Membrane-associated G protein D. Platelet-derived growth factor E. Growth factor receptor
- Wilms tumor 1, or nephroblastoma, is caused by mutations in the WT1 gene, which encodes a transcription factor. You have identified a novel variant in WT1: Arg422Pro. You have control cells and cells that have been engineered to carry the homozygous WT1 p.Arg422Pro mutation. You want to assess effects of this mutation on a variety of endpoints. For each endpoint listed below, choose the one technique is best suited to answer the question. Choose from: array CGH, qRT-PCR, qPCR, RNA-seq, FISH, in situ hybridization, western blot, immunostaining, WT1 ChIP-seq, WT1 ChIP-PCR, ATAC-seq, 3C Endpoint Technique? WT1 protein amount (quantitative) Western blot WT1 protein binding to all enhancers, genome-wide Chip-seq WT1 mRNA amount (quantitative) WT1 protein subcellular localization Quantitative assessment of all mRNAs in these cells (genome-wide) RNAseq Chromatin interactions between a specific WT1 chromatin binding site (identified above)…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.Which of the following drugs would you expect would prevent transformation of cells by the Rous Sarcoma Virus (RSV) (select all that appy)? A. Tyrosine Kinase Inhibitor B. Integrase Inhibitor C. Inhibitor GTPase Activity ✓ D. Reverse Transcriptase Inhibitor E. Staurosporine (inhibitor of Ser/Thr kinases)