Concept explainers
To determine: What would be the difficulties of finding cancer drugs that works by inhibiting tyrosine kinase given that similar kinases also function in normal cells.
Introduction: Enzyme-linked receptor is a transmembrane protein with a binding site for signaling molecule outside the cell and an enzyme component inside the cell. An example of enzyme-linked receptor is tyrosine kinase. On binding of ligands with the enzyme-linked receptors, receptor protein comes close together in the plasma membrane and forms dimer which initiates activation of downstream molecules and causes cellular response.
To suggest: Whether it could be possible to develop such new medication through government-sponsored research. Why or why not.
Introduction: Enzyme-linked receptor is a transmembrane protein with a binding site for signaling molecule outside the cell and an enzyme component inside the cell. An example of enzyme-linked receptor is tyrosine kinase. On binding of ligands with the enzyme-linked receptors, receptor protein comes close together in the plasma membrane and forms dimer which initiates activation of downstream molecules and causes cellular response.
To suggest: Alternatives if it is not possible to develop new such medication through government-sponsored research.
Introduction: Enzyme-linked receptor is a transmembrane protein with a binding site for signaling molecule outside the cell and an enzyme component inside the cell. An example of enzyme-linked receptor is tyrosine kinase. On binding of ligands with the enzyme-linked receptors, receptor protein comes close together in the plasma membrane and forms dimer which initiates activation of downstream molecules and causes cellular response.
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- 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.arrow_forwardPay close attention to the information related to figure 3.14a and the structure of the PKA catalytic site in this figure. In a few well-written sentences, propose the following: A mutation that would result in PKA becoming a dead kinase*. A mutation that would result in PKA becoming a constitutively active** kinase.arrow_forwardSuppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: a. Which of the ligands, based on the table, has the highest specificity in binding to the target Protein J?arrow_forward
- Suppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: Describe the relative binding affinities of Ligand A to Protein K and to the active and inactive forms of Protein J. Determine which will Ligand A bind with the highest, medium, and lowest affinity.arrow_forwardSuppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: a. Which of the ligands, based on the table, may be expected to be the most potent or have the highest activity against cancer? Explain. b. Which of the ligands, based on the table, may be expected to be least toxic to normal cells? Explain.arrow_forwardCyclin-dependent kinases are a type of "microchip" protein that require multiple inputs (i.e., structural alterations) to be activated-- and thus are active only under specific conditions (as shown in the diagram below). How does limiting activity to when all conditions have been met help the cell function properly? INPUTS has this phosphate been removed? been added? has this is cyclin present? phosphatearrow_forward
- Working out the order in which the individual components in a signaling pathway act is an essential step in defining the pathway. Imagine that two protein kinases, PK1 and PK2, act sequentially in a kinase cascade. When either kinase is completely inactivated, cells do not respond to the normal extracellular signal. By contrast, cells containing a mutant form of PK1 that is permanently active respond even in the absence of an extracellular signal. Double mutant cells that contain inactivated PK2 and permanently active PK1 respond in the absence of a signal. Draw out the signaling pathway in a wild-type cell. What outcome is predicted for a double mutant cell with an activating mutation in PK2 and an inactivating mutation in PK1? Explain your reasoningarrow_forwardplease help me with this problemarrow_forwardYou are a scientist studying two related congenital diseases, Noonan syndrome and Tiger syndrome. People with these syndromes are characterized by differences in heart development and skeletal morphology. Individuals with either syndrome are also susceptible to certain types of cancer, such as leukemia. Some cases of Noonan syndrome are caused by dominant activating variants of the MAP kinase-kinase-kinase protein Raf. The genetic basis of Tiger syndrome is unknown. Your team is involved in a clinical trial, which finds that drugs that inhibit Raf are associated with improved outcomes in cancer patients with Noonan syndrome. You find that Tiger syndrome patients also respond to the treatment, so you sequence the Raf gene in several patients, but find no mutations. Based on what you know about the MAP kinase pathway, you sequence the Sos gene in Tiger syndrome patients. You find that 5 out of 10 patients in your trial have a SNP that changes the amino acid Thr266 to Lys (T266K).…arrow_forward
- GTP binding proteins are molecular switches. How do GTP binding proteins work? Provide two examples of GTP binding proteins that function in intracellular protein transport. Make a drawing that illustrates the function of each of these proteins in their respective roles. Predict the direct outcome of a mutation that: Inhibits GTPase activity Inhibits interaction with the GEFarrow_forwardHelparrow_forwardIf you have a protein kinase that is regulated by both small molecule inhibitors as well as by phosphorylation, and is part of a cooperative enzyme complex that works as part of a larger pathway involving kinase and GTPase proteins please explain where on this protein regulation could occur, how different types of inhibition could control the function of the protein as well as the function of the complex, and how the protein could regulate other proteins. (This question was previously answered but it was answered incompletely mentioning an herbicide developed in the 1950's. Apparently, it was a plagiarized excerpt from an NCBI article. This is a repost for a full and complete answer. Thank you so much for your help! :) )arrow_forward
- Biology (MindTap Course List)BiologyISBN:9781337392938Author:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. BergPublisher:Cengage Learning