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BMS2062 - Introduction to bioinformatics S2 2025
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In the image below, there is a comparison of DMSO-treated (control) & ivacaftor treated epithelial lung cells, which contain ∆508 CFTR proteins. How could an additional experiment be used to determine how effective ivacaftor is at restoring the beat frequency of the cilia in epithelial lung cells, which contain the ∆508 CFTR proteins?
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For a patient who was found to have the ∆508 deletion in their CFTR gene, why should the patient take both lumacaftor and ivacaftor?
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Based on the image below, which of the following best describes how lumacaftor binds to the CFTR transmembrane domain 1?
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How did the QSAR modelling assist in lowering the EC50 of the lead compound being developed to treat people with cystic fibrosis who have the ∆508 CFTR mutation?
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The activity of drug candidates targeting CFTR has been presented as EC50. What is the difference between EC50 and Kd?
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During the drug development process referred in Applied session 11 activity 1, where a drug was being developed that bound to the CFTR protein, both the high throughput screen and the patch clamp assay were used. Why were both assays required during the drug development process, given that both techniques are membrane potential assays?
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Ivacaftor restores only 40 to 50% of ∆508 CFTR protein activity in individuals with cystic fibrosis. Why doesn’t Ivacaftor restore the ∆508 CFTR function to 100% of the native CFTR function?
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Based on the image above, which CFTR domains form the binding pocket that facilitates the Ivacaftor binding?
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After ATP hydrolysis, the CFTR chloride channel must be able to switch from an open to a closed state because:
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What scenario would cause the chloride ion channel within CFTR to be unable to open (remain stuck in the closed conformation)?
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