Join us for an in-depth analysis of the differing roles of antagonist and agonist in the medical field, with our session providing clear, relatable explanations to ensure your understanding. Discover the processes behind combination therapy, including the activation or inactivation of modulators, using cystic fibrosis as an example. We also delve into stop codon readthrough and nonsense mutations, specifically focusing on Duchenne Muscular Dystrophy. Learn about the implications of protein-related therapies, their mutation-specific nature, and their role in mitigating disease severity rather than providing an outright cure. This enlightening session promises to enhance your understanding and professional application of these crucial concepts.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.
OK. I think um med metal does not wanna work at all today. Um Thank you for uh whoever's actually telling me everything F T next week. OK. Antagonist versus agonist, you guys should understand that antagonists block agonists activate. Are you all right with that? I hope so. Uh And hopefully, I went through modulate as well. Combination therapy uh is a chaperone which folds and an a, an activator or a modulator which activates or inactivates depending on what it needs to do. Uh An example of this is Trita for cystic fibrosis electro afta or tether cafta will fold the protein correctly, the chloride ion channel and then it will uh make it work when it's at the epithelium. Uh That's pretty simple to remember. I hope. Um now we have stop codon readthrough. Uh So these are called by nonsense mutations. I like to think of nonsense as, as if someone's speaking nonsense, I'll tell them to stop talking. Similarly, a nonsense mutation is a premature stop codon. It means that the rest of the DNA sequence isn't transcribed. Therefore, you have a shorter amino acid sequence and therefore a truncated protein. In this case, it is for Duchenne muscular dystrophy, which makes, uh, a truncated dystrophin after urine, basically ignores it, uh, and make sure you have a slightly longer protein which would be semi functional or functional. But once again, like most of the protein related therapies, they will be mutation specific and will not be a cure. They'll simply call it to be a less severe version of the original disease and treat symptoms. Uh, can everyone has me still, uh, like and cool.
