Channel: In Vivo Podcast clear
| # | Channel | Title | Views | Likes | Cmts | Score | Sentiment | Duration | Transcript | Link |
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| 1 | In Vivo Podcast | Yamanaka's 4 Proteins: Unlocking Stem Cell Rejuvenation #shorts | 222 | 3 | 49.5 | 3:00 | Dr. Yamanaka was the one to show that by introduction of only four proteins, you can revert a skin cell into a stem cell. So how do you see that perhaps playing into these efforts of longevity? I think that's going to turn out to be like very important, huge, you know, reprogramming epigenetic reprogramming. I think it still needs refinement. We've done experiments in my lab, like basically taking progerias, you know, skin cells, bringing them into stem cells. So it works even in progeria. You can sort of, despite the damaged, despite the compromised telomeres, you can still like revert those cells back to the embryonic state. It's interesting. You know, infastinatingly, yeah, this is a good point, like the, so lamin A, the protein that's mutated produces progerin, but interestingly, lamin A and progerin are not expressed in embryonic stem cells. So if you take a skin cell from a progeria patient and reprogram it back to an embryonic form, you're effectively removing the consequence of the mutation, at least temporarily, because the protein is no longer produced in those embryonic cells. So phenotypically, they look normal. You know, they look quite normal at that point. So it gives you an opportunity to go in, you know, perhaps and do gene editing, you know, fix the mutation. And then when you rederive somatic cells from those embryonic cells, they should not undergo early senescence, because you basically fix the mutation at the embryonic. So that's my question for you. When you, when you induce progeria fiber blast back into a stem cell like state, and then don't intervene and then differentiate them again, they then present the same progeria phenotypes before. They do. Yes. Interesting. No, the, yeah, the, you know, because the DNA sequence is still there, and it's going to start making progerian again. Right. And, you know, the cells reacquire the progeria phenotype. And so the gene is silenced when it's in that embryonic state. Exactly. Yeah. Very interesting. Which is kind of like a nice sort of caveat to that reprogramming story, and that it gives you like a temporal window. Because the, you know, to intervene to use CRISPR or something like that, the mutation is not active in that cell type. | ↗ |