As someone interested in the topic but not having the background in this field it would be a lot easier to understand just by adding some natural retorical pauses (as we normally do when we talk) 😀 It is better better to speed up the video pase than to slow it down since the quality differs. Just a tip! Thanks for making this information available! (even though I only grasp half of it just because some retorical details 😉)
But is it necessarily a bad thing that SIRT1 gets degraded within a cell that is already senescent? It would be important to know if autophagy degrades SIRT1 in a normal cell which would be bad. My takeaway is that activating/upregulating SIRT1 with resveratrol etc may prevent the onset of senescence, but once senescence has set in, I don't see how rescuing SIRT1 in those senescent cells helps with anything at all.
Please help me answer this .., why would Sirt1 have a higher expression in high fat diet than in mice fed with NMN ? Would really appreciate your response Thankyou
Hello, so it has always been stated that deacetylation of p53 reduced its dna binding ability, so short answer yes. But, i am certain the situation is a lot more complex and given that p53 has >300 PTMs i doubt it would be that simple!! This question bugs me a lot!
