Alex K Chen Posted November 13 Report Share Posted November 13 (edited) https://pmc.ncbi.nlm.nih.gov/articles/PMC10742131/ Spliceosome disruption in aging (which is part of the cause of longer transcripts going down far more than other transcripts) is one of the most universally expressed features [see a kejun ying paper] yet it is also slightly ameliorated by CR. I'm esp interested in whether the spliceosome has VERY LONG proteins that are more likely to go way down with age (tough this is really most common for neuron proteins like prolly neurexin) aging results in deregulation of AS transcripts (part of the reason why older people have slightly more progerin), including mis-sense AS transcripts, cryptic splice sites, and skipped exons... [the question is are mis-sense AS transcripts or skipped exons more common?] Or inappropriately spliced exons? Quote These studies in cells have highlighted over 400 differential splicing events associated with the senescent phenotype and have found that exon skipping is the overrepresented splicing event. The studies on human tissues focused their investigation on events occurring in brain [10,11] or 48 primary tissues [20]. There's one paper coming from Gladyshev lab on this soon! Edited November 13 by Alex K Chen Quote Link to comment Share on other sites More sharing options...
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