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CRISPR-dCas9 epigenome editing platforms employ catalytically dead Cas9 fused to epigenetic effectors ( TET1 for active demethylation, DNMT3A for targeted methylation) without DNA breaks, enabling precise chromatin manipulation

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doi: 10.1007/s007020100013

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As expected, Ampk, known to inhibit mTORC1, is less active upon Stard7 deficiency in Apc +/Min mice

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