Experimental study reveals feedback loops between DNMT1, autophagy, and cellular senescence in aging tissues, highlighting epigenetic mechanisms behind organ decline and canities.
: 4-OHT, 4-hydroxytamoxifen; ChIP, chromatinimmunoprecipitation; D, dasatinib; D-gal, D-galactose; DCT/Trp-2, dopachrometautomerase; DMRs, differentially methylated regions; DNAm, DNA methylation; DNMTs,DNA methyltransferases; DSBs, double-stranded breaks; ETO, etoposide; GST, glutathione-S-transferase; HEK293T,human embryonic kidney 293T; HEM, human epidermal melanocytes; Hydr, hydralazine;IP, immunoprecipitation; IR, ionizingradiation; KIF1A, kinesin family member 1A; M, methylated; MmIMCD3,mouse inner-medullary collecting duct 3; MITF, melanocyte inducingtranscription factor; MSP, methylation specific PCR; NCBI, national center for biotechnologyinformation; N-me, N-methyladenosine; PBMCs, peripheral blood mononuclear cells;Pro, proliferating; Q, quercetin; Rapa, rapamycin; RRBS, reduced representationbisulfite sequencing; RT, reverse transcription; SA-GLB1/β-Gal, senescence-associatedgalactosidase beta 1; SASP, senescence-associated secretory phenotype; Sen, senescent; SNP, single nucleotidepolymorphism; TYR, tyrosinase; TYRP1/Trp-1, tyrosinase related protein 1; UHRF1,ubiquitin like with PHD and ring finger domains 1; UM, unmethylated; UTR, untranslatedregion; WGBS, whole-genome bisulfite sequencing.
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