Project description:We discovered that the cell-free chromatin assembly system senses free DNA ends and mounts a DNA double-strand break response. DNA ends are first recognized by the Ku complex and later resected. The phosphorylation of H2A.V (homologous to gH2A.X) initiates at DNA breaks and spreads over ten thousands of base pairs of DNA within a few minutes. The phosphorylation of gH2A.V remains tightly associated with the damaged DNA in cis and does not transfer to intact DNA circles in the same reaction. Our descriptions of the damage-related proteome and phospho-proteome provide a rich resource for in-depth mechanistic analyses of the DNA chromosome break response in this model system.

2019-07-22 | GSE126415 | GEO

Vaping Dose, Device Type, and E-Liquid Flavor are Determinants of DNA Damage in Electronic Cigarette Users.

Project description: Not available

| S-EPMC10202635 | biostudies-literature

Chromosomal reinsertion of broken RSS ends during T cell development.

Project description: Not available

| S-EPMC2118463 | biostudies-literature

Sociodemographic characteristics and vaping motives as potential correlates of early vaping initiation.

Project description: Not available

| S-EPMC11747700 | biostudies-literature

Psychological and Demographic Predictors of Vaping and Vaping Susceptibility in Young Adults.

Project description: Not available

| S-EPMC8415821 | biostudies-literature

Peroxiredoxin 1 protects telomeres from oxidative damage preserving chromosome ends for extension by telomerase

Project description:With the increase of atmospheric oxygen 2.3 billion years ago, mechanisms evolved to mitigate the toxic effects of oxygen radicals. Telomeres appear particularly susceptible to oxidative damage, which leads to cellular and organismal aging, cancer, cardiac failure and other diseases. Specific mechanisms of telomere protection from oxidative damage and the molecular consequences of the damage have not been described. Here, we identify the antioxidant enzyme peroxiredoxin 1 (PRDX1) enriched in telomeric chromatin in S and G2 phases of the cell cycle during which telomeres become replicated. PRDX1 depletion leads to oxidative damage of telomeric DNA without affecting the bulk of genomic DNA. The oxidized nucleotide 8-oxo-2’deoxyguanosine-5’-triphosphate (8oxodGTP) can be incorporated by telomerase into telomeric repeats but it mediates premature chain termination when incorporated as first G in the telomeric 5’-TTAGGG-3’ sequence. In dependency of the alignment position within the telomerase RNA template, terminus 8oxoG containing DNA substrates also completely block extension by telomerase. We propose two major mechanisms by which PRDX1 counteracts telomere damage and aging. In safeguarding telomeres from oxygen radicals, PRDX1 prevents DNA damage, telomere replication defects and mutations that will perturb recognition of telomeric DNA by shelterin components. In preventing modification of the telomeric DNA substrate and the dNTP pool, PRDX1 preserves telomeres for elongation by telomerase.

2016-12-07 | PXD002626 | Pride

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