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In healthy humans after age 50, endogenous DNA single- and double-strand breaks increase linearly, and other forms of DNA damage also increase with age in blood mononuclear cells. [120] Also, after age 50 DNA repair capability decreases with age.
In eukaryotes, ATP-dependent chromatin remodeling complexes and histone-modifying enzymes are two factors that act to accomplish this remodeling process after DNA damage occurs. [60] Further DNA repair steps, involving multiple enzymes, usually follow. Some of the first responses to DNA damage, with their timing, are described below.
In the human hematopoietic stem cell compartment DNA damage accumulates with age. [90] In healthy humans after 50 years of age, chronological age shows a linear association with DNA damage accumulation in blood mononuclear cells. [91] Genome-wide profiles of DNA damage can be used as highly accurate predictors of mammalian age. [92]
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to repair the damage before continuing to divide. DNA damage checkpoints occur at the G1/S and G2/M boundaries. An intra-S checkpoint also exists. Checkpoint activation is controlled by two master kinases, ATM and ATR.
Healthy humans after age 50, accumulate endogenous DNA single- and double-strand breaks in a linear fashion in cellular DNA. [134] Other forms of DNA damage also increase with age. [134] After age 50 a decline in DNA repair capability also occurs. [134] These findings are in accord with the theory that DNA damage is a fundamental aspect of ...
Endogenous DNA damages occur frequently including about 50 double-strand DNA breaks per cell cycle [69] and about 10,000 oxidative damages per day (see DNA damage (naturally occurring)). During repair of double-strand breaks many epigenetic alterations are introduced, and in a percentage of cases epigenetic alterations remain after repair is ...
As a response to DNA damage, one of the responses triggered by oxidative stress is the activation of the p53. [31] The p53 protein binds to DNA, then stimulates the production of a p21, which is also known as cyclin-dependent kinase inhibitor 1. This ensures that the cell cannot enter the next stage of cell division unless the DNA damage is ...
Nucleotide excision repair (NER) is a particularly important excision mechanism that removes DNA damage induced by ultraviolet light (UV). UV DNA damage results in bulky DNA adducts — these adducts are mostly thymine dimers and 6,4-photoproducts. Recognition of the damage leads to removal of a short single-stranded DNA segment that contains ...