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It is involved in base excision repair.
AP sites can be formed by spontaneous depurination, but also occur as intermediates in base excision repair.
Most damage to bases in DNA is repaired by the base excision repair pathway.
DNA polymerase beta maintains genome integrity by participating in base excision repair.
Both mechanisms form a single-strand break, which is then repaired by either short-patch or long-patch base excision repair.
Base excision repair is the mechanism by which damaged bases in DNA are removed and replaced.
It initiates base excision repair by removing damaged bases to create abasic sites that are subsequently repaired.
Nucleotidyl transferase is a component of the repair pathway for single nucleotide base excision repair.
This is called base excision repair (BER).
Correction of this mutation involves the use of alkyladenine glycosylase (Aag) during base excision repair.
Caloric restriction promotes genomic stability by induction of base excision repair and reversal of its age-related decline.
Both the deamination and the oxidation products have been shown to be repaired by TDG, a glycosylase which is involved in base excision repair.
AICDA can deaminate 5-methylcytosine, which can then be replaced with cytosine by base excision repair.
Base excision repair of ionizing radiation-induced DNA damage in G1 and G2 cell cycle phases.
When base excision repair in the cell is compromised, mutations in other genes build up, leading to cell overgrowth and possibly tumor formation.
MYH is another important example of a stability gene that confers risk of colorectal cancer on the basis of defective base excision repair.
The few that survived had developed enzymes that verified the genetic material and broke up thymine dimer bonds, known as base excision repair enzymes.
Base excision repair (BER), which repairs damage to a single base caused by oxidation, alkylation, hydrolysis, or deamination.
DNA glycosylases are a family of enzymes involved in base excision repair, classified under EC number EC 3.2.2.
Apurinic sites in double-stranded DNA are efficiently repaired by portions of the base excision repair (BER) pathway.
MYH glycosylase fixes these mistakes by base excision repair, such that mutations do not accumulate in the DNA and lead to tumor formation.
But elimination of any gene essential for base excision repair kills the embryo-it is too lethal to display symptoms (much less symptoms of cancer or "accelerated aging").
MSH2 is involved in many different forms of DNA repair, including transcription-coupled repair, homologous recombination, and base excision repair.
In biochemistry and genetics, base excision repair (BER) is a cellular mechanism that repairs damaged DNA throughout the cell cycle.
These include the nucleotide excision repair, the mismatch repair, the base excision repair, the double strand break repair and the cross link repair pathways.