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Basic steps of base excision repair. Base excision repair (BER) is a cellular mechanism, studied in the fields of biochemistry and genetics, that repairs damaged DNA throughout the cell cycle. It is responsible primarily for removing small, non-helix-distorting base lesions from the genome. The related nucleotide excision repair pathway repairs
22256 Ensembl ENSG00000076248 ENSMUSG00000029591 UniProt P13051 P97931 RefSeq (mRNA) NM_080911 NM_003362 NM_001040691 NM_011677 RefSeq (protein) NP_003353 NP_550433 NP_001035781 NP_035807 Location (UCSC) Chr 12: 109.1 – 109.11 Mb Chr 5: 114.27 – 114.28 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Uracil-DNA glycosylase (also known as UNG or UDG) is an enzyme. Its most ...
Enzymes, namely DNA glycosylases, also commonly create AP sites, as part of the base excision repair pathway. In a given mammalian cell, 5000–10,000 apurinic sites are estimated to form per day. Apyrimidinic sites form at a rate roughly 20 times slower, with estimates at around 500 formation events per day, per cell.
Uracil-DNA glycosylases are DNA repair enzymes that excise uracil residues from DNA by cleaving the N-glycosydic bond, initiating the base excision repair pathway. Uracil in DNA can arise either through the deamination of cytosine to form mutagenic U:G mispairs, or through the incorporation of dUMP by DNA polymerase to form U:A pairs. [18]
Apurinic/apyrimidinic (AP) endonuclease is an enzyme that is involved in the DNA base excision repair pathway (BER). Its main role in the repair of damaged or mismatched nucleotides in DNA is to create a nick in the phosphodiester backbone of the AP site created when DNA glycosylase removes the damaged base.
AP sites are pre-mutagenic lesions that can prevent normal DNA replication. All cells, from simple prokaryotes to humans, have evolved systems to identify and repair such sites. Class II AP endonucleases cleave the phosphodiester backbone 5' to the AP site, thereby initiating a process known as base excision repair (BER). The APEX gene ...
The XRCC1 protein does not have enzymatic activity, but acts as a scaffolding protein that interacts with multiple repair enzymes. The scaffolding allows these repair enzymes to then carry out their enzymatic steps in repairing DNA. XRCC1 is involved in single-strand break repair, base excision repair and nucleotide excision repair. [6]
Microhomology-mediated end joining (MMEJ), also known as alternative nonhomologous end-joining (Alt-NHEJ) is one of the pathways for repairing double-strand breaks in DNA. As reviewed by McVey and Lee, [1] the foremost distinguishing property of MMEJ is the use of microhomologous sequences during the alignment of broken ends before joining, thereby resulting in deletions flanking the original ...