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- Apoptosis
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- DNA Repair
- Base Excision Repair
- Checkpoint signaling
- Chromatin Research
- Direct Reversal of DNA Damage
- DNA Double Strand Break Repair
- DNA Polymerases
- DNA replication, Transcription, Translation and Splicing
- Editing and Processing Endonucleases
- Genes Sensitive to DNA Damaging Agents
- Homologous Recombination
- Mismatch Repair
- Modulation of DNA Pools
- Non-homologous end-joining
- Nucleotide-Excision Repair
- Zinc Finger
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- Translation Control
- Tyrosine Kinases
- Wnt Signaling Pathway
- modENCODE Antibodies
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Base Excision Repair
Base excision repair (BER) is a cellular mechanism that repairs damaged or incorrect bases in DNA. Although several variations of this mechanism exist, three general steps are present in each. First, DNA glycosylase breaks the beta-N glycosidic bond to create an AP site, a location along the DNA strand where there is neither a purine or pyrimidine base. AP endonuclease then recognizes this site and cuts the damaged DNA strand upstream of the AP site, thus producing a 3?-OH terminus. Lastly, DNA polymerase uses endonuclease activity to replace the damaged nucleotide and extend the 3?-OH terminus and DNA ligase seals the new DNA strand.
All Base-excision Repair Antibodies, Lysates, Proteins and RNAi
Research Cloud — Top terms most co-occuring with "Base-excision Repair" in scientific publications. Click to explore.
