The major human abasic endonuclease: formation, consequences and repair of abasic lesions in DNA.
DNA continuously suffers the loss of its constituent bases, and thereby, a loss of potentially vital genetic information. Sites of missing bases--termed abasic or apurinic/apyrimidinic (AP) sites--form spontaneously, through damage-induced hydrolytic base release, or by enzyme-catalyzed removal of modified or mismatched bases during base excision repair (BER). In this review, we discuss the structural and biological consequences of abasic lesions in DNA, as well as the multiple repair pathways for such damage, while emphasizing the mechanistic operation of the multi-functional human abasic endonuclease APE1 (or REF-1) and its potential relationship to disease.
Wilson
D M
DM
Molecular and Structural Biology Division, Lawrence Livermore National Laboratory, Livermore, CA 94551, USA. wilson61@llnl.gov
Barsky
D
D
D000818:Animals; D019757:Carbon-Oxygen Lyases / Q000096:biosynthesis* / Q000737:chemistry / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase; D043223:Deoxyribonuclease IV (Phage T4-Induced); D011487:Protein Conformation
D043223:Deoxyribonuclease IV (Phage T4-Induced); D019757:Carbon-Oxygen Lyases; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase