| Literature DB >> 6348032 |
A F Wahl, J W Hockensmith, S Kowalski, R A Bambara.
Abstract
An investigation of the mechanism of the polAex1 mutation in vitro suggested that the excision repair deficiency observed in vivo does not result from an inability of the enzyme to nick translate. The defect appears to reside in the inability of the enzyme to effectively generate a nick structure to serve as a substrate for DNA ligase.Mesh:
Substances:
Year: 1983 PMID: 6348032 PMCID: PMC217772 DOI: 10.1128/jb.155.2.922-925.1983
Source DB: PubMed Journal: J Bacteriol ISSN: 0021-9193 Impact factor: 3.490