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Abstract

An investigation of the mechanism of the polAexl 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.

Publication Date

1-1-1983

Journal Title

Journal of Bacteriology

Document Type

Article

Included in

Life Sciences Commons

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