A single hydrophobic cleft in the Escherichia coli processivity clamp is sufficient to support cell viability and DNA damage-induced mutagenesis in vivo |
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Authors: | Mark D Sutton Jill M Duzen Sarah K Scouten Ponticelli |
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Affiliation: | (1) Department of Biochemistry, and Witebsky Center for Microbial Pathogenesis and Immunology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 3435 Main Street, 140 Farber Hall, 14214 Buffalo, NY, USA;(2) Department of Biochemistry, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 3435 Main Street, 140 Farber Hall, 14214 Buffalo, NY, USA;(3) Department of Immunology, Roswell Park Cancer Institute, 14263 Buffalo, NY, USA |
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Abstract: | Background The ubiquitous family of DnaN sliding processivity clamp proteins plays essential roles in DNA replication, DNA repair, and cell cycle progression, in part by managing the actions of the different proteins involved in these processes. Interactions of the homodimeric Escherichia coli β clamp with its known partners involves multiple surfaces, including a hydrophobic cleft located near the C-terminus of each clamp protomer. |
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