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1 of Escherichia coli to a virulent mutant of phage P1.
2 oter, thereby supporting the lytic growth of phage P1.
3 plementary in supporting the lytic growth of phage P1 and acid resistance of an E. coli sspA mutant.
4 her recombinases in the Int family (Cre from phage P1 and Int from Haemophilus influenzae phage HP1)
5 ional activator for the lytic development of phage P1 and is essential for stationary phase-induced a
6 E. coli MLK217 into S. typhimurium MGS-7 via phage P1 and subsequently via phage P22 into the virulen
13 t for both transcriptional activation of the phage P1 late promoter and acid resistance of E. coli.
14 E. coli and to activate transcription from a phage P1 late promoter, thereby supporting the lytic gro
15 L4 and L22 mutations into wild-type cells by phage P1-mediated transduction demonstrated that each al
17 anipulated using the generalized transducing phage P1, presumably because its extensive O antigen obs
18 are lysogenic for P1 and when infected with phage P1 produce only approximately 1% the number of inf
20 sts of a promoterless derivative of cre, the phage P1 recombinase, carried on a plasmid, and two chro
21 nto the same plasmid via the two loxP sites (phage P1 recombination sites), one located downstream fr
22 Two additional peptides, derived from the phage P1 RepA protein and the E. coli HemA protein, whic
23 ily of recombinases, Flp of yeast and Cre of phage P1, show the same intrinsic chirality as lambda In
24 roteins, human mitochondrial SSB (Hsmt SSB), phage P1 SSB, and F episome-encoded SSB, as well as a Hs
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