Abstract: The present invention relates to novel Amido-Substituted Heterocycle Compounds of Formula (I): and pharmaceutically acceptable salts thereof, wherein R1, R2, R3, R4, and R5 are as defined herein. The present invention also relates to compositions comprising at least one Amido-Substituted Heterocycle Compounds for treating or preventing a herpesvirus infection in a patient.

Abstract: The present invention relates to novel Amido-Substituted Heterocycle Compounds of Formula (I): and pharmaceutically acceptable salts thereof, wherein R1, R2, R3, R4, R7, and R8 are as defined herein. The present invention also relates to compositions comprising at least one Amido-Substituted Heterocycle Compound, and methods of using the Amido-Substituted Heterocycle Compounds for treating or preventing a herpesvirus infection in a patient.

Abstract: Purified Ref polypeptides with increased nuclease site-specific targeting activity, recombinant nucleic acids and cells for expression of such Ref polypeptides, and methods for using the Ref polypeptides in combination with RecA protein and variants thereof to effect targeted nuclease cleavage of a DNA duplex are disclosed.

Abstract: Purified Ref polypeptides with increased nuclease site-specific targeting activity, recombinant nucleic acids and cells for expression of such Ref polypeptides, and methods for using the Ref polypeptides in combination with RecA protein and variants thereof to effect targeted nuclease cleavage of a DNA duplex are disclosed.

Abstract: A system and a method for DNA double-strand break repair in vitro are disclosed. Applications of the disclosed method in multiple areas are also disclosed.

Abstract: Kits and a method for cleaving double-stranded DNA using Ref and RecA protein and variants thereof at a site having a DNA sequence homologous to the sequence on a single-stranded DNA targeting fragment are disclosed.

Abstract: A system and a method for DNA double-strand break repair in vitro are disclosed. Applications of the disclosed method in multiple areas are also disclosed.

Abstract: A system and a method for DNA double-strand break repair in vitro are disclosed. Applications of the disclosed method in multiple areas are also disclosed.

Abstract: Kits and a method for cleaving double-stranded DNA using Ref and RecA protein and variants thereof at a site having a DNA sequence homologous to the sequence on a single-stranded DNA targeting fragment are disclosed.

Abstract: A system and a method for DNA double-strand break repair in vitro are disclosed. Applications of the disclosed method in multiple areas are also disclosed.

Abstract: A method of protecting the 3? end of a DNA molecule from nuclease damage is disclosed. In one embodiment, the method comprises the step of exposing the DNA molecule to a preparation of DdrA protein.

Abstract: A method of protecting the 3? end of a DNA molecule from nuclease damage is disclosed. In one embodiment, the method comprises the step of exposing the DNA molecule to a preparation of DdrA protein.

Abstract: The present invention provides RecA mutant proteins, having either a single mutation or a double mutation. The RecA mutant proteins are highly proficient in both SSB displacement and steady state binding of DNA in the presence or absence of SSB as compared to the wild-type protein. The single RecA mutant, RecA?C17, has 17 amino acid residues removed from the carboxyl terminus. The double mutant RecA, RecA?C17/E38K, combines the 17 amino acid residue C-terminal deletion of RecA?C17, with a single amino acid change from Glutamate to Lysine at position 38. These RecA mutant proteins are pH sensitive allowing control over formation of products. Hence, methods of using the novel RecA mutants and kits having the RecA mutants as components thereof are also contemplated by the present invention.

Abstract: The present invention provides RecA mutant proteins, having either a single mutation or a double mutation. The RecA mutant proteins are highly proficient in both SSB displacement and steady state binding of DNA in the presence or absence of SSB as compared to the wild-type protein. The single RecA mutant, RecA&Dgr;C 17, has 17 amino acid residues removed from the carboxyl terminus. The double mutant RecA, RecA&Dgr;C17/E38K, combines the 17 amino acid residue C-terminal deletion of RecA&Dgr;C17, with a single amino acid change from Glutamate to Lysine at position 38. These RecA mutant proteins are pH sensitive allowing control over formation of products. Hence, methods of using the novel RecA mutants and kits having the RecA mutants as components thereof are also contemplated by the present invention.

Abstract: A method of introducing exogenous cloned DNA into a bacterial chromosome of a bacteria in which the transposon Tn5 and the FLP recombinase are functional in vivo is disclosed. In one embodiment, the method comprises the steps of: (a) introducing FLP recombination target sites (FRTs) permanently at random locations in a bacterial chromosome using a plasmid vector that contains an FRT within a modified Tn5 transposon, two selectable markers, and a removable replication origin; (b) mapping the FRT introduced into the bacterial chromosome; (c) cloning exogenous DNA into a vector comprising two FRT sites, two selectable markers, and a removable replication origin; (d) removing the replication origin in the vector of step (c); (e) introducing the altered plasmid vector into bacterial cells, wherein the bacteria cells comprise a functional FLP recombinase; and (f) obtaining targeted integrants.