The present invention refers to a fusion protein or a protein complex comprising a DNA binding protein (DnaBP), a nucleobase modifying protein (NMP), and a Base Excision Repair associated protein (BERAP. Also, described herein are a method of replacing a cytosine with a guanine on a DNA strand in a cell and a method of treating a subject having or suspected of having a disease or disorder.

The present disclosure features useful compositions and methods to treat trinucleotide repeat expansion disorders, e.g., in a subject in need thereof. In some aspects, the compositions and methods described herein are useful in the treatment of disorders associated with OGG1 activity.

A method for nucleic acid synthesis and regeneration of a reusable synthesis initiator includes incorporating a linking nucleotide to an immobilized initiator using a polymerase, synthesizing a nucleic acid right after the linking nucleotide using the polymerase, subjecting a substrate base of the linking nucleotide in the nucleic acid to base-excision by a DNA glycosylase to generate an abasic site, subjecting the abasic site to cleavage by an endonuclease to release the nucleic acid from the initiator, and converting the 3′ terminus of the initiator back to its original form by a 3′ phosphatase activity-possessing enzyme. A kit based on the aforesaid method and a method for regenerating a reusable initiator are also disclosed.

Provided herein are methods and compositions for highly precise base editing and single strand nicking. In particular, provided herein are methods for producing a genetically modified cell where the methods employ a universal, highly precise base editor or staggered Cas9 editor for precise base editing with minimal off-target or bystander effects.

Certain embodiments are directed to methods for treating a virus induced dysregulated inflammatory response in a subject in need of such treatment. The methods can include the administration a NEIL2 peptide or a composition comprising the NEIL2 peptide to the subject.

Provided is a gene editing system for editing a target sequence in the genome of a cell, comprising a CRISPR nuclease, a cytosine deaminase, an AP lyase, a guide RNA and optionally an uracil-DNA glycosylase. Also provided are a method of producing a genetically modified cell, and a kit comprising the gene editing system.

The present invention provides isolated peptides or the fragments derived from SEQ ID NO: 45, which bind to an HLA antigen and induce cytotoxic T lymphocytes (CTL). The peptides may include the above mentioned amino acid sequence with substitution deletion, or addition of one, two, or several amino acids sequences. The invention also provides pharmaceutical compositions including these peptides. The peptides of this invention can be used for diagnosing or treating cancer.

The present invention relates to a pharmaceutical composition for inhibiting cancer cell metastasis, the pharmaceutical composition including at least one of: (1) si-rpS3/203 binding to a 203.sup.rd base sequence of rpS3 mRNA; (2) si-rpS3/635 binding to a base sequence corresponding to a position 635 of the rpS3 mRNA; (3) si-rpS3/747 binding to a base sequence corresponding to a position 747 of the rpS3 mRNA; and (4) si-rpS3/766 binding to a base sequence corresponding to a position 766 of the rpS3 mRNA.

The invention relates to the identification of genetic signatures and expression profiles that are a part of the Base Excision Repair (BER) pathway, a major DNA repair pathway that modifies base lesions. In one embodiment, the present invention provides a method of determining responsiveness of treatment by BER inhibitors for malignant glioma by determining the presence of a low level of expression of Apex 1, a low level of expression of Apex 2, and a high level of expression of MPG.

Among other things, a method for performing multiple enzyme reactions in a single tube is provided. In some embodiments, the method may comprise producing a reaction mix comprising a thermolabile UDG, an AP lyase and DNA fragments that comprise one or more uracil residues, incubating the reaction mix at a relatively low temperature to cleave fragments at the one or more uracil residues, raising the temperature of the reaction mix to a relatively high temperature to inactivate the thermolabile UDG; and deaminating the fragments, thereby converting any cytosine in the fragments of DNA to uracil.