Enzymes that remove amine groups from cytosine bases in DNA are likely involved in generating the clusters of mutations (kataegis) seen in breast cancer.

Systematic screen of HIV-1 Vif mutants identifies synthetic and naturally occurring amino acid polymorphisms separating PPP2R5 and APOBEC3 family protein depletion and uncovers the mechanism of Vif-dependent cell cycle arrest.

The antiviral and genomic DNA deaminase APOBEC3B is repressed in normal cells by PRC1.6/E2F6 and DREAM/E2F4 complexes and deregulation of this axis provides a unifying mechanism for overexpression in cancer.

Transcribed promoters are highly susceptible to mutation by cytidine deaminases, implicating stable exposure of single stranded DNA structures, rather than cofactors, in localising mutation during tumourigenesis and antibody maturation.

Combining in vitro and in vivo assays demonstrates that the cytidine deaminase APOBEC3A can inhibit LINE-1 retrotransposition by deaminating transiently exposed single-strand DNA that arises during the process of LINE-1 integration.

A comprehensive whole cell proteomic map describing expression time courses of >6,500 viral and cellular proteins during HIV infection identifies Vif-dependent antagonism of key cellular phosphatase PP2A.

The repair of spontaneous DNA damage can introduce mutators that lead to further genetic changes, which could underlie evolutionary change, disease and aging.

USP49 can increase A3G protein expression and enhance its anti-HIV-1 activity, which is also correlated with hypermutations and affects the HIV-1 latent reservoir.

A novel DNA/RNA modifying enzyme catalyzing a previously unknown 5-carbamoyloxymethylcytosine modification has been discovered using a novel framework called Metagenomics Genome-Phenome Association.

The birth of the antiviral gene APOBEC3B in ancient primates is linked to the evolution of a potent counterdefense by herpesviruses, a host-pathogen interaction maintained to present day.