Abstract
Barrier-to-autointegration factor (BAF; encoded by BANF1) is a small highly conserved, ubiquitous and self-associating protein that coordinates with numerous binding partners to accomplish several key cellular processes. By interacting with double-stranded DNA, histones and various other nuclear proteins, including those enriched at the nuclear envelope, BAF appears to be essential for replicating cells to protect the genome and enable cell division. Cellular processes, such as innate immunity, post-mitotic nuclear reformation, repair of interphase nuclear envelope rupture, genomic regulation, and the DNA damage and repair response have all been shown to depend on BAF. This Review focuses on the regulation of the numerous interactions of BAF, which underlie the mechanisms by which BAF accomplishes its essential cellular functions. We will also discuss how perturbation of BAF function may contribute to human disease.