53BP1

The p53-binding protein 1 (53BP1) is a DNA damage response factor, which is recruited to nuclear structures at the site of DNA damage.  DNA double-strand breaks (DSBs) are mutations that are detrimental to cell viability and genome stability, and must be repaired either through homologous recombination (HR) or non-homologous end joining (NHEJ). 53BP1 specifically promotes both NHEJ as well as the inhibition of HR repair, yet the decision making on a molecular level between these two routes not clearly understood.

53BP1 (p53 binding protein 1) was originally thought to be an enhancer for p53 transcriptional, but later studies have demonstrated that it is actually a substrate for ataxia telangiectasia mutated (ATM). 53BP1 is a classic late DNA damage response (DDR) marker that is present during the cell cycle phases of telophase and cytokinesis (within mitotic mammalian cells).

The 53BP1 (p53 binding protein 1) was initially believed to be a p53 transcriptional enhancing partner, but it has now been established as an ataxia telangiectasia mutated (ATM) substrate. As a late DNA damage response (DDR) marker, 53BP1 appears during the telophase and cytokinesis phase of mitotic mammalian cells¹.

53BP1 (p53 binding protein 1) was originally thought to be a p53 transcriptional enhancing partner, but now has been shown to be an ataxia telangiectasia mutated (ATM) substrate. It is a late DNA damage response (DDR) marker, appearing in the telophase/cytokinesis phase in mitotic mammalian cells (1).

53BP1 (p53 binding protein 1) was originally thought to be a p53 transcriptional enhancing partner, but now has been shown to be an ataxia telangiectasia mutated (ATM) substrate. It is a late DNA damage response (DDR) marker, appearing in the telophase/cytokinesis phase in mitotic mammalian cells (1).

Mediating DNA damage is a crucial process, and one of the most important cellular guards against cancer. In response to DNA damage, sophisticated cellular machinery is recruited to repair the breaks, and if it fails, the cell is committed to death.

Our antibody database at Novus Biologicals provides research tools for the forefront of cancer research. Recently, a mouse study using 53BP1 and BRCA1 antibodies showed that deletion of 53BP1 greatly lessened the incidence of tumor development in mice carrying the mutated BRCA1 gene.