DNA Repair

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.

DNA repair protein RAD50 is a component of the MRN complex (Mre11-RAD50-Nbs1) responsible for DNA double strand break (DSB) repair.

Dnmt1 belongs to the C5-methyltransferase family that repairs cytosines in dsDNA using a nucleophilic attack mechanism. Dnmt1 is the most abundant mammalian DNA methyltransferase. It is the key methylation maintenance enzyme for both DNA replication/repair and de novo methylation during somatic cell development and differentiation.

Ataxia Telangiectasia Mutated (ATM) is a serine/threonine protein kinase that is the master regulator of the DNA double-strand break (DSB) repair pathway. ATM is a key part of the cell cycle machinery that activates checkpoint signaling in response to DSBs, apoptosis, and genotoxic insults. ATM normally exists in its inactive state as a dimer or tetramer - upon DNA damage, it dissociates into monomers triggered by its own autophosphorylation.

Apurinic/apyrimidinic (AP) endonuclease 1 (APE1) plays an important role in the DNA base excision repair pathway.

NBS1 (Nijmegen breakage syndrome protein 1) is a component of the MRN complex (Mre11-Rad50-Nbs1) that plays important role in detecting DNA double strand breaks (DSBs) and triggering the downstream cascade. DSBs can be caused by ionizing radiation, chemotherapy drugs, metabolic ROS, replication errors, programmed enzymatic activities during meiosis/V(D)J recombination, etc.

APE1 is involved in repairing oxidative DNA damages in vitro, regulates the redox of transcriptional factors, repairs AP sites in DNA, and is important for embryonic development in mice. Learn more about APE1 in our infographic below.

Novus Biologicals offers APE1 reagents for your research needs including:

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).

Fanconi anemia (FANC) is a heterogenous, autosomal-recessive cancer susceptibility genetic disorder that is characterized by a wide array of symptoms, including congenital defects, progressive bone marrow failure due to DNA-damage hypersensitivity, chromosomal instability, and poor DNA repair. The protein FANCD2 is involved in mediating cellular resistance to DNA cross-linking and DNA synthesis arrest that is triggered by ionizing radiation (IR).