ATR, also named as FRP1, belongs to the PI3/PI4-kinase family and ATM subfamily. ATR is a serine/threonine protein kinase which activates checkpoint signaling upon genotoxic stresses such as ionizing radiation (IR), ultraviolet light (UV), or DNA replication stalling, thereby acting as a DNA damage sensor. ATR recognizes the substrate consensus sequence [ST]-Q. ATR phosphorylates BRCA1, CHEK1, MCM2, RAD17, RPA2, SMC1 and TP53/p53, which collectively inhibit DNA replication and mitosis and promote DNA repair, recombination and apoptosis. ATR phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at sites of DNA damage, thereby regulating DNA damage response mechanism. It is required for FANCD2 ubiquitination. It is critical for maintenance of fragile site stability and efficient regulation of centrosome duplication. ATR catalyze the reaction: ATP + a protein = ADP + a phosphoprotein. Defects in ATR are a cause of Seckel syndrome type 1 (SCKL1) which is a rare autosomal recessive disorder characterized by growth retardation, microcephaly with mental retardation, and a characteristic 'bird-headed' facial appearance. The antibody can recognize all the isoforms of ATR.