RAD1 polyclonal antibody

DNA damage or incomplete replication of DNA results in inhibition of cell cycle progression at the G1-S or G2-M checkpoints by conserved regulatory mechanisms. Rad17 is involved in regulation of cell cycle arrest at the G1 checkpoint, whereas Chk1, Rad1, Rad9 and Hus1 are involved in regulation of cell cycle arrest at the G2 checkpoint. Over- expression of Rad17 results in p53 activation and an accumulation of cells in G1 phase. Chk1 functions as an essential component in the G2 DNA damage checkpoint by phosphorylating Cdc25C in response to DNA damage, thus inhibiting mitosis. Hus1 and Rad9 exhibit conserved function in fission yeast and higher eukaryotes. Hus1 has been shown to be phosphorylated in response to DNA damage, a process which requires rad checkpoint genes. Rad9 is thought to be a candidate tumor sup-pressor gene because it is localized to a region of human chromosome 11 containing a number of tumor suppressor loci.