The G2/ M checkpoint response is mediated by both p53 dependent and p53 independent process, both of which regulate the activation of Cdc2 cyclin B1. The p53 dependent and p53independent pathways are set off by the kinases ATM and ATR, which act as sensors of DNA damage and coordinate the DNA damage response pathways. ATM and ATR stimulate numerous kinases, including the signal transducers Chk1 and Chk2 and may secure p53 by immediate phosphorylation or indirectly through Chk1 or Chk2. Today’s study price A66 showed that the G2/M phase arrest of osteoblasts caused by treatment with 6 mM ATO wasn’t permanent and that, at the time of arrest, appearance of the central aspects of the equipment, ATR and ATM, was increased. More over, appearance of NBS1, whereby ATM initiates DNA repair, however not that of ATRIP, the ATR discussion issue, was also increased. These data show that ATO induced DNA damage could generally be fixed by an ATMdependent pathway. Since DNA PK, one of the PI3 Ks, and its DNA lesion conversation factor, Ku 80, weren’t examined in this study, the likelihood of these participation in the osteoblast response to ATO treatment cannot be overlooked. Phosphorylation of Chk1, Chk2, and p53 was increased by ATO therapy and was paid down by the existence of an ATM or ATR inhibitor. This suggests that ATM mediates Chk2, Chk1, and p53 phosphorylation in ATO treated osteoblasts. p53 protein plays a critical role in controlling cell cycle progression Lymph node after DNA damage. The process by which it mediates cell cycle arrest at the G2 checkpoint involves transactivation of the cyclin dependent kinase inhibitor p21waf1/ cip1. Moreover, p21waf1/cip1 may connect with the activated Tyr 15 dephosphorylated kind of Cdc2, rendering it inactive, revealing that p21waf1/cip1 may play a in Cdc2 inhibition and G2 arrest. It has been noted that p21waf1/ cip1 expression is rarely p53 independent, e. g. p21waf1/cip1 AP26113 expression is blocked in cells from p53 knockout mice. However, p53 independent p21waf1/cip1 expression is induced in antioxidanttreated colorectal cancer cells. We suppose that p53dependent p21waf1/cip1 expression may possibly occur in ATO treated osteoblasts, because our results showed that, after p21waf1/cip1 upregulation was attenuated when phosphorylated p53 levels were paid off by an ATM chemical and that ATO therapy, osteoblasts showed elevated levels of active/phosphorylated p53 and of p21waf1/cip1. However, p53 independent p21waf1/cip1 expression cannot be overlooked, since the effects of the ATM chemical on p53 phosphorylation and expression appear to be quantitatively different, together with the former being affected to a better degree.