The G2/ M checkpoint reaction is mediated by both p53 dependent and p53 independent procedure, both that determine the activation of Cdc2 cyclin B1. The p53 dependent and p53independent pathways are brought about by the kinases ATM and ATR, which act as sensors of DNA damage and co-ordinate the DNA damage response pathways. ATM and ATR activate numerous kinases, including the signal transducers Chk1 and Chk2 and can strengthen p53 by direct phosphorylation or indirectly through Chk1 or Chk2. Today’s study Afatinib molecular weight showed that the G2/M cycle arrest of osteoblasts due to treatment with 6 mM ATO wasn’t permanent and that, at the time of arrest, expression of the central aspects of the gate equipment, ATM and ATR, was increased. More over, expression of NBS1, through which ATM stimulates DNA repair, however not that of ATRIP, the ATR interaction element, was also increased. These data suggest that ATO induced DNA damage would generally be restored by an ATMdependent path. Because DNA PK, one of the PI3 Ks, and its DNA lesion interaction aspect, Ku 80, were not examined in this study, the possibility of the involvement within the osteoblast response to ATO therapy can’t be ignored. Phosphorylation of Chk1, Chk2, and p53 was increased by ATO therapy and was reduced by the presence of an ATM or ATR chemical. This implies that ATM mediates Chk2, Chk1, and p53 phosphorylation in ATO treated osteoblasts. p53 protein plays a critical role in controlling cell cycle progression Inguinal canal after DNA damage. The process by which it mediates cell cycle arrest in the G2 checkpoint requires transactivation of the cyclin dependent kinase inhibitor p21waf1/ cip1. In addition, p21waf1/cip1 could associate with the activated Tyr 15 dephosphorylated type of Cdc2, making it inactive, suggesting that p21waf1/cip1 might play a in Cdc2 inhibition and G2 arrest. It has been reported that p21waf1/ cip1 expression is seldom p53 independent, e. g. p21waf1/cip1 Flupirtine expression is blocked in cells from p53 knockout mice. However, p53 independent p21waf1/cip1 expression is induced in antioxidanttreated colorectal cancer cells. We imagine that p53dependent p21waf1/cip1 phrase might occur in ATO addressed 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 can’t be overlooked, as the effects of the ATM inhibitor on p53 phosphorylation and p21waf1/cip1 expression seem to be quantitatively different, with the former being influenced to a better degree.