Anti-Cdc25A Anticorps (A29458)

GL331, a topoisomerase II inhibitor, has been found to trigger DNA damage response (DDR) to induce cell cycle arrest. However, the underlying mechanism has not yet been fully understood. This study investigated the molecular mechanism involved in the GL331-induced cell cycle arrest via DDR in human hepatocellular carcinoma HepG2 cells. As a result, GL331 could induce S arrest and up-regulate the phosphorylation of the histone H2AX variant (γ-H2AX). Ataxia telangiectasia mutated protein kinase (ATM) was activated by GL331 through its autophosphorylation at Ser1981, which led to the activation of DNA damage signaling pathways including p53/p21 and Chk2/Cdc25A cascades. The DNA damage cascades triggered by GL331 finally induced the inactivation of cyclin A/Cdk2 complexes to some extent. These phenomena could be reversed by ATM siRNA, followed by a partial disruption of S arrest. The present results suggested that the S arrest induced by GL331 via DDR was in an ATM-dependent manner to some degree.

Three forms of nano-trititanate (H(2)Ti(3)O(7) nanomaterial) were prepared by a hydrothermal method to replace nano-TiO(2) for sterilizing the environment. The bactericidal capabilities of these nano-trititanates were observed to be more significant compared to nano-TiO(2) both with and without exposure to UV light. For the future commercial applications of those nano-trititanates, we investigated their cytotoxicity and genotoxicity to HEp-2 cells. As data in our study shows, nanoplate, one of the nano-trititanates, possesses the lowest toxicity to HEp-2 cells. The results indicated that the shape and length of the material only affect the toxicity of nano-trititanate but not its bactericidal effect. Thus, through manipulating the shape or length of nano-trititanate, we may obtain a more powerful bactericidal reagent with lower toxicity to the human body.