In a signal to the other DNA repair enzymes such as DNA ligase III, DNA polymerase beta. IR is known to strongly stimulate the activity t of PARP to DNA-Sch To repair the. Sun mediated inhibition of PARP poly ation leads to inhibition of DNA repair. Blocking repair mediated PARP lead to apoptosis can also be very effective in combination with IR. Many small molecule inhibitors of PARP activity were t been developed as a potential chemo-and radiosensitizing agents. In fact, cell studies with PARP inhibitors has been shown that cells with a coverage factor radiosensitize mean dose of 1.4. Recently, a protein other than genes to be involved in apoptosis involved in the development of radioresistance in the cells. This is a redoxinducible and evolutionary conserved zinc finger protein, the cells RING redox agent-induced apoptosis protects. The anti-apoptotic function of SAG has been known to spread through the antioxidant activity of t through the Sunitinib 341031-54-7 metal of the free radicals and the bond-inhibiting ROS-induced cytochrome c release and caspase activation. In the study showed that SAG ROS production induced by IR stands, what to protect against cell death by apoptosis, and D Attenuation caused by SAG using antisense to an increased Hten apoptosis and sensitization of the PC 3, the cells of the prostate . The induction of apoptosis is one of the most desired of all anti-cancer strategy.
Most therapies are aimed at this way, but the development of radioresistance caused by overexpression of the fight against apoptotic factors and regulation of pro-apoptotic mediators are not welcome. Many agents have explored in this direction for their radiosensitizing function through modulation of apoptotic signaling pathways that have been discussed in the following sections. The investigation of molecular mechanisms of cancer development has been largely on the belief that cancer cells differ from normal cells in their Imiquimod genetic makeup and genetic aberrations are responsible for the Ver Changes in gene expression profile focus necessary for malignant transformation. Sp To ter studies have continued as it was found that Ver changes In chromatin, the change is not it, The tats Chliche sequence of the genetic material was also important, and k Nnte influence the gene expression profile of an individual. These changes were Ver Sp Ter than epigenetic changes Ver, All hereditary Ver Changes in chromatin that bring one Change in gene expression, but not contains a Change in the DNA sequence Lt underlying known . This inputted dinner chemical modifications of the DNA itself, such as DNA methylation or of proteins that are closely linked to the DNA, such as histones, which bind and the DNA packaging in a compact chromatin. Although epigenetic regulation of gene expression has long been known, but its R Has in the development of cancer in the past two decades, accelerated. Epigenetic Ver Modifications of the genome are much more dynamic and h Changes more frequently than mutations and other genetic Ver. The cells are st YOUR BIDDING Modify DNA and histones to Ver To regulate changes in gene expression. epigenetic occur Haupts chlich at the level of chromatin, the packaging the DNA VER changed and thereby on the transcriptional activity of t. Ground Tzlich this would mean.