Lines and contributes to radio-and chemoresistance. Inactivation of the ISP via antisense or RNA interference resulted in the sensitization of cells overexpressing IAP to radiation. Are the use of IAP inhibitors therapeutic potential in inhibiting or resistance to prostate cancer cells overcome and leads to growth inhibition shown. Therefore, k Can these compounds, which can be achieved by erh Seem to increase in apoptosis, acting as a radiosensitizer. Another protein that plays a role Significant radiationinduced apoptosis in the response is p53. It can prevent the formation and tumor progression through mechanisms dependent ZD6474 Zactima Ngigen and independent Ngigen transcription. Mechanisms of p53-dependent Independent transcription include the classical system of repression of genes by binding to the promoter region of the downstream targets of growth and apoptosis. These targets go More Ren pro apoptotic Bcl-2 such as Bax, Puma, Noxa, Bak and Bid. In addition, f Promotes apoptosis through transcriptional repression of antiapoptotic genes Bcl-2, Bcl xL and survivin. Wild-type p53 induces the synthesis of a p21/Waf, in the cellular growth arrest in G1 through Culminates re apoptotic regulatory mechanisms followed each. Recent studies on the r Of p53 in the induction of apoptosis, showed that p53 gene regulation by transcription was independent Independent and provide mechanisms. An earlier report, which induces the presence of nontranscriptional regulation of genes by p53 in apoptosis came from a study that showed a nuclear accumulation of p53 is not, according to apoptotic stimuli in a variety of experimental systems. It was suggested that when p53 accumulates in the cytosol it mediates cell death by a independent Independent transcriptional activity t of p53 as a BH3, which can bind to its mitochondrial translocation of Bcl-2, Bcl xL and Bak. It is also known to facilitate the expression of Fas on the cell Surface by the transport of the Golgi apparatus increased Ht has. Bim, another pro apoptotic Bcl-2 was shown to be activated by cytoplasmic p53.
Bim is determined by the anti-apoptotic, thereby preventing permeabilization of the U Eren membrane of the mitochondria isolated. p53 has been shown that Fluorouracil Bim is displaced from sequestration nts by inhibition of Bcl-2, Bcl xL, Mcl or 1. Although it is known that wild-type p53 usually sensitizes cells to radiation, mutations in p53 have been shown different effects on the radiation sensitivity. Show for over 50% of advanced tumors, a mutation in p53, it is important to understand and decipher, the R The p53-game, that in sensitizing cells to radiation, in its mutated state It is well documented that most mutations that inactivate p53 is known to occur in the DNA-binding sharing plans. Therefore, it is m Possible that tumors that have mutated p53, the F Ability to induce apoptosis in transcription not get the tie does not necessarily lead to promoters of target genes. Therefore, it is much more deeply into the consequences of p53 mutations in therapy-mediated IR. As a member of the street s base excision repair, poly-polymerase activity t module repair single-strand breaks in DNA. Once PARP detects an SSB, it binds to DNA, and after a structural Ver Change, begins the synthesis of a poly-cha.