CCR-4, IL-2, IL-6, COX-2, cyclin D1, Bcl 2, Bcl xL, p53, STAT, MMP-9, vimentin, XIAP, survivin and AKT, NF-kB binding sites have in their promoters. IR has been reported that NF-kB, both in vitro and in vivo to activate. The mechanisms of IR-induced activation of NF-kB are not YOUR BIDDING clarified Rt. IR is known that the efficiency of DNA binding of NF-kB to erh Hen and erh ht Also the mRNA levels of NF-kB. Training of Bezirksschulr-run ataxia telangiectasia after irradiation and activated mutant PIDD that l St the degradation of IkB alpha and thus activates NF-kB. Another mechanism is secreted by TNF in response to radiation induced degradation of IkB mediated but the method is known, in particular at h Work higher doses of radiation. Yakovlev et al. shown a new mechanism that the IR can be used in the therapeutic dose range further comprises the NF-kB-activity t by a mechanism in which tyrosine 181 IkBa nitro is as a result of constitutive activation of nitric acid synthase oxidation showed, resulting in the dissociation of NF-kB IkBa intact. This mechanism does not seem to require IKK phosphorylation or dependent Ngigen proteolytic degradation of IkBa. In view of the r The pleiotropic NF-kB in cell proliferation and growth, many studies have examined whether the blockade of NF-kB signaling pathway Gemcitabine Gemzar sensitize k Nnte cells against radiation These studies on the duration of a decade created the R The NF-kB in acquired resistance of cancer cells against radiation. It has been found that NF kB for a Gro Part of radioresistance in a cell population of cells that is fractionated IR HK18 observed derived. Radioresistance was of active NF-kB by involving crosstalk with other signaling pathways confinement Lich EGFR, PK A and PI3K/AKT, which also conveys important intermediates in the development of radioresistance.
Downstream targets of NF kB for induction of resistant Ph Genotype are COX-2 which has been brought in mediating radioresistance in various tumor cells in context. The overexpression of COX-2 was found which was radioresistant tumors of the larynx and oral squamous cell, and the inhibition of COX-2 demonstrated that the effect of inducing the radiosensitization in the cells of lung cancer. NF-kB is known to activate the transcription of several genes suppress cell death involved both mitochondrial and death receptor pathways. One of these target proteins Is the cellular Ren FLICE like inhibitory protein. c FLIP is a high degree of homology shared with caspase-8, but has no protease activity t. It competes with caspase 8 for binding to the induction of the death signaling complex. Thereby preventing high c FLIP caspase 8 recruitment to the hard disk. Up regulation of c FLIP has been reported in many tumors. It is assumed that c expression can FLIP the Best RESISTANCE to apoptosis by death receptor in tumors induced explained Ren. However, requires a clear Gain Ndnis of the R The c-FLIP apoptosis in other studies. In most reports, inhibit FLIP c has described as the struggle against apoptosis has been, principally Chlich for their F Ability, apoptosis at high ectopic expression. Other than blocking the extrinsic pathway of apoptosis seems to flip, have a C r The separate as a mediator of proliferation induced by Fas.