The phenomenon of apoptosis, programming cell death, repeatedly became the cause of heated arguments in the scientific circles. In is not surprising, as its importance for life and functioning of cell and organism in the whole is difficult to overstate. Apoptosis plays significant role in the processes which are connected with development of cancer cells and formation of cancerous growth. It is significant to add, that Nobel price in medicine was given for discovery of this phenomenon in 2002. The great amount of all kinds of researches is connected with apoptosis, but nevertheless a lot of unsolved problems remain for researchers. It is quite explainable, because many factors influence the processes connected with apoptosis anyhow and it is difficult to understand this phenomenon in one sight.

Antiapoptosis could be considered as one of the processes connected with programming cell death but it has not got proper attention until recently. It is known that there is the system in the cell which is responsible for apoptosis prevention. It works permanently and it is possible to say that one of the stages of apoptotic response is antoapoptosis inhibition. In any words, cell is balancing all the time between apoptotic and antiapoptotic regimen of functioning. In dependence on the process which has managed to overweight, cell will live or will not. The weights for this balance are great number of various extracellular and intracellular factors and effectors, which take part in these processes. In this connection it is possible to say that apoptosis and their antagonist are different sides of one phenomenon.

The researchers dealing with such problem confront in increasing frequency with duality of phenomenon of programming cell death and pay more and more attention to the antiapoptosic pathways. For example, in some cells it has not managed to start apoptosis without switching off the process-antagonist. Antiapoptosis in cancer cells should not be ignored as well, because thanks to it cancerous growths obtain the immunity to drugs.

Basing on considerable amount of experimental data accumulated in this question, we have started the kinetic model development of the main from the pathways of antiapoptotical signal transmission – activation of NFkB-dependent genes transcription. This project allows receiving the power instrument for estimation of impact various intra- and extracellular factors in the apoptosis/antiapoptosis processes. Moreover, by means of that it is possible to reveal the number of unsolved problem, existing in the understanding of these processes up to now.

The response of organism on the changing of environment conditions reveals in the increasing or decreasing of synthesis of certain proteins. Usually such regulation happens on the level of genes and realizes by special molecules – transcriptional factors. One of such molecules is NFkB (nuclear factor kappa B), which plays central role in the cell immune response during various inflammatory process, during cell reaction in the response of several stress action (heat shock, irradiation, action of heavy metals, etc.), and stimulates processes which prevents apoptosis. NFkB binds with promoters of more than 120 various genes, activating the synthesis of corresponding proteins.

NFkB usually presents in cell as a complex with its inhibitor IkB (inhibitor of kappa B). In such binding state NFkB is inactive and do not influence gene expression. Activation of NFkB happens under the influence of definite signal molecules which come through blood to the various cells of the organisms and interact with special cell receptors. As a result of such interaction the cascade of reaction start leading to degradation of inhibitor IkB and formation of free NFkB which are able to bind with DNA. One of genes whose expression NFkB increases, coding IkB. In that way, during NkB activation the synthesis of its inhibitor (IkB) increases together with other protein, that lead to NFkB and IkB binding and formation of inactive complex. As a result of NFkB return in the inactive state the oversythesis of proteins does not happen. It is one of the great numbers of various method of active (free) NFkB regulation in cell.

At present time in the framework of research the role of NFkB in various metabolic pathways, one of the main signal pathways of NFkB activation being induced by TNF (tumor necrosis factor) molecule is investigated. The common scheme of this signal pathway is presented on the figure. On the basis of literary and experimental data the kinetic model of signal pathway have been developed. The model describes reactions which are going in the cell after interaction of TNF with special TNF receptor and are leading to the NFkB activation and increase of expression of NFkB-dependent genes. The main task of this work is to develop the kinetic model of TNF-induced signal pathway of NFkB activation in according to data being observed in the experiment and to analyse this model with aim to reveal the reactions and metabolites whish play key role in the regulation of signal pathway being into consideration.