Protein XXXX --structure, function, and possible therapeutic implications.

@entity1 @entity5 @entity876 @entity272 @entity105
Cell cycle is driven by a number of positive and negative regulatory phosphorylation and dephosphorylation events that ultimately influence the activity of transcription factors. Normal skin architecture depends on the regulation mechanisms of cell proliferation and differentiation and on apoptosis. Complex interaction of different factors in the regulation of these mechanisms, aimed at maintaining constant desquamation, is often changed in @entity272 . The main difference between normal cells and @entity5 cells results from discrete changes in specific genes important for cell proliferation control mechanisms and tissue homeostasis. These genes are mainly proto-oncogenes or @entity5 -suppressor genes, and their mutation could play a role in cell hyperproliferation and @entity105 . Tumor-suppressor genes normally function as a physiological barrier against clonal expansion or mutation accumulation in the genome. They also control and arrest growth of the cells that hyperproliferate due to oncogene activity. Alteration or DNA damage in @entity5 -suppressor genes and oncogenes are considered key events in @entity1 @entity105 . Tumor-suppressor protein @entity876 is an important transcription factor, which plays a central role in the cell cycle regulation mechanisms and cell proliferation control, and its inactivation is considered a key event in @entity1 @entity105 . The role of @entity876 protein in the cell cycle, high proportion of @entity5 with mutated @entity876 gene, and accumulation of significant amount of knowledge on molecular biology of this protein make this molecule especially attractive for development of new therapeutic approaches. Main strategies for development of new antineoplastic therapies are based on "wild-type" @entity876 protein acting as a @entity5 suppressor, selective apoptosis inductor, and a protein able to arrest cell cycle.
