الفهرس 
INTROOUCTION AND AIM OF THE WORKOnly 14 pages are availabe for public view
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Abstract
The tumor suppressor gene P53 was discovered at 1979 and forming 16 -20 k-b on the short arm ofchromosome-17 at locus 13.1 (17 Pi3). This gene contains 11 exons producing its mRNA that is translated into P53 protein. The P53 protein is a nuclear phosphoprotein of393 amino- acids and structilraUy of 53 k.d., but functionally has 3 domians, acidic domian responsible for its phosphorylation (stabilization), DNA binding domian that combines with the DNA at specific sequences and basic domain signalling for nuclear localization. The P53 protein acts normally as a guardian of the cell genome controlling the cell cycle being antiproliferative, induces both cell differentiation and apoptosis, also P53 induces DNA renaturation and strand transfer in the stressed cell, moreover, it induces transcription activation of apoptotic genes and transcription repression of oncogenes. . The mechanisms of P53 protein inactivation include mutation of P53 gene, interaction with viral or cellular proteins and cytoplasmic exclusion. Different P53 mutation are identified but the hot spot mutation predominate and that mutant forms may have transdominant function, loss of function or gain of neo function. So, research on P53 protein is at fever pitch and in the past couple of years it has become clear that inactivation of its tumor suppressor activity is an utmost universal step in the development of human cancers.