Nucleotide excision repair (NER) is one of the main cellular reaction to DNA damage, contribu- ting to genomic stability. NER is a major cellular pathway that removes bulky DNA adducts and helix- distorting lesions, such as the UV-induced photoproducts cyclobutane pyrimidine dimers and 6–4 pyri- midine photoproducts. The heterogeneity of NER seems to be governed by the functional compartmen- talization of chromatin into transcriptionally active and inactive domains as well as by functional role of sequences within genes.

DNA repair in mammalian cell

The infection caused by Helicobacter pylori is an important risk factor for gastric and duodenal ulcer. Infection with the bacterium causes a disturbance in the structure and function of cells of the gastric mucosa which may be the beginning of a number of pathological processes, including neoplastic transformation. Infection is associated with the development of chronic inflammation of the gastric epithelial cells of the microorganism caused by adaptation to the environment, defined by the chemical structure and specificity of the bacterial adhesins, the enzymatic activity of H.

DNA triplex can be formed by interaction of double-stranded sequence-specific single-stranded DNA oligonucleotides called TFO. There are many potential uses triple-stranded structures induction strategies for these molecules. They allow specific blocking sequence replication, and regulation of gene expression by inhibiting transcription. Particularly promising, due to the potential for use in gene therapy is the ability to introduce mutations TFO into the genomic DNA, and the induction of homologous recombination.

Philadelphia chromosome (Ph) is the result of a chromosomal translocation leads to malignant transformation of hematopoietic cells . The reason is oncogenic tyrosine kinase activity of the BCR / ABL fusion gene resulting from following the transfer of a fragment of chromosome 9 to chromosome 22 [ t ( 9 , 22 )] . There is a whole family of tyrosine kinases fusion ( FTKs ) related to BCR / ABL , such as the TEL / ABL , TEL/JAK2 , TEL / TRKC (L) , TEL / PDGFâR and NPM / ALK , which induce both acute and chronic myelogenous leukemias and lymphomas.