Formed by arachidonic acid or other unsaturated fa y acids Tetrahydroberberine following free Benzoylpaeoniflorin radicals a ack, can bind to proteins by Michael addition, with preferential amino acidic binding sites to cysteine, hystidine or lysine residues. Therefore, 4-HNE protein adducts could be considered a reliable OS markers and have a biological impact on protein function. In this regard, the amino acid sequence of the human beta-actin shows several potential 4-HNE binding sites on all the major conformational subdomains of the protein. 
A total of 6 C, 8 H and 19 K residues are present in the sequence, and potential 4-HNE binding amino acid residues are present in all the relevant conformational subdomains of the protein, for a total of 2 C, 4 H and 7 K in the subdomain 1, a total of 1 H and 3 K in the subdomain 2, a total of 2 C, 2 H and 5 K in the subdomain 3, and a total of 3 C and 4 K in the subdomain 4. In particular, the subdomain 2 of the molecule is of critical importance for DNAase 1 binding and protein polymerization, while a very crucial C 374 residue and potential binding site for 4-HNE is present in the conformationally critical hydrophobic pocket of the molecule. Our findings indicate that the observed reduction in beta-actin band intensity is independent of the employed monoclonal antibodies and are compatible with a real decrease in the betaactin expression in the R patients erythrocytes membrane. Moreover, the reported evidence exhaustively addresses the question of whether the observed decrease in beta-actin protein expression might be related to oxidative PTMs potentially preventing antibody recognition. Taken together, our data indicate that major alterations exist in the beta-actin of R erythrocytes which results both from changes in expression and as a consequence of oxidative damage. To this regard, beta-actin is a well-known major target for OS processes, while erythrocytes represent ����cellular detectors���� revealing the co-existence of major cytoskeletal changes in this key genetic model for neurodevelopmental disorders. In particular, this work suggests a novel role for MeCP2 as a stabilizing protein in microtubule dynamics. To date, no definitive cure for R exists, although several approaches to a potential therapy have been either a empted or hypothesized, including activation of the silenced Mecp2 gene, gene therapy, modulation of some of the downstream effects from MeCP2-deficiency. Our study indicates that a proteomic approach in R is able to reveal additional downstream effects of the MECP2-deficiency, and therefore could identify potentially novel therapeutical targets for the disease. The four serotypes of dengue virus cause the most important arthropod-borne viral disease of humans. DENV infection results in a range of clinical outcomes ranging from the milder dengue fever to the potentially life threatening dengue haemorrhagic fever/dengue shock syndrome. A recent study estimates that up to 390 million people are infected with DENV annually, making dengue a serious global public-health problem. Despite much effort, there are neither vaccines nor antiviral therapies in clinical use to prevent or treat dengue, and our understanding of dengue pathogenesis is still limited. DENV is a member of the Flavivirus genus of the Flaviviridae family and has a RNA genome of,11 kb in size.