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By Ngu T. T. V.

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Many complex diseases are linked to various heritable dispositions like single nucleotide polymorphisms (SNP) or allelic translocations. Consequently they have become a main focus in modern biomedical research and have also started to raise public interest. Single nucleotide polymorphisms are common rather than exceptions. SNPs may determine the efficiency of gene transcription, gene translation or protein structure, leading to an altered amount of enzyme and/or enzyme activity, thus influencing further metabolic pathways.

For example, the MBD1 and a histone H3 methyltransferase enzyme (SetDB1) interact during the cell cycle, linking DNA methylation to rearrangement of chromatin by histone methylation [23]. Even if mechanisms for an active demethylation for DNA are not well understood [28], gene silencing by DNA methylation is reversible. For example, Il-4 expression in undifferentiated T cells is silenced via binding of MBD2 on the methylated promoter of the gene [29]. After differentiation, TH2 cells express the transcription factor GATA-3 which competes with MBD2 for binding to the IL-4 promoter.

I) DNMT3 enzymes themselves might recognize DNA or chromatin via their conserved PWWP (relatively well-conserved Pro-Trp-Trp-Pro residues, present in all eukaryotes) domain. (ii) By interaction of DNMTs with site-specific transcriptional repressor proteins DNMTs can be targeted to gene promoter regions. 1 DNA methylation pathway. DNA methylation mechanism. However, further efforts are needed to clarify these pathways [23]. DNMTs also seem to mediate gene silencing by modifying chromatin via protein–protein interactions.

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A bundle method for solving equilibrium problems by Ngu T. T. V.

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