International research team with the participation of the University of Stuttgart decodes the role of the DNA methyltransferases DNMT3A and DNMT3B [Picture: University of Stuttgart /Max Kovalenko]
International research team with the participation of the University of Stuttgart decodes the role of the DNA methyltransferases DNMT3A and DNMT3B [ Picture: University of Stuttgart /Max Kovalenko] The ICF syndrome is a genetic developmental disorder that, among other things, leads to an immune deficiency and therefore increases the susceptibility of those affected to other diseases. Pioneering genetic observations around 20 years ago showed that the key to this disease lies in inadequate activity of the DNMT3B enzyme. An international research team led by Prof. Albert Jeltsch from the Institute of Biochemistry and Technical Biochemistry (IBTB) at the University of Stuttgart has now been able to explain these relationships from a biochemical-molecular point of view. In the course of the evolution of higher organisms such as mammals, gene duplication often occurs. The resulting "twin genes" have a very similar genetic makeup, but are independent of each other and can therefore specialize in certain tasks. An example of this is DNA methylation, a chemical change in the basic building blocks of the genetic material of a cell, which is caused by the transfer of methyl groups by enzymes (DNA methyl transferases, DNMT) to certain locations in the DNA. The DNA-methyltransferases DNMT3A and DNMT3B are two forms of these enzymes in human cells that have arisen from gene duplication.
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