A research group led by Assistant Professor Keiichi Izumikawa and Professor Nobuhiro Takahashi of Tokyo University of Agriculture and Technology, and Specially Appointed Professor Toshiaki Isobe of Tokyo University of Agriculture and Technology has analyzed the latest mass analysis of the complex formed by the binding of RNA to a protein called CHTOP, which is involved in RNA metabolism abnormalities. Analysis by the method revealed that CHTOP regulates the expression level by degrading messenger RNA. It can be said that the onset mechanism has been elucidated because the increase in CHTOP promotes the formation of malignant brain tumors.
According to Tokyo University of Agriculture and Technology and Tokyo Metropolitan University, CHTOP is known as a protein involved in the formation of malignant brain tumors and the regulation of hereditary anemia. It was found that the intracellular concentration is regulated by degrading the messenger RNA to which CHTOP is bound.In normal cells, the amount of CHTOP is kept constant by this mechanism, but in malignant brain tumors, this is thought to be broken, and the amount of CHTOP is abnormally increased to promote proliferation.
The research team believes that the elucidation of the mechanism of CHTOP expression regulation has paved the way for the treatment of malignant brain tumors by developing a drug that inhibits expression.Furthermore, it is expected that this discovery will lead to the development of therapeutic agents for hereditary anemia.Hereditary anemia is a potentially fatal disease, partly due to mutations in the hemoglobin gene that carries oxygen in the blood.
Human hemoglobin is made from different genes in the fetal and adult.It is known that even if there is an abnormality in the gene that works in the adult, the gene that works in the fetal period is normal, and when CHTOP increases the expression level during the growth process, the gene that works in the fetal period is converted into the gene that works in the adult. There is.If this mechanism is used to make genes in the fetal period produce normal hemoglobin, treatment will be possible.
