Publications by authors named "Yuka Matsuyama"
The chitinolytic bacterium, Chitiniphilus shinanonensis SAY3 was examined to characterize its chitin-degrading enzymes in view of its potential to convert biomass chitin into useful saccharides. A survey of the whole-genome sequence revealed 49 putative genes encoding polypeptides that are thought to be related to chitin degradation. Based on an analysis of the relative quantity of each transcript and an assay for chitin-degrading activity of recombinant proteins, a chitin degradation system driven by 19 chitinolytic enzymes was proposed.
View Article and Find Full Text PDFPeroxiredoxin is an abundant peroxidase, but its non-peroxidase function is also important. In this study, we discovered that Tsa1, a major peroxiredoxin of budding yeast cells, is required for the efficient flux of gluconeogenesis. We found that the suppression of pyruvate kinase (Pyk1) via the interaction with Tsa1 contributes in part to gluconeogenic enhancement.
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- Liver-specific knockout of Nrf1 in mice leads to the development of nonalcoholic steatohepatitis, characterized by significant lipid accumulation in the liver and altered fatty acid composition.
- Inducing Nrf1 knockout with 3-methylcholanthrene results in increased levels of glutathione and upregulation of the xCT antiporter gene, suggesting a complex role for Nrf1 in regulating antioxidant defenses.
- Nrf1's regulatory function is critical in managing both fatty acid metabolism and the balance of cysteine content in liver cells, indicating its involvement in a larger stress response mechanism.
Nrf1 (NF-E2-related factor 1) is a basic region leucine zipper-type transcription factor belonging to the CNC (cap-'n'-collar) family. Major pathophysiological contribution of Nrf1 remains unclear. As single nucleotide polymorphism rs3764400 in 5'-flanking region of NRF1 gene appears to associate with obesity, in this study, we focused on the Nrf1 function on metabolism.
View Article and Find Full Text PDFGiant cell tumors of bone (GCTB) are benign and locally destructive tumors that include osteoclast-type multinuclear giant cells. No available treatment is definitively effective in curing GCTB, especially in surgically unresectable cases. Isocitrate dehydrogenase (IDH) mutations have been reported not only in gliomas and acute myeloid leukemias, but also in cartilaginous tumors and osteosarcomas.
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