Publications by authors named "Keita Nagaoka"
Dynamic kinetic resolution (DKR) of unprotected amino acids (AAs), via intermediate formation of Ni(II) complexes, is currently a leading methodology for preparation of natural and tailor-made AAs in enantiomerically pure form. In this work, we conduct a comparative case study of synthetic performance of four different ligands in DKR of six AAs representing aryl-, benzyl-, alkyl-, and long alkyl-type derivatives. The results of this study allow for rational selection of ligand/AA type to develop a practical procedure for preparation of target enantiomerically pure AAs.
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- The study investigates the impact of knocking out the cystine transporter xCT on ferroptosis in mouse embryonic fibroblasts and the mechanisms that support macrophage survival despite this deficiency.
- Proteomic analysis revealed that levels of carnosine dipeptidase II (CNDP2) increased significantly in xCT KO macrophages, enhancing their ability to break down cysteinylglycine, which contributes to cell survival.
- When tested in CNDP2 KO mice, an acetaminophen overdose led to severe liver and kidney damage, indicating that CNDP2 plays a critical role in protecting these organs from oxidative stress and ferroptosis-related cell death.
γ-Glutamylpeptides are largely produced via the action of γ-glutamylcysteine synthetase or γ-glutamyltransferase (GGT). GGT transfers the γ-glutamyl moiety from glutathione (GSH) and other γ-glutamyl compounds to amino acids, peptides, or water. A conventional GGT assay employs a synthetic donor substrate, which facilitates monitoring cleavage activity by means of colorimetric analyses but provides no information on the resulting γ-glutamylpeptides.
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- - ASK1 is a kinase that responds to oxidative stress and is regulated by several molecules and modifications, but the details of this regulation are not well understood.
- - The study found that TRIM48 plays a key role in controlling ASK1 activation in response to oxidative stress by promoting the degradation of PRMT1, which normally inhibits ASK1.
- - TRIM48's influence on ASK1 can affect cell death; its knockdown reduces ASK1 activation and cell death, while increasing TRIM48 levels can enhance cancer cell death in experimental models.