Keiko Kato

TL;DR: It is shown that a large bowel microbial fermentation product, butyrate, induces the differentiation of colonic Treg cells in mice and ameliorated the development of colitis induced by adoptive transfer of CD4+ CD45RBhi T cells in Rag1−/− mice.

TL;DR: It is shown that metabolic reprogramming of colorectal cancer is caused chiefly by aberrant MYC expression, and inhibition of MYC target pyrimidine synthesis genes such as CAD, UMPS, and CTPS blocked cell growth, and thus are potential targets for coloreCTal cancer therapy.

TL;DR: Evidence is provided that succination, resulting from FH deficiency, targets and potentially alters the function of multiple proteins and may contribute to the dysregulated metabolism observed in HLRCC.

TL;DR: It is concluded that glutaminolysis is activated in gliomas with IDH1-R132H mutation and that development of novel therapeutic approaches targeting activated glutaminosynthesis is warranted.

TL;DR: It is demonstrated that FH1-deficient cells and tissues exhibit defects in the urea cycle/arginine metabolism, and the importance of extramitochondrial metabolic pathways in FH-associated oncogenesis and the Urea Cycle/argInine metabolism as a potential therapeutic target is highlighted.