Glucosamine-induced OGT activation mediates glucose production through cleaved Notch1 and FoxO1, which coordinately contributed to the regulation of maintenance of self-renewal in mouse embryonic stem cells.

@article{Jeon2014GlucosamineinducedOA,
  title={Glucosamine-induced OGT activation mediates glucose production through cleaved Notch1 and FoxO1, which coordinately contributed to the regulation of maintenance of self-renewal in mouse embryonic stem cells.},
  author={Ji Hoon Jeon and Han Na Suh and Mi Ok Kim and Jung Min Ryu and Ho Jae Han},
  journal={Stem cells and development},
  year={2014},
  volume={23 17},
  pages={
          2067-79
        }
}
We aimed to study the relationship between glucosamine and FoxO1/Notch in gluconeogenesis and maintenance of mouse embryonic stem cell (mESC) self-renewal. Glucosamine (GlcN) increased glucose production and gluconeogenic enzyme (G6Pase and PEPCK) expression. GlcN also increased the percentage of cells in S phase, number of cells, and the protein expression of cell cycle regulatory proteins that were blocked by 3-mercaptopicolinic acid (gluconeogenesis inhibitor) or glucose transporter (GLUT) 1… Expand
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Embryonic Stem Cell Proliferation Stimulated By Altered Anabolic Metabolism From Glucose Transporter 2-Transported Glucosamine
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Chemical Modulation of Protein O-GlcNAcylation via OGT Inhibition Promotes Human Neural Cell Differentiation.
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It is suggested that chemical inhibition of OGT and perturbation of protein O-GlcNAcylation accelerate the differentiation of hESCs along the neuronal lineage, thus providing further insight into the dynamic molecular mechanisms involved in neuronal development. Expand
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It is demonstrated that nutritional stress reproduced in colon cancer cells the effects obtained with OGT inhibition, which strongly suggests that stemness is regulated by HBP/O- GlcNAcylation nutrient sensing pathway, and that O-GlcNAc nutrient sensor represents an important survival mechanism in cancer cells under nutritional stressful conditions. Expand
O-Linked N-Acetylglucosamine (O-GlcNAc) Expression Levels Epigenetically Regulate Colon Cancer Tumorigenesis by Affecting the Cancer Stem Cell Compartment via Modulating Expression of Transcriptional Factor MYBL1*
TLDR
The aberrant CCSC compartment observed after modulating O-GlcNAc levels is likely to result, at least in part, from the epigenetic regulation of MYBL1 expression by O- GloverNAc, thereby significantly affecting tumor progression. Expand
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TLDR
It is demonstrated that glucosamine impedes Th1, Th2, and iTreg cells but promotes Th17 differentiation through down-regulating N-linked glycosylation of CD25 and subsequently inhibiting its downstream Stat5 signaling in a dose-dependent manner. Expand
Intracellular protein O-GlcNAc modification integrates nutrient status with transcriptional and metabolic regulation.
TLDR
It is established that increased expression of OGT and hyper-O-GlcNAcylation is common to human cancers of breast, prostate, colon, lung, and pancreas and attenuating OGT activity reduces tumor growth in vitro and metastasis in vivo. Expand
Role of O-linked N-acetylglucosamine (O-GlcNAc) modification of proteins in diabetic cardiovascular complications.
TLDR
An overview of the regulation of protein O-GlcNAcylation is provided followed by a discussion of potential mechanisms by which dysregulation in O- GlcNAc cycling contributes to the adverse effects of diabetes on the cardiovascular system. Expand
Diabetic Embryopathy Susceptibility in Mice Is Associated with Differential Dependence on Glucosamine and Modulation of High Glucose-Induced Oxidative Stress
TLDR
FVB embryos are more dependent on exogenous GlcN for glycosylation, but also for stimulation of the PPP and NADPH production, than are B6 embryos, thereby rendering FVB embryos more susceptible to high glucose to induce oxidative stress. Expand
Reprint of: Role of O-linked N-acetylglucosamine (O-GlcNAc) modification of proteins in diabetic cardiovascular complications.
TLDR
An overview of the regulation of protein O-GlcNAcylation is provided followed by a discussion of potential mechanisms by which dysregulation in O- GlcNAc cycling contributes to the adverse effects of diabetes on the cardiovascular system. Expand
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