Title : Glucose-regulated phosphorylation of TET2 by AMPK reveals a pathway linking diabetes to cancer.

Pub. Date : 2018 Jul

PMID : 30022161






4 Functional Relationships(s)
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1 We identify the tumour suppressor TET2 as a substrate of the AMP-activated kinase (AMPK), which phosphorylates TET2 at serine 99, thereby stabilizing the tumour suppressor. Serine protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens
2 We identify the tumour suppressor TET2 as a substrate of the AMP-activated kinase (AMPK), which phosphorylates TET2 at serine 99, thereby stabilizing the tumour suppressor. Serine protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens
3 Increased glucose levels impede AMPK-mediated phosphorylation at serine 99, which results in the destabilization of TET2 followed by dysregulation of both 5-hydroxymethylcytosine (5hmC) and the tumour suppressive function of TET2 in vitro and in vivo. Serine protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens
4 Treatment with the anti-diabetic drug metformin protects AMPK-mediated phosphorylation of serine 99, thereby increasing TET2 stability and 5hmC levels. Serine protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens